Remarkable T2 Diabetes Reversal: From VLC to Starches and Resistant Starch

You gotta see this. Diagnosed T2, with diabetic ketoacidosis and blood glucose of 680 and afterward, readings around 200+. Tried controlling with very low carbohydrate, got down to fasting readings of 140, but then worse and worse as time went on.

Here’s what happened when she added resistant starch and later, 100-200 grams daily of starchy carbohydrates.

Michelle // Feb 12, 2014 at 19:58

I have what might seem a silly question. Is a (non insulin or diabetes drug-using) person still technically a T2 diabetic if they eat a few of tbs of potato starch a day, prepare their starches to maximize RS, along side eating mostly Perfect Health Diet-style (plus beans and occasionally bread) for a few months and their blood glucose reading goes from difficult to keep under 200 to under 100 almost all the time? That’s me.

I was following VLC for a few months after being diagnosed this last summer as a T2 with great results at first, diminishing with each subsequent month. I had no signs of diabetes blood-work wise in previous years. I got sick and keeled over from diabetic ketoacidosis, in August. My BG was 680 at the time.

This last fall, all I had to do is look at carbs for BG to spike. Even with VLC, I was having more and more trouble with the dawn phenomenon, waking up with BG of 180+ every day. It got to where I was only able to eat a few fat bombs a day to keep my BG under 140, and I started looking for answers. Found FTA in November and ran with the starch. Huzzah for the starch!

I started upping my carbs two months into my personal n=1 PS experiment that started in November and now eat between 100-200 grams of carbs (tho I’ve had days where I ate up to 600) and my blood glucose per my meter is great. I ate a mound of Richard’s garlic fried rice with a steak and green beans tonight, and my BG before: 95, to one hour after: 110. Two hours, down to 90. It seems like the more carbs I eat the lower my reading goes.

I am very gratified, and wonder: am I really still diabetic? I imagine “yes” if I go back to SAD. I just don’t know.


She posted some some follow-on info below that linked comment. Pretty amazing story. I think it really, once again, calls into question everything about very low carb, even for T2 diabetics, at minimum. Perhaps not applicable to T1s, since they’re not producing insulin at all.

Starchy food for thought? I wonder if any other T2s will give this a try. But remember her protocol. She stayed VLC for 2 months wile on the potato starch, then transitioned to a Perfect Health Diet-style of between 100g and 200g daily. Plus, she’s eating clean: starches from white rice, potatoes and beans. Don’t try this with gluten grains and sugar water. I’d also suggest that once you ramp up your RS over a couple of months to 2-3 TBS per day, that you add in the starches slowly (discount non-starch vegetable carbs), like perhaps 50g additional per week, spread between all of your meals.

Update: Lots more background info at these comments below, here and here.

Update 2: In case you may happen to run across a schizophrenic, bipolar, OCB female who laughingly pretends she knows more than everyone else put together, is so ignorant about resistant starch that she thinks she “get[s] a lot” (direct quote) from her corn wraps, and asserts that type 2 diabetics don’t present with ketoacidosis: Diabetic Ketoacidosis in Type 2 Diabetics: A Novel Presentation of Pancreatic Adenocarcinoma.

Richard Nikoley

I'm Richard Nikoley. Free The Animal began in 2003 and as of 2021, contains 5,000 posts. I blog what I wish...from health, diet, and food to travel and lifestyle; to politics, social antagonism, expat-living location and time independent—while you sleep—income. I celebrate the audacity and hubris to live by your own exclusive authority and take your own chances. Read More


  1. MrPotatoStarchHead on February 13, 2014 at 07:32

    How much protein was she eating on VLC?

  2. AJ on February 13, 2014 at 08:27

    Great story.
    Would be helpful to know how much PS she is using?
    Would be helpful to know when she takes it, all at once or spread out through the day?
    I’m happy for her.

    For me as a Type II and taking 4Tbs of PS a day(twice a day) for 2 months, my blood sugars remain high and even higher with Rice & Bean. Fasting glucose remains unchanged unfortunately. Sleep is noticeably better though.

    Wondering if I should take the 4Tbs all at once.
    I do know my gut health is compromised and is a work in progress to heal which may be leading to the minimal results on my blood glucose.

    Thanks for the continuing series on RS Richard.


    • Richard Nikoley on February 13, 2014 at 08:55

      AJ, I believe she said 3 TBS.

      What I would suggest is a slow ramp up, maybe 1/2 C of rice per meal. You might need to “exercise” with light weights before going to 2 C heavyweight in a single meal. You might ask Paul on the PHD site what he thinks.

      Or, it just might be something that doesn’t work for you.

      Another idea is that you do this same thing but maybe first with beans, then with potatoes, then with rice, so you can see which starch works best for you.

    • AJ on February 13, 2014 at 09:45

      Thanks for the recommendations.
      Luckily the tinkering process and individual adaption of this is the part I love.

    • Pone on February 20, 2014 at 22:08

      AJ, how much exercise do you do? On days when my glucose does go out of control, a one hour postmeal glucose can be reduced about 30 points just by a 30 minute walk. Two 30 minute walks during a day can make a huge difference.

    • Joyce Barron on September 6, 2015 at 19:33

      Have you ever tried an Indian herb named holy basil or tulsi? I learned about it when my husband was having a hard time with the dawn phenomenon and looked into its properties. It has a chemical compound that increases gaba. I have narcolepsy and am familiar with xyrem being used for this purpose. I have tried it for both him and me and it’s helping with fragmentation of sleep and vivid dreams as well

  3. Julie on February 13, 2014 at 09:02

    Hope this isn’t off-topic but I’ve just started Chris Kresser’s 30-day ‘Paleo Reset’ diet in which he says that people with a possible autoimmune disease (like me) shouldn’t eat white potatoes. I’ve been taking potato starch for the last month (no effects yet) and wondered if I should switch to another source of RS.

    I live in the UK, which is a further complication – we don’t seem to have plantain flour, tapioca flour and so on easily available.

    Has anyone in the UK (or Europe) found a non-potato RS product?

    Richard and Tim – I expect you’ve already thought of this but in your book it would be great if you could include product info for those of us outside the US (perhaps by crowdsourcing it via your blog).

  4. Michelle on February 13, 2014 at 09:04

    I got to where I could hardly eat protein on VLC without BG spiking. I tried to stick to 3 oz of any kind of meat at any meal, and ate cheese/dairy. Like i said in my comments, I ended up eating 3 or 4 fat bombs a day and nothing else in a desperate attempt to control BG, so near the beginning of the N=1 experiment I was eating very little.
    I take 4 -6 tbs starch a day over the average. I don’t take the same amount each time, I vary it like Richard suggested. I’ll take 2 tbs with milk, water or kefir and slug it down, or mix a couple of tbs in yogurt and eat it for a treat. I take the second two, or whatever amount, in the evening in a bit of water before bed. Got rid of horrific heart burn doing that. My husband and adult daughter are on the starch now as well. Too soon to say anything about results but they don’t have the health challenges I’ve had.

    I worked my way up to the larger amount of PS over the first month and was seeing small changes in my BG but not enough to really say it was working well. When I read in multiple comments that there’s hardly any response when in ketosis, I decided it was time to start adding carbs. I started with beans, as I discovered quickly potatoes and rice would send BG spiking up. Once I adjusted to eating *properly prepared for RS* beans, I started adding in rice *UB parboiled, prepared for RS*. It took a couple of weeks to adjust. After I stopped spiking over rice, I added potatoes. I figure out what I am going to eat for the whole day, then break up my percentages of protein, carb and fat per PHD amounts, then eat that in two or three meals. I seem to have gravitated towards an 18/6 eating pattern without consciously attempting it. I don’t start getting hungry until 10 or after, so eat my first meal when I get hungry, usually close to noon. I don’t eat after 6 pm as I am not anxious to tempt the heartburn into coming back.

    I am still not touching fruit or sugar. I plan on trying strawberries and in-season fruit this spring, seeing if I can readapt to them the same way I have with starches. I don’t know if it will work but I am willing to try.

    It is not a perfect curve; I still get the odd spike, especially in the morning. But overall, my BG is remaining in “normal” range 95% of the time. I am warm, I am starting to get some lovely fuzz on my forehead where the hair is starting to grow again, I am sleeping all night for the first time in my adult life and I feel REALLY good, physically and mentally. The starch calm high is amazing.

    • Pone on February 20, 2014 at 22:13

      For me, so far, the raw potato starch has improved sleep and stool volume. But I feel it has made my blood glucose control worse not better.

      I don’t have enough data yet to make positive statements or quantify. Some of these data points could change as my gut evolves. I’ve backed down my dose to one or two tablespoons each night until I get a better handle on the impact of starch on my blood glucose.

  5. Michelle on February 13, 2014 at 09:15

    For those curious, I am female, turned 47 in January. I am tall and fat as a house and starting to move from sedentary to ambulatory now that I feel human again. No regular exercise pattern other than keeping an eye toward MovNat type jumping around and walking the dogs. I have abused my body with the worst kind of yoyo dieting since I was age 6, including a failed 4 year experiment with a lap band that almost killed me by cutting my stomach open. Thank goodness it’s gone. I am amazed I am still alive with all the foolishness I have committed.

    Sorry I am blah blahing about myself so much but I am trying to add any datapoints that are useful in pinning down why this is working.
    Oh yeah, the cons:

    At times, the fartage is unreal. for me it seems to be linked with how much carbs I have consumed. The higher the carbs, the greater the fartage. Dark beer is the WORST for fartage. I love the stuff but I can clear a house with the gas afterward. At some point I am going to have to do something to make adjustments.

    PS is a hunger crusher. I find I am bored with food in a way I’ve never been, even on VLC. I mean BORED.

    Also, other dietary additions that started in January: daily dosing with Vit D drops, weekly dosing of Vit B complex drops, one K2 capsule a day, and Vit E when I can remember it.

    • Charles on February 13, 2014 at 16:32

      I think the PS fixes the gut biome which fixes satiety signaling. In my case that’s been dramatic. I don’t have too many cravings, and I’ve really learned to ignore them after doing this for 40+ years. It was mostly out of self-defense. I was a fat kid and very carb sensitive. I never wanted to be fat again, and I wanted to have energy and good health. So I trained myself to eat right, consciously. After five months on potato starch, I don’t crave anything much anymore. I enjoy food, but the background of dietary discipline that I’ve built up over four decades no longer seems necessary. It’s a hell of a lot easier to make good choices.

  6. Resurgent on February 13, 2014 at 09:25

    “I think it really, once again, calls into question everything about very low carb, even for T2 diabetics, at minimum. Perhaps not applicable to T1s, since they’re not producing insulin at all.”

    Richard – I would wait till a T1 person tries this and reports the results. Our ‘health’ is a condition heavily modulated by our gut biome. We are still scratching the surface.

    • Charles on February 13, 2014 at 16:33

      T1’s have tried this and have reported results, and they have been able to reduce insulin.

  7. Paul Jaminet on February 13, 2014 at 10:37
  8. Kim on February 13, 2014 at 12:08

    I am a T2 diabetic and am currently taking 500 mg ER of Metformin x 4 per day. Since I started eating vlc, probably ketogenic, my fasting blood sugar is under 100 (usually in the high 90s) and when testing before dinner, I have had some readings around 88. I may try the RS protocol and then try to ramp up my carb intake and see what happens. I really want to get off the metformin as it causes unpleasant side effects for me. I have some potato starch at home already. I know that my gut is not working great as any time I eat vegetables or fruit (like the little bit of apple in chicken/apple sausage), it sends me to the bathroom. I do have low thryroid and also am on blood pressure meds. My doctor told me my thyroid wasn’t low because of a low carb diet but because since I am so overweight and have the diabetes, that it’s probably affecting my thyroid right now.

    • Pone on February 20, 2014 at 22:16

      One THIRD of all people of European descent have fructose malabsorption. You can confirm it with a hydrogen breath test, and these tend to only be offered through labs of major hospitals or universities with hospitals.

      I wouldn’t assume that a compromised gut accounts for the problems with fructose.

  9. rs711 on February 13, 2014 at 12:26

    I’m glad you’re feeling better Michelle, kudos on your continued efforts!

    Did you every measure your urine, breath or blood ketones when trying to VLC?
    What kind of milk were you drinking? Whole? skimmed? pasteurized? UHT? (same Q for the yoghurt)
    When you mention fat bombs – what kind of fat was it? Poly 3 &/or 6? Mono? Sat?
    Did you eat veggies?
    Were you taking those supplements you mentioned while VLCing &/or after adding in some PS? What about when you switched to the recommended PHD ratios of 30/30/40?

    Sorry for all the questions but I’m trying to understand your case more exactly – on the surface it seems to be a curious result.

    All the best!

  10. Michelle on February 13, 2014 at 13:01

    I used ketostix to check and see if I was in ketosis. Purple as all get out. Interestingly, I lost absolutely no weight, after the big drop just before the DK episode. I did gain 10 pounds in January, adding carbs. I’ve lost a few of those this month but I am not attempting to diet beyond working on keeping the PHD ratios.

    I drink one teaspoon of whole milk in tea, plus maybe 1/4 cup with the PS. I can’t stand low fat milk. I use heavy whipping cream in coffee, one tsp per cup, 2 cups daily. That uses up almost all the fat I have in a day. Butter is about the only other fat I use. If I eat the PS in yogurt, I eat a scant 1/4 cup of full fat plain greek yogurt.

    I made fat bombs from coconut oil, cream cheese, sometimes unsalted butter, occasionally cocoa powder or 85% dark chocolate. When I was eating fat bombs I ate them exclusively as it seemed like my BG would spike when I ate any food :/ I was eating a small amount of salad and green or nonstarchy veg during the beginning of VLC. I eat veggies now, in the form of small salads, or a side veg, plus the occasional bite of jarred kimchee from the store.

    I started taking the supps approximately the same time I started the PHD, on Jan. 1.

    I hope this helps. I don’t mind questions; it helps me to think carefully about what I’ve one with this N=1. If the data is useful, I am glad.

  11. Michelle on February 13, 2014 at 13:05

    To adjust a poorly worded comment: the heavy whipping cream uses up all the extra added fat I will have during the day, over the top of butter in cooking, fat in the meat and dairy I eat. The majority of the fat I eat comes from butter for cooking, although I will use coconut oil if I have it *and can afford it:)*

  12. Jane Karlsson on February 14, 2014 at 07:07

    Richard, I think you need to talk to Paul Jaminet about white rice. He said in 2011 ‘We like white rice, but if evidence showed it to be unhealthy we’d be equally quick to stop eating it.’ This evidence is now available, in a 2012 study from China showing an association between white rice and diabetes.

    White rice has had nearly all its magnesium removed. Magnesium deficiency has been linked to diabetes in many human and animal studies.

    • SteveRN on February 14, 2014 at 11:27

      I don’t think that means it is unhealthy, just that you don’t get any magnesium from it. Lots is foods are missing some nutrients but are still healthy. That’s why you have a variety of foods you should eat, to cover all your bases. Personally, I think mag is so important and so depleted from the soil that I supplement it heavily, Almost next to impossible get enough via food.

    • DuckDodgers on February 14, 2014 at 11:35


      That study certainly doesn’t show that rice causes diabetes. All it shows is that rice causes an increase in blood sugar (duh).

      Paul Jaminet already addressed these poorly designed studies here:

      In a country, increase in any carb consumption (i.e. in China, that just happens to be rice) correlates with a greater chance of being diagnosed with diabetes. That doesn’t necessarily mean that rice or carbs cause diabetes. It just means that increasing carb consumption makes the symptoms of diabetes more visible.

      In any case, in that link, Jaminet shows quite convincingly that the countries that tend to eat the most white rice also tend to have the lowest incidence of diabetes.

    • Pone on February 20, 2014 at 22:27

      Jane, that is a pretty horrible study. First, they are comparing rice, against more rice, against even more rice. It’s difficult to evaluate rice against other starches when you don’t make any comparison.

      Second, they don’t control for other factors in the diet. The person who ate >400 grams of white rice might also be more likely to down seven sodas and eat huge bowls of fruit and lots of grains. That person is a walking war chest of metabolic syndrome precursors. How do we place any blame on rice there?

      Rice is the key starch used in most long-lived asian geographies. I think Paul has it right.

    • Jane Karlsson on February 21, 2014 at 04:48

      Pone, the study does that. Look at Table 3 and you will see that as rice intake goes up, flour intake goes down. In the north they eat wheat and in the south they eat rice. Table 3 also shows that as rice intake goes up, so does vegetable intake.

      If you take the work of this group as a whole, what they seem to have shown is that white flour makes you fat and diabetic, and white rice makes you thin and diabetic. We are often told white rice is OK because the Japanese are thin. Actually they have more diabetes than we do.

    • DuckDodgers on February 21, 2014 at 20:21


      The Japanese study clearly implicates “recent” changes for the growth in Japanese diabetes. Since rice has been around for thousands of years, it’s an unlikely culprit.

      Sounds like you are grasping for straws to demonize rice for some reason — as if one or two studies could really pinpoint rice as being a sole cause for diabetes. Fact of the matter is that your hypothesis doesn’t account for the countries that eat the most white rice and have the lowest incidence of diabetes:

    • Pone on February 21, 2014 at 21:21

      To me the most obvious evidence is that when you take Japanese on their traditional diets and bring them to the West, their disease progression – including diabetes – occurs as they shift from the traditional diet to Western processed food diets and grains.

      To me the research Jane quotes is a very very bad study design. They do not control for many other things, and the fact that people at the high end of rice consumption consume “less grains” doesn’t really address the fact that these people are consuming LOTS of UNSAFE STARCH, in addition to the rice. All bets off once you cross that line and start eating large quantities of processed and unsafe starch. They are loaded with Omega-6 in processed foods, imbalanced against Omega-3, etc, lots of irritation and autoimmune triggers from proteins in grains, etc etc.

      What I do believe is that if you eat processed foods, toxic grains, and get substantially large amounts of caloric intake from carbohydrates (say >40%), then probably additional carb intake will provoke glucose control problems. In that case you are forcing the body to deal with excess glucose intake, and it really doesn’t matter where you get that excess glucose from. Rice is just a placeholder but it could be any kind of starch and if you overeat calories and carbs, you are at extra risk of diabetes.

    • Jane Karlsson on February 22, 2014 at 04:20

      Please read the comment I just posted to Pone. White rice has had nearly all its magnesium and most of its manganese removed. The starch cannot be metabolised without these metals. Eating it without them is going to cause diabetes in susceptible people.

      I have biology degrees from Oxford and Cambridge, and I have spent 30 years studying the biomedical literature full time. I was fortunate enough to inherit money so I could do this. No academic institution will fund someone who wants to read the literature.

    • Richard Nikoley on February 22, 2014 at 07:44


      Any info on the Mg and Mn content of parboiled vs. plain white rice? Googling around, appears to be higher. I did a post on parboiled rice, not sure if you saw it.

      At any rate, the previous point I made still stands.

      1. Even in the PHD diet, rice is not a staple and it’s to be consumed with protein and veggies.

      2. Paul also has storage organs, so even at 30% carbs total, maybe you’re looking 15-20% from rice.

      3. If you add legumes (garbanzos high in Mn, I see), you get more Mg and Mn, and reduce rice load even further.

      I really don’t understand why you keep beating this drum, as though someone is advocating white rice as a 60% staple or something.

    • gabriella kadar on February 22, 2014 at 08:03

      Duckie, it looks like it’s not the rice. More like overeating in general, lots of abdominal fat, and in those countries where diabetes is now skyrocketing, low lean muscle mass.

      The BMI is adjusted for those societies where lean muscle mass is low. In India, a BMI of 25 is considered to be obese.!po=2.50000

      They have skinny legs and arms but marshmallow tummies.

    • DuckDodgers on February 22, 2014 at 11:06

      Jane, That’s all very interesting, but I think you’re going to need to do better than that in terms of presenting evidence. I’m sure you can find a few papers that show deficiencies can exacerbate insulin issues, but that still doesn’t explain why the countries that consume the most white rice have the lowest incidence of diabetes. Vietnam, Bangladesh, Myanmar, Indonesia, Cambodia, etc. those countries consume the most white rice but have the lowest incidence of diabetes. If anything, those countries show that white rice consumption is protective of diabetes.

      Now, you can continue to ignore that paradox, or you can address it here.

      And, as Richard pointed out, nobody here is advocating making rice a staple. We all eat a variety of carbs.

    • Pone on February 22, 2014 at 16:02

      Wow, Jane, you would be my dream girl being able to spend a lot of time reading science, and then not have the pressure of publication or commercial job. And if you were Taylor Swift, then I could spend another one third of my time writing poetry and song lyrics.

      Ah, the dream. 🙂

    • Jane Karlsson on February 23, 2014 at 04:00

      Yes I saw your post on parboiled rice. As you say, the Mg content is not improved.

      I don’t understand why you keep beating this drum. Brown rice is delicious.

    • Jane Karlsson on February 23, 2014 at 04:03

      I’m doing something wrong here. I wanted to reply to Richard and my post ended up somewhere else.

    • Jane Karlsson on February 23, 2014 at 04:58

      White rice may appear to be protective because white flour is worse. In many countries white flour is ‘fortified’ with iron. Diabetes is linked to iron overload. Some scientists are trying to argue iron fortification is counter productive but no-one is listening.

      Why do you think people eat too much? Guyenet’s group has found brain damage in obese people, in the satiety centre of the hypothalamus. The damage appears to be due to oxidative stress. The most important antioxidant enzyme is MnSOD, a manganese enzyme.

    • gabriella kadar on February 23, 2014 at 05:05

      Jane, I bought germinated brown rice a while back because it’s supposed to have GABA. I’m not doing it anymore because it came out my backside looking exactly like it went in the front. Waste of money as far as I can tell. I’m not going to chew every mouthful 50 times. I don’t need to wear down my teeth. When I made an effort to chew it more often, the ‘end product’ was somewhat less ‘ricey’ but still indicated poor digestion of product.

      I get my magnesium from coconut water, Epsom salt baths, and the occasional 200 mg tablet. 1 litre of coconut water = 200+ mg of magnesium. The potassium can’t hurt either. Calories are not really an issue approx. 200 kcal per 1 litre. I don’t eat peanut butter which apparently is a good source of magnesium.

      I buy the huge containers of Epsom salt from Costco. Keep two containers and decant the salt into the empty one, fill with water, so that I add solution to the bath, not crystals. My tender bum doesn’t like sitting on salt crystals. Full body soak for 20 to 30 minutes.

    • DuckDodgers on February 23, 2014 at 06:07


      Brown rice tastes like ass, and as I’m sure you’re aware, has a good amount of toxins and antinutrients:

      From Rice in human nutrition:

      Antinutrition factors in the rice grain are concentrated in the bran fraction (embryo and aleurone layer). They include phytin (phytate), trypsin inhibitor, oryzacystatin and haemagglutinin-lectin. All except oryzacystatin have been previously reviewed (Juliano, 1985b).

      All the antinutrition factors are proteins and all except phytin (phytate) are subject to heat denaturation. Phytin is located in 1 – to 3-µm globoids in the aleurone and embryo protein bodies as the potassium magnesium salt. Its phosphate groups can readily complex with cations such as calcium, zinc and iron and with protein. It is heat stable and is responsible for the observed poorer mineral balance of subjects fed brown rice diets in comparison to that of subjects fed milled rice diets (Miyoshi et al., 1987a, 1987b).

      Trypsin inhibitor has also been isolated from rice bran and characterized (Juliano, 1985b). The partially purified inhibitor is stable at acidic and neutral pH and retained more than 50 percent of its activity after 30 minutes of incubation at 90°C at pH 2 and 7. Steaming rice bran for 6 minutes at 100°C inactivates the trypsin inhibitor, but dry heating at 100°C for up to 30 minutes is not as effective. The inhibitor distribution is 85 to 95 percent in the embryo, 5 to 10 percent in germ-free bran and none in milled rice.

      Haemagglutinins (lectins) are globulins that agglutinate mammalian red blood cells and precipitate glycoconjugates or polysaccharides. The toxicity of lectins stems from their ability to bind specific carbohydrate receptor sites on the intestinal mucosal cells and to interfere with the absorption of nutrients across the intestinal wall. Rice-bran lectin binds specifically to 2-acetamido-2-deoxy-Dglucose (Poole, 1989). It is stable for 2 hours at 75°C but sharply loses activity after 30 minutes at 80°C or 2 minutes at 100°C (Ory, Bog-Hansen and Mod, 1981). Rice lectin agglutinates human A, B and O group erythrocytes. It is located in the embryo but has receptors in both rice embryo and endosperm (Miao and Tang, 1986).

      Oryzacystatin is a proteinaceous (globulin) cysteine proteinase inhibitor (cystatin) from rice seed and is probably the first well-defined cystatin superfamily member of plant origin (Kondo, Abe and Arai, 1989). Incubation at pH 7 for 30 minutes at 100°C had no effect on its activity but inhibition decreased IS percent at 110°C and 45 percent at 120°C. Oryzacystatin effectively inhibited cysteine proteinases such as papain, ficin, chymopapain and cathepsin C and had no effect on serine proteinases (trypsin, chymotrypsin and subtilisin) or carboxyl proteinase (pepsin).

      An allergenic protein in rice grain, causing rice-associated atopic dermatitis in Japan, is an a-globulin and shows stable immunoreactivity (60 percent) even on heating for 60 minutes at 100°C (Matsuda et al., 1988). It is present mainly in milled rice rather than in the bran. Hypoallergenic rice grains may be prepared by incubating milled rice in actinase to hydrolyse globulins in the presence of a surfactant at an alkaline pH (Watanabe et al., 1990a) and washing. The color of the processed grain is improved by treatment with 0.5-N hydrochloric acid and washing with water (Watanabe et al., 1990b).

      Brown rice has a lot of negative aspects. White rice is fairly benign in the context of a balanced diet and within the context of fatty and fibrous meals.

      And honestly, nobody here plans on getting their “nutrition” from white rice. We are all well aware that it is a nutritionless food. We all find our minerals elsewhere.

    • gabriella kadar on February 23, 2014 at 06:15

      Duckie, maybe that’s why I don’t process the stuff at all. I thought that germinated brown rice would be easier but no. It does taste way better than the regular brown rice. It’s expensive.

    • DuckDodgers on February 23, 2014 at 06:33

      White rice may appear to be protective because white flour is worse. In many countries white flour is ‘fortified’ with iron. Diabetes is linked to iron overload. Some scientists are trying to argue iron fortification is counter productive but no-one is listening.

      Then that would simply implicate iron as a major cause of diabetes, not rice. You’re still ignoring the fact that the countries that consume the most white rice have the lowest incidence of diabetes because it simply goes against your hypothesis.

    • gabriella kadar on February 23, 2014 at 06:51

      Duckie, it’s an n=1, but one of my employees who lives on an Indian Hindu style diet (with small amounts of limited species animal meat) has literally free-based roti and rice all of her adult life. She is iron anemic (low hgb and low ferritin). We’ve checked for Thalassemia trait. Negative. We’ve tested folic acid and B12 = high normal. Her HgbA1c is in the pre-diabetic range. I guess it’s not the iron. Iron pills don’t work. They are not absorbed. So unless she eats lots of lamb/goat liver lamb/goat meat, she won’t improve her status. She seems to have trouble absorbing minerals, including zinc.

      What she does have is chronically inadequate dietary protein. Split peas just don’t cut it. This eating plan is entirely suboptimal.

      Unfortunately, regardless of what she learns at work, the traditional marriage and male dominated home means that the husband can ‘not allow’ changes which may improve health status. His hair has all fallen out too. You’d think, eh?

    • DuckDodgers on February 23, 2014 at 07:10



    • gabriella kadar on February 23, 2014 at 07:37

      Duckie, yikes is right.

      She’s kinda balding on top too. I don’t think it’s ‘male pattern baldness’ in a woman. Ever since, I’ve been paying attention when I’m out and about. I live in the most ethnically diverse ‘riding’ in Canada. What I see is Muslim women don’t have this balding phenomenon. But it’s relatively common with Hindu women. I don’t think the genetics is all that different between the two groups.

      I think also that protein malnutrition causes digestion difficulties. Possibly this is the reason that mineral absorption is poor. They get early menopause due to primary ovarian failure. Early menopause does not auger well for chronic disease like diabetes, heart disease etc. Correlation.

    • Richard Nikoley on February 23, 2014 at 12:37

      “free-based roti and rice all of her adult life”

      If I were Indian, I’d free-base naan with basmati rice, alongside copious rogan josh and butter chicken. 🙂

    • Richard Nikoley on February 23, 2014 at 12:59

      “Brown rice tastes like ass”

      I have a nephew and one of the first complex dots he connected to form a metaphorical sentence was after he smelled something, looked up to his mom and said: “It smells like butt.”

    • gabriella kadar on February 23, 2014 at 13:06

      Aye Richard, there’s the rub: those other dishes you mention are not current with the Hindu pantheon of recipes. Them thars Muslim recipes.

      These people eat maybe 1 ounce of meat when they eat it. Vegetables are merely a garnish. Mostly it’s roti, rice and little bits of greenery (unripe papaya, guar beans, shit, shit, shit and more shit, (sorry).) It’s been a big eye opener for moi. You can save a lot of money this way. You may drop dead of heart attack, stroke, and diabetes before age 50 but you do save a lot of money.

    • Richard Nikoley on February 23, 2014 at 14:35

      For many years, I had a Pakistani (Wasim) as my single in-house CRM software developer. He has 2 kids still in Pakistan and went there at least once per year and brought them over at least once per year.

      He always told me when I talked of how I love Indian food, “find a Pakistani restaurant.” Now I know, but at the time asked the difference.


      He was a very lean and healthy looking man, young for his years, always (drank no alcohol, either). He could fast like crazy. One time, he was at the office working on the database for well over a day straight when we were closed down for the Xmas Holidays, and was there so long he called on my cell, just to ask if he could maybe have an apple he saw in the refrigerator. 🙂

      I closed my company down almost a year ago, but just prior, I got a call from him. He sounded awful, weak. He’d just come out of a 3-month coma. he was attending a family wedding in LA, tripped and fell down a flight of stairs. Didn’t know if he’d make it and wanted to give me the passwords to get to everything in terms of the front-end code.

      I told him: “Wasim, eat lots of meat.” “I know,” he replied.

      A few months later I began getting calls from companies, as Wasim uses me a a reference when seeking new clients.

      He’s well into his 60s, looks late 40s.

      I’m such a pathetic little pussy sucker for happy endings.

    • gabriella kadar on February 23, 2014 at 15:42

      Cripes. Amazing he remembered to look up the passwords, wherever he’d had them stashed.

      Most of the cooks in Indian restaurants are from Bangladesh. Around here the Pakistanis drive taxis.

    • Richard Nikoley on February 23, 2014 at 20:03

      Oh, no mystery. Very meticulous man. It came out in the software he wrote for us, his art.

    • Richard Nikoley on February 23, 2014 at 20:08

      ….I should add that in the space from ’02 to maybe ‘o8’ he made better than an half million working from home from me, 90% of the time.

    • Jane Karlsson on February 24, 2014 at 02:49

      All the antinutrition factors in rice can be broken down by gut enzymes, so if you find brown rice indigestible it’s because these enzymes aren’t working too well. Some of them need metal cofactors (see ‘Activation of intestinal peptidases by manganese’), and the one that breaks down phytic acid comes from gut bacteria.

      I believe the reason brown rice doesn’t qualify as ‘safe starch’ is because of the phytic acid? Actually phytic acid has been found to improve copper absorption.
      This could be very important, because getting enough copper nowadays is difficult.

    • DuckDodgers on February 24, 2014 at 04:27


      Can you provide evidence that Oryzacystatin is “broken down by gut enzymes”? How about Trypsin inhibitor and haemagglutinin-lectin?

      I’m not sure how you can convince anyone considering the observed poorer mineral balance of subjects fed brown rice diets in comparison to that of subjects fed milled rice diets (Miyoshi et al., 1987a, 1987b).

    • Jane Karlsson on February 25, 2014 at 02:41

      I don’t understand your question about rice proteins. Are you doubting that your gut has enzymes which break down proteins, any proteins? Or that some of them require cofactors which have been removed from white rice?

      I have seen one of the two Miyoshi papers, and the experiment was short term. The subjects had 14 days on white rice and 8 days on brown rice. Gut bacteria need time to adjust. Here is a paper showing that people accustomed to a diet high in phytic acid can break down nearly 90% of it.
      Nobody doubts that phytic acid can inhibit mineral absorption. It really isn’t a big deal. Your body adjusts to lower mineral availability by upregulating absorption and downregulating excretion. Phytic acid only causes problems in people eating a very deficient diet.

    • Jane Karlsson on February 25, 2014 at 03:20

      Yes it does look like iron is a major cause of diabetes. Most studies implicate iron from meat. Perhaps the countries that eat the most white rice eat the least meat, I haven’t looked them up to find out. Perhaps you could do it?

    • DuckDodgers on February 25, 2014 at 04:39


      Oryzacyststin is an inhibitor of protein-digesting enzymes. It’s not a good thing. That’s why they call it an “anti-nutrient.”

    • DuckDodgers on February 25, 2014 at 06:19

      Perhaps the countries that eat the most white rice eat the least meat, I haven’t looked them up to find out. Perhaps you could do it?

      I don’t have the time to devote to this like you do 🙂 but glancing at this I don’t see any correlations. For instance, some of the countries that have the most incidence of diabetes (Egypt, Bosnia, Jamaica, Saudi Arabia, Latvia, Jordan, Armenia, Fiji, Nicaragua, Samoa) seem to have moderate to low intakes of meat consumption per capita. On the other hand, there are some countries with high meat consumption and high incidence of diabetes (US, Bahamas, Spain). And then there are some countries with low meat consumption and low diabetes. But Bangladesh has some of the lowest meat consumption in the world and Myanmar, while low, eats 3x as much meat as Bangladesh and yet Bangladesh has much more diabetes than Myanmar.

      Anyway, I don’t see a significant correlation at first glance, And don’t have the time to investigate it.

      And furthermore, you aren’t going to solve this by just looking at one or two foods. For all we know, diabetes is caused by something gut related and is just more easily diagnosed with increased consumption of any carb.

    • gabriella kadar on February 25, 2014 at 06:42

      Duckie, there are a number of type 2 diabetes/gut microbiome studies which correlate low or no bifidobacteria and lactobacillus fecal analysis. Plus there are also supposedly some pathogens found. The resistant starch, PS, feeds these bacteria. Other plant fibres do too.

      India, for example:
      Br J Nutr. 2009 Feb;101(4):465-73. doi: 10.1017/S0007114508073649.
      A high dietary intake of fat has been reported in Asian Indians(9,10). Fat consumption ranged from 13 to 59 g/d in different regions and states in India. Further, individuals in rural areas in India consume lower (17 %) energy intake from dietary fat as compared with urban residents (22 %)(11). Yagalla et al.(10) have reported a higher average energy intake from total fat (32 %) in migrant Asian Indians in the USA. Further, vegetarian migrant Asian Indians had higher values of BMI than non-vegetarians due to an increased intake of high-fat dairy products… Many studies in rural populations in India(57), including a subset of rural pregnant women(58), have shown a poor intake of fruits and vegetables. Even in migrant Asian Indians or South Asians,fibre intake has been reported to be low, particularly in vegetarians; however, it varied by region of origin in India and dietary profile of the migrants from India and other South Asian countries(59).

    • gabriella kadar on February 25, 2014 at 06:49

      Duck, I’ve noticed this here. Rice, roti, noodles are the primary source of calories. Lots of sugar in chai and there’s all sorts of super high sugar content Indian sweets. Vegetables are more like a garnish than an actual significant part of a meal. Lots of fried stuff based on ground pulses. Lots of ‘vegetable oil’ aka soybean oil because it’s very cheap.

      The BMI for this group is not the same as for Europeans. They have very low lean muscle mass, so BMI 25 is obese.

    • DuckDodgers on February 25, 2014 at 06:56

      Very interesting, gab!

    • Jane Karlsson on February 25, 2014 at 06:59

      The proteins you eat get denatured in your stomach acid. Oryzacystatin is supposed to repel insects, not humans. Insects don’t have acid stomachs.

    • DuckDodgers on February 25, 2014 at 11:38

      Ah, my mistake. I see the GMO-researchers have cleared all cystatins for safety. 🙂

      Anyway, as we keep telling you. Nobody here eats rice as a staple. Everyone gets plenty of manganese from a variety of foods.

    • Jane Karlsson on February 26, 2014 at 02:26

      Yes I should have done it and I’m glad you did. So it isn’t meat. Perhaps it’s fat. Saturated fat increases iron absorption and inhibits manganese absorption.

    • DuckDodgers on February 26, 2014 at 04:42

      Interesting. That might explain some of the worsening blood sugar control over the long term on keto that many experience. But it doesn’t explain the many, many cultures who consumed lots of saturated fats without problems.

  13. SteveRN on February 14, 2014 at 09:49

    I think I know who you are referring to regarding the bipolar who says type 2’s do not get ketoacidosis. Weird, because as a icu rn for around 8 years, I have seen a lot of patients, type 2, admitted with DKA as the official diagnosis, DKA related to the type 2 mentioned by doctors in progress notes and H&P’s. I will have to tell all these doctors in the future they have no idea what the hell they are talking about.

  14. Charles on February 14, 2014 at 10:24

    Interesting, Dr. Jay Wortman stated to me that it’s very rare. I tend to trust him on these issues, but apparently he’s not aware of increased incidence.

    • Paul Jaminet on February 16, 2014 at 06:50

      Hi Charles,

      Probably a lot more common on VLC than on normal diets, as carbs promote insulin release and suppress free fatty acid release and ketone production. As the low-carb movement catches on doctors will see more cases.

    • Jane Karlsson on February 17, 2014 at 04:11

      Paul Jaminet

      I have some information for you. You have written about micronutrients important in mucin synthesis and didn’t mention manganese. Glycosyltransferases are activated specifically by manganese. Here’s a paper about it.

  15. Jane Karlsson on February 15, 2014 at 02:35


    Yes lots of foods are missing some nutrients and are still healthy. But I don’t know of any foods which have had nutrients deliberately removed and are still healthy. Carbohydrate foods should not be eaten without the minerals that activate enzymes of carbohydrate metabolism. You can’t rely on vegetables to provide the minerals, as the Chinese study showed: people eating the most white rice also ate the most vegetables.

    And it isn’t just magnesium. Most of the manganese has been removed from white rice too, and manganese is if anything even more important in diabetes.

    ‘Manganese supplementation protects against diet-induced diabetes in wild type mice by enhancing insulin secretion’

    • GTR on February 15, 2014 at 15:29

      You also can’t rely on food and even water to provide you with the minerals, as the mineral contents of both soils and water vary considerably from place to place.

      And by the way – doesn’t too much manganese make one crazy?

    • Jane Karlsson on February 16, 2014 at 04:52

      Yes, very high doses of manganese cause parkinsonism. Lower doses prevent it.

      ‘Manganese: a transition metal protects nigrostriatal neurons from oxidative stress in the iron-induced animal model of parkinsonism’

    • gabriella kadar on February 16, 2014 at 14:59

      Don’t forget Jane, high levels of manganese result in learning disability.

    • Jane Karlsson on February 17, 2014 at 02:33

      Gabriella, we have discussed this at length on Wooo’s blog. You believe that an amount of manganese in drinking water 100 times less (ONE HUNDRED times less) than the amount in food can damage children’s brains. I don’t believe it. For me, that paper shows correlation not causation. The manganese in water was correlated with iron in water, and the authors never considered the possibility that the problems were caused by iron. Iron overload has been found in many neurodegenerative diseases, and it’s a far more plausible candidate than manganese, which is protective in much larger amounts than were found in that water.

      Remember, Wooo has told everybody who will listen that I am insane. She knows now I am not, but she can’t get out of it now. You are not helping. Well actually, you are, by giving me the opportunity to explain my position.

  16. Jane Karlsson on February 15, 2014 at 03:00


    In fact the study doesn’t even show that. It shows an association, which might be cause and effect and might not be. It has to be considered together with other work including Robert McCarrison’s on white rice in India. He found that people eating machine polished rice had ten times more beriberi than people eating home pounded rice, which has some bran/germ left.

    Yes it does seem that white flour is worse than white rice. Zumin Shi, the lead author of the Chinese study, says that in China white flour has more iron than white rice. He and others have found a link between iron overload and diabetes.

    • Richard Nikoley on February 15, 2014 at 08:27

      I’m not sure what the point is, Jane. Nobody here is advocating rice as a staple. If if you flow PHD and use it as your exclusive starch, you’re at 30% of calories. Toss in potatoes and legumes and mix then up, you’re at 10-15% of starch.

      No big.

    • Jane Karlsson on February 16, 2014 at 04:55

      Ok. Just so you know. Your favourite female blogger is hoping you will trip up, and I’m hoping you won’t.

    • Richard Nikoley on February 16, 2014 at 09:12

      You talking about the bi-polar, OCD crazy who’s so far gone she can’t even help herself anymore?


      Yea, used to like her blog rants and shit, but when I saw her behavior on Twitter, literally 24/7 sometimes, no sleep, total self-absorption selfies throughout the day I realized that it’s very unhealthy to pay attention to this person. I trolled her for a while on Twitter, for fun, but then had enough of it.

      All in all, a big distraction to have every paid any attention to her.

    • Jane Karlsson on February 17, 2014 at 02:42

      Richard, don’t underestimate Wooo. She is getting her act together. I spent a lot of time correcting her mistakes, and she has taken it on board although she would never admit it.

    • Richard Nikoley on February 17, 2014 at 22:07


      Please, I have tried everything with her. Without exception, she believes it’s mal intentioned. Hell, I even once popped my cell number on Twitter, said just call, let’s chat (I’ve chatted with many over the years and once did that in a Reddit r/Paleo flame and got a call immediately and it turned out cool). Yea, like I’m scamming right out in front of my 7000 followers. This happened before. Every good intention was rebuffed and characterized as the worst of intention.

      No matter what I say nice or complimentary about her, it’s not only not believed, but pumped out to others as actually manipulative, which just tells me that she’s quite dumb because in my observation even of lots of people who hate me, they have at least some understanding of how I operate all up front, never from scheming or manipulation of hidden agenda.

      Accordingly, I’ve given up for good. If she ever comes to me, I will listen (always, anytime, I never hold a grudge) but that’s how it would have to be. No groveling or anything like that, but she will need to approach me and if she never does, I won’t be worrying about it.

      And in all cases, I always wish her well.

    • Jane Karlsson on February 18, 2014 at 02:24

      Well I can’t disagree with any of that. But I do think you should take what I say about magnesium and manganese seriously, precisely because she is pretending it isn’t true and that I am insane. She is doing this partly because she’s stuck with it but partly, I suspect, so that people like you won’t think it’s important. The Mg-Mn story is very important indeed. Removal of these and other metals from white flour/rice/sugar has the potential to explain modern disease. I have spent 30 years studying the literature, I have a PhD in biology, and this is what I have found.

    • Richard Nikoley on February 18, 2014 at 13:39


      Interested in writing something up on it for the blog, like 2,000ish words?

    • Jane Karlsson on February 19, 2014 at 03:53

      Thanks Richard, but I have to say no. People are far too terrified of Wooo to believe what I say.

      You can always email me if you have a question.

    • Richard Nikoley on February 20, 2014 at 07:30

      Just to clarify, I meant about Mg-Mn stuff, not about whatever Wooo is up to, because almost nobody cares.

    • Jane Karlsson on February 21, 2014 at 05:06

      Yes, I did realise that. Perhaps I will do it. I need to think about it. I know what will happen if I do, and I don’t want that shit.

  17. Jane Karlsson on February 15, 2014 at 05:39


    I think I was talking garbage about foods that have had nutrients removed. What about butter and cheese? They’ve had stuff removed and are still healthy.

  18. […] Animal site recently, and my comments were blogged about by Richard N, the proprietor of that blog. HERE is his post. I am going to take all my comments over a couple of threads and roll them into one […]

  19. […] Michelle from a few days back, the one who  presented at the hospital with a BG of 680, diagnosed diabetic (type 2) […]

  20. Chupo on February 18, 2014 at 16:34

    Michelle, you ROCK!!! You have diabetes by the balls! Don’t let go and keep up the good work! You’re truly an inspiration! 🙂


    “get[s] a lot” (direct quote) from her corn wraps”

    I think she gets a lot more RS from Carbquik which is made from enzymatically changed, highly processed, WHEAT starch!!! :-O Apparently it doesn’t degrade with cooking as her blood ketones were higher after the Carbquik pancakes. She attributes it to lower protein that day but I wonder if the RS might have played a part.

    • Richard Nikoley on February 18, 2014 at 17:01

      RS has zero to do with it and she’s too ignorant to understand how ignorant she is.

      I told her she was ignorant about the corn. And for such a big mouth: crickets. And she still thinks she knows something about resistant starch and pretends, while she knows nothing at all. Average reader of comments here knows 10 times more.

      Enzymes don’t create RS. RS4, the one synthetic variant, has nothing to do with enzymes but trade secret processes, likely repeated heating and cooling.

      She’s just too dumb to know how dumb about this (point of no return, dumb), and she struts it around with hubris.

      It’s a good laf, though.

  21. Chupo on February 18, 2014 at 18:07

    “RS has zero to do with it ”

    With higher ketones? I have experienced ketosis while eating resistant starch even while eating carbs.

    Ketosis and carb consumption isn’t mutually exclusive.
    SCFA are much like MCT in this respect. The lower digestive systems of rabbits will convert SCFA to ketones in vitro much like liver.

    Yeah’ it’s rabbits and in vitro but I don’t know what else could explain it. I was in ketosis on the potato hack and I still am while eating potato starch while not eating ketogenically.

    Not a fan of Carbquick no matter how they make it. lol.

  22. Pone on February 20, 2014 at 21:35

    Maybe Paul or others could comment on this. My experience has been along the lines of the person described in this post. I was at a prediabetic 115 fasting glucose, with excursions after meals above 140 mg/dL. After starting 3/4 to 1 cup of starchy white rice after four meals a day, now I see fasting glucose around 90 mg/dL and on *most* days my one hour post-meal glucose is 110 mg/dL. So ironically enough, by challenging my body with small amounts of dietary glucose, I end up with lower glucose levels than by removing dietary glucose.

    What explains that perplexing result? Intuition tells you that ingestion of starch will make glucose rise, so how can you get to a lower average glucose level by eating more glucose?

    As I understand it (just barely), the key may be in how the body triggers insulin release. When in a fasting state, insulin is at some endogenous background level. It may be that as insulin resistance increases, the body’s response to this endogenous insulin levels progressively fails, leaving glucose levels more and more elevated. I think they call this endogenous insulin release the basal insulin release.

    Dietary glucose derived from starches appear to use a different type of insulin release. In the scenario where you eat starch, the pancreas goes through a two phase insulin release, and that second phase appears to push the glucose to lower levels than where they go with just the basal insulin release.

    So eating small amounts of starch / glucose can push you to a lower glucose level than a ketogenic diet. With ketogenic, you are just staying at a prediabetic physiologic insulin resistance level all the time, because you never get the second phase insulin release from starchy meals.

    As I have said elsewhere, my frustration with this whole experiment is I have no way currently to track my insulin levels. The disease here is about insulin resistance, not about glucose production, perse. In type 2 diabetes, the body is not losing any ability to create glucose from starch. Rather, the body is losing an ability to respond to insulin. So it’s actually monitoring the insulin level that tracks the disease. The glucose is an important piece of co-joined data, but to me you need both pieces of information.

    I’m looking for a portable insulin tester, which I’m guessing must be made somewhere as an in-hospital device. If anyone knows of a cost effective one I would love the referral.

  23. Paul Jaminet on February 21, 2014 at 05:25

    Hi Pone,

    It’s not perplexing when you realize that the body is always trying to restore homeostasis, which it achieves naturally with a carb intake around 30% of energy. At lower carb intakes, you become insulin resistant and create a hormonal environment (stress/starvation response) that discourages glucose utilization by cells and promotes cannibalization eg turning protein into glucose. In this state, you have no way to dispose of dietary carbs so postprandial glucose is high, and fasting glucose can also go high due to the circadian rhythms of the stress hormones leading to a peak of gluconeogenesis at a time of minimal glucose utilization.

    When you return carb intake toward 30%, insulin sensitivity is restored, normal glucose utilization is restored, and stress hormones go down, so your glycemic response improves.

  24. Jane Karlsson on February 21, 2014 at 06:26

    Pone, have a look at this. It suggests insulin resistance comes from abnormal insulin secretion.

    ‘The presence of oscillations in peripheral insulin concentrations has sparked a number of studies evaluating the impact of the insulin release pattern on the action of insulin on target organs. These have convincingly shown that equal amounts of insulin presented to target organs have improved action when delivered in a pulsatile manner. In addition, impaired (not absent) pulsatility of insulin secretion has been demonstrated in Type II (non-insulin-dependent) diabetes mellitus, suggesting a possible mechanism to explain impaired insulin action in Type II diabetes. …’

    ‘Routine screening procedures for insulin secretion yield little predictive value for later development of diabetes but more sophisticated methods using time-series analysis of diurnal, ultradian and rapid oscillatory insulin secretion reveal the presence of profound defects in glucose-intolerant individuals. Furthermore, studies of rapid pulsatile insulin secretion have revealed defects in glucose-tolerant first-degree relatives of patients with Type 2 diabetes. …’

    The oscillations depend on adequate amounts of micronutrients, of which magnesium and manganese are likely the most important.

  25. Christoph Dollis on February 21, 2014 at 08:55

    30% is a pretty blanket recommendation.

    Doesn’t a person’s genetic ancestry factor in in a major way?

  26. Pone on February 21, 2014 at 13:52

    Paul, I appreciate that there is some kind of complex biofeedback at work, and that some combination of insulin sensitivity and insulin production might give better glycemic response. But I am making a different point that I think may have importance here.

    My point was that when you *EAT* the foods that become glucose, you get *TWO* phases of insulin response. And it is that second push of insulin that drives your glucose down to a lower number. I think this effect is completely independent of any systemic regulation of your baseline.

    In my own case, I might have glucose of 90 mg/dL on waking, but if I don’t eat and extend my fast, my glucose starts to rise pretty quickly. On a good day it might stop at 100 and on a bad day it might go to 115 again. It’s only the constant cycle of small amounts of dietary glucose that give me that second push of insulin that does send my baseline down.

    All of this seems pretty complex to me. It’s not clear to me (yet) what part of my now-lower glucose readings is attributable to a healthy restoration of insulin sensitivity, and what part is attributable to exposing myself to the added insulin generation from eating glucose.

    I can’t prove that getting lower glucose readings that result from added insulin is healthier than living in physiological insulin resistance, like ketogenic dieters do. But the data seems to suggest that people at 115 mg/dL fasting glucose have substantial added health risks over 100 mg/dL. It bothers me that Rosedale and other ketogenic advocates say that glucose is bad yet consistently ignore that their diets successfully push *many* (NOT ALL) people to much higher fasting glucose levels. If glucose is bad, it is bad no matter how you get to the place where you have high fasting glucose.

  27. gabriella kadar on February 21, 2014 at 15:06

    Pone, that’s because endogenously produced glucose does not stimulate beta cells to produce insulin.

    When digestible carbs hit the stomach, a small peptide molecule is produced which lets the beta cells know ‘glucose incoming’. Therefore, insulin begins to be secreted as glucose is entering the blood.

    When glucose is produced through gluconeogenesis, this response is blunted. This is why an IV dextrose push does not increase insulin levels the way ingested dextrose will.

  28. Pone on February 21, 2014 at 15:24

    Gabriella, I am not doubting you, but I asked you to show references for that and you did not. I tried to Google this phenomena and it was mixed into detail of complex and unrelated articles or books. Do you have something short and to the point in a scientific reference that would prove your point?

    I certainly believe the biofeedback loop is different between endogenous and dietary glucose. But I have a hard time believing there is no biofeedback loop.

    In any case, my point remains that dietary glucose causes two phases of insulin response, and it is that second push that gets the insulin resistant person down to a lower glucose reading.

  29. Charles on February 21, 2014 at 15:41

    While this doesn’t speak directly to your question, it’s an interesting article about insulin release and resistance.

  30. Pone on February 21, 2014 at 16:33

    Jane, that is interesting about pulsating insulin, but the tests required to establish this defect would be impossible to get? They are talking about sampling your blood once a minute. My guess is this is only done in experimental settings, never in a clinical practice?

    Do you have any research references to prove that magnesium and manganese are the critical nutrients for insulin? Doesn’t sound correct.

  31. Pone on February 21, 2014 at 16:52

    The research Jane pointed to suggests a possible reason there is not a home insulin tester: spot testing once an hour probably just misses the picture entirely. Insulin is rising and falling pretty rapidly, minute to minute. An effective insulin tester would probably need to be integrated into a device that you wear on your body constantly, which can do spot tests every 15 seconds or so.

    Anyone else have a thought on that?

  32. Pone on February 21, 2014 at 16:58

    Charles that is interesting and supports Jane’s links as well. But the question for the patient is:

    1) So who exactly is going to do the testing to establish a failed first phase insulin response? If I’m understanding it correctly, no clinical setting is going to test you every minute to measure that response.

    2) Assuming you have a failed first and second phase insulin response, then how do you re-establish it?

    Look how frustrating this is to the patient. You have no clue is pancreas failing to produce insulin, or is the insulin there and the body is just not responding to that insulin? These two things are like night and day. They suggest totally different problems, and the solution to each is somewhat different. The technology is there to make this diagnosis, yet the system turns a blind eye to the patient and doesn’t diagnose.

    It’s not enough to say everyone with elevated glucose is “insulin resistant”. Maybe they just have bad genes and as they get older the pancreas under-performs. Why isn’t the medical system more concerned with making that diagnosis?

  33. gabriella kadar on February 21, 2014 at 17:34

    Pone: enjoy. It’s long. Dr. Bernie Zinman discovered the little peptide molecule.

  34. Pone on February 21, 2014 at 17:55

    Gabriella, I have not read more than a few pages and will read more later. But what the intro seems to be saying is that GIP and GLP are stimulated by eating and in type 2 diabetes GIP fails to control release of more insulin.

    Is there a section there that indicates there are no analogs to GIP or GLP for endogenous glucose produced by the liver in the fasting state?

  35. gabriella kadar on February 21, 2014 at 18:52

    The physiology of endogenous glucose production happening when adrenalin is released due to the sympathetic nervous system is needed for muscles and brain, neither of which require insulin for glucose to pass into the cells. If insulin were released by the beta cells at the rate they are when glucose in ingested, then a lot of glucose would go into the adipocytes and compromise the ‘fight flight’ response.

    I’ve gone out on a empty stomach with low fasting BG and found two hours later that it was elevated. My body made more glucose in order to supply the muscles. If I wold have continued to be physically active, eventually the blood glucose would go down because if it’s floating around like that, eventually some insulin will be released.

    Have you tried testing for this over hours? And how fast the glucose goes down after activity, no food, and relaxation? Have you continued with moderate exercise for several hours on an empty stomah to find out at which stage your glycogen runs out and blood sugars go down?

    It would be interesting.

  36. Pone on February 21, 2014 at 19:08

    Doesn’t glycogenolysis to the muscle requires insulin?

    I am still not seeing any reference that says endogenous glucose production is not regulated by insulin. I do believe you that the regulation system is different than eating. I just can’t believe there is NO regulation system.

    Regarding exercise, it seems to make my muscles “thirsty” to replenish glycogen, and my glucose will drop 20 to 30 points after completing even 30 minutes of walking. High intensity exercise drops it a bit more. I’ve never tried exercising at a slower pace for two hours. Why would blood sugar going down be tied to exhaustion of glycogen? Wouldn’t it be enough to just have glycogen levels lowered and the muscles start to drink up any available glucose they can find?

    Of course I test over hours, particularly when it is a bad day. I had everything under control for several weeks but since I started the potato starch it is going haywire the last week. Today was just insane and the worst it has been in a long time:

    On waking I am at 91 mg/dL

    One hour later extending my fast and not eating I am at 100 mg/dL. Two hours after eating breakfast (salmon, frittata, and one cup starchy white rice) I am at 126 mg/dL. That’s rare for me.

    One hour later: 129 mg/dL. That is insulin resistance probably and what is causing it. That never happens to me that I would be higher at hour 2 than hour 1, and above 120 at hour 2 is just unusual for me.

    One hour later: 125 mg/dL. Three straight hours of very high glucose. No explanation.

    Two hours later after a salad: 97 mg/dL

    At that point I had a big lunch without any real starch (maybe 1/4 cup starchy white rice) and one hour later I am at 107 mg/dL.

    I cannot explain days like today at all. I eat the same foods that for three weeks had me peaking at 110 mg/dL one hour after meals and then slipping below 100 mg/dL two hours after meals. Yet something today has made me either more insulin resistant, and alternately my body is producing less insulin. Either way, the doors kind of fell off and I have no idea why. Very frustrating. I will go exercise and that will probably drop the glucose significantly. But to some extent that is cheating and why is my normal sedentary glucose is behaving badly.

  37. Richard Nikoley on February 21, 2014 at 21:45

    Wow, talk about freaking yourself out by deranged obsession and blaming everyone else, demanding proof.

    How about you prove up your assertions and lay off on demanding others do your research for you.

    No animal ever tested their BG ever.

  38. Pone on February 21, 2014 at 22:41

    Richard, there is no blaming anyone else for anything. That’s just weird of you to say.

    In these discussions, when people make claims, it is fair to ask them where they got their information. There is no demand either. There is a polite request.

    I’m not asking anyone to research questions I originate.

    No animal ever tested their blood glucose ever, but that’s because most animals live in a near starvation state and eat a natural diet they are evolved to eat. Once they do get old and metabolism fails, they die pretty rapidly. Is that our goal, to be like animals and die as soon as our metabolism fails? Is it an unreasonable thing for a prediabetic to monitor their blood sugar and just want to understand their disease?

  39. Pone on February 21, 2014 at 22:43

    That should have been written “No animal ever tested their blood glucose ever, but most animals live in a near starvation state and eat a natural diet they are evolved to eat….”

  40. Pone on February 21, 2014 at 23:56

    Jane, I read your references on insulin oscillation and did some additional research, and this was very helpful thanks.

    Here is a study with graphs that show how “normal” people cycle insulin in their endogenous state:

    There are such amplitude swings in the cycle, that taking a spot reading for insulin isn’t going to be very helpful. You would probably need to measure at least every five minutes to capture even the general shape of the cycles.

    So the suggestion appears to be that most type 2 diabetics have a failure in these pulsing cycles, and as a result they are not able to clear fasting / endogenous glucose efficiently. It may be that the tissues of the body act less efficiently to absorb glucose when the pulsing pattern of insulin is not normal. After exercise, however, the muscle become much more sensitive to whatever background insulin exists, and they therefore can store glycogen in spite of any defects in the insulin pulsing cycle.

    I was not able to find any studies with graphs that show what a “defective” pulsing pattern looks like. If you have one please share. I was not able to find full text for the links you shared.

    Unlike endogenous insulin release, the insulin response curves that I have seen for post-meal events look like more normal curves. So really it looks like insulin release behaves totally different when you eat than when you are in a fasting state. Having a portable meter for insulin when you are testing after meals might be a very useful thing. Doing insulin testing in your fasting state would be extremely difficult (and very very damn expensive if each test is costing you $10 and you have to test every few minutes).

    Thanks for this information. I learned a lot here.

  41. Pone on February 22, 2014 at 15:26

    Jane, the magnesium research is really interesting, thanks. And since most everyone is not getting enough magnesium, it’s a no brainer to supplement it. Do you have any opinions on what dose of magnesium is optimal? Perfect Health Diet recommends 200 mg daily. Does the science say anything about taking it spread over the day versus once?

    Any opinion on the type of magnesium or brand? This is one Perfect Health Diet recommends:

    The maganese I want to be much much more cautious and studied about. The first point is that very few people who eat a nutritious diet have a shortage. And the second point is that manganese is a dangerous neurotoxin. So overdose is a real possibility if you supplement this, and the effects are nightmarish. I think this is something you would only do if you very carefully took apart your diet and assessed your manganese intake. And even then if you supplemented I think it would be at the low end of the scale.

    I don’t have full text on the mouse manganese study you published. What kind of dose were the rats receiving, normalized to a human dose? It’s interesting research, but it’s not a no-brainer to supplement.

  42. Jane Karlsson on February 22, 2014 at 03:53

    Pone, if you google ‘magnesium insulin resistance’ you will find many papers showing that insulin resistance correlates with low blood Mg and/or low Mg intake. Mg is needed both for insulin action and for insulin production. Beta cells produce insulin in response to glucose metabolism, which requires Mg at many points. Glycolytic enzymes are generally activated by Mg, for instance, and beta cell oscillations are dependent on oscillations of glycolysis, which is a natural oscillator. Mitochondrial metabolism oscillates and so does ATP synthesis, which is dependent on Mg and is critical for insulin secretion. Calcium oscillates, membrane potential oscillates, and the pumps responsible require Mg and/or MgATP. Every aspect of beta cell oscillations needs Mg.

    As for manganese, an important paper was published a year ago showing how Mn interacts with iron to cause diabetes. The authors had shown earlier in mice with hereditary iron overload, that the excess iron stops Mn from getting into mitochondria. They have now shown that the same thing happens in wild type mice on a diabetogenic diet. No Mn in mitochondria = diabetes.

  43. Richard Nikoley on February 22, 2014 at 07:34


    I supp magnesium (malate – the Source Naturals brand). Just Googling around, seems to be quite a lot of foods with decent amounts of Manganese. You think it’s necessary to supplement it?

  44. DuckDodgers on February 22, 2014 at 16:39

    Ugh.. Stay away from Manganese supplementation. Most people get way more than enough from a variety of foods. Pone is correct. Overdoing Manganese can fuck you up, big time. (Hat tip to the Jaminets for highlighting the dangers of Manganese supplementation in Chapter 36 of the PHD).

    Manganese neurotoxicity: a model for free radical mediated neurodegeneration? Donaldson J et al. Canadian Journal of Physiology and Pharmacology 1982 Nov;60(11):1398–405,

    Possible health effects of high manganese concentration in drinking water. Kondakis XG et al. Archives of Environmental Health 1989 May-Jun;44(3):175–8,

    Water manganese exposure and children’s intellectual function in Araihazar, Bangladesh. Wasserman GA et al. Environmental Health Perspectives 2006 Jan;114(1):124–9.

    Hair manganese and hyperactive behaviors: pilot study of school-age children exposed through tap water. Environmental Health Perspectives Bouchard M et al. 2007 Jan;115(1):122–7,

    Parkinson’s disease risks associated with dietary iron, manganese, and other nutrient intakes. Powers KM et al. Neurology 2003 Jun 10;60(11):1761–6

  45. Pone on February 22, 2014 at 17:27

    Jane, I found some pretty remarkable studies regarding magnesium. This one stood out:

    They are claiming nearly very large reductions in fasting glucose, strangely at the same time reductions in fasting insulin, large reductions in LDL, and huge increases in HDL. BUT…the dose they supplemented in that study is 2.5g = 2500 mg, which is about four times the highest recommended supplement dose I have ever seen. At levels above 2 grams, Magnesium is a laxative.

    If Paul is still lurking around this thread, I would be interested in knowing if in your reading of the literature, were people seeing major results at more reasonable supplementation levels?

  46. Pone on February 22, 2014 at 17:35

    It looks like Magnesium Chloride needs to be converted to elemental Magnesium, and a 2500 mg dose of Magnesium Chloride is somewhere around 300 mg of elemental Magnesium.

    So based on this study a 400 mg dose of elemental Magnesium (maybe split 200 mg twice a day) would be a reasonable upper limit.

  47. Paul Jaminet on February 22, 2014 at 17:36

    Pone, that’s 2.5 g MgCl2 which is about 625 mg magnesium. They want to see significant effects within 3 months and it can take months to relieve a whole body magnesium deficiency, so it is reasonable to oversupplement in a short term study. I don’t think you want to take 625 mg daily forever. 200 mg daily is something you can take forever.

  48. Pone on February 22, 2014 at 19:59

    Thanks Paul. For my calculation I just grabbed a product label here:

    They give roughly 500 mg Magnesium Chloride against 60 mg Elemental Magnesium. That suggests that 2500 mg of MgCl would be 300 mg Elemental?

  49. Jane Karlsson on February 23, 2014 at 05:49

    This is a difficult question. I don’t take supplements myself. 30 years ago I changed my diet to the one found by McCarrison to produce good health, and it seems to have worked. I haven’t seen a doctor for 25 years except for a thorn in my thumb. I had deformed feet and they’re fine now. Connective tissue turnover is dependent on manganese and copper, so I think I must be getting enough of them.

    Yes I do realise the literature suggests manganese is a dangerous neurotoxin. You may be surprised to hear that it’s actually one of the least toxic metals. It has received a very bad press which is almost completely undeserved. The Wikipedia entry claims there is strong evidence for Mn overload in neurodegenerative disease, for instance, and gives no references. Because there are none.

    The mice in that study were injected with manganese. The authors tried Mn in drinking water and it didn’t work. They think it was excreted. Mn is very easily excreted, and in fact Mn that’s actually needed gets excreted in the bile in a process called enterohepatic circulation. It’s supposed to be re-absorbed further down the gut. I suspect gut bacteria help. This is why I am so interested in Richard’s work on resistant starch.

  50. DuckDodgers on February 23, 2014 at 06:15


    If manganese isn’t a problem, why is it showing up in the hair of hyperactive children?

    Hair manganese and hyperactive behaviors: pilot study of school-age children exposed through tap water.

  51. gabriella kadar on February 23, 2014 at 06:56

    Duckie, Jane has already told me that this study is BS. She thinks it’s iron in the water which wasn’t tested apparently.

    Funny thing: my six cousins grew up on well water which tasted of iron. When we’d visit, I thought the water tasted disgusting but that’s what they had. Not one of them has grown up to be diabetic. Not one. They are between 57 and 45 years old now. Neither were any of them exhibiting behavioural issues as children or as adults. My uncle, who drank that stuff since 1955, recently died aged 86. He wasn’t diabetic either. Neither is my aunt who is now 84 years old.

  52. DuckDodgers on February 23, 2014 at 07:21


    And, as Grace pointed out, you have millennia of asians cooking in iron woks and low incidence of diabetes. My guess is that it’s more complex than Jane wants to admit. Sounds like she wants white rice to be the culprit when the evidence to demonize it is fairly weak.

  53. DuckDodgers on February 23, 2014 at 07:39

    The Wikipedia entry claims there is strong evidence for Mn overload in neurodegenerative disease, for instance, and gives no references. Because there are none.

    Probably because they put all the references into its own Wikipedia article for “Manganism”

  54. Paul Jaminet on February 23, 2014 at 07:58

    The atomic weight of Magnesium is 24 and that of Chlorine is 35. So magnesium is 24 / (24+70) = 25% of MgCl2 by weight.

    You have misread that label. The pill has both MgCl2 and Mg. 520 mg Mg from MgCl2 and 62 mg free Mg.

  55. Pone on February 23, 2014 at 16:30

    Paul thanks for clarifying, particularly for using atomic weights.

    That label is a mess, but your message is clear.

  56. Jane Karlsson on February 24, 2014 at 03:33

    Why is manganese showing up in the hair of hyperactive children? Here’s a possible explanation given by the authors themselves in their follow up paper.
    ‘Despite measures taken to wash hair samples, residual external contamination cannot be ruled out completely. For instance, arsenic present in water has been shown to bind to the hair surface and was not removable by sample washing (Concha et al. 2006); it is not known whether this could also apply to manganese.’

    The problem with these studies is that there is no known mechanism by which the tiny amount of Mn could have caused problems. The authors say Mn in food is fine but 100 times less in water is not fine at all. It makes no sense. Mn is so easily excreted that to get any effect on diabetes in mice you have to inject it. How can it have got into the children’s brains, and how could it have damaged them even if it did? Scientists have tried injecting Mn directly into rats’ brains to solve this mystery, but unless the dose was extremely high the Mn was actually protective. Injected iron caused parkinsonism, and injected Mn prevented it. The authors were very surprised.

  57. SteveRN on February 24, 2014 at 03:38

    For my Mag education, I have been reading a lot of stuff from this guy… Not as entertaining as Richard, but I think he knows his stuff regarding Mg. He recommends getting an Mg RBC test instead of the standard Mg blood test, as the body can make itself short Mg in the tissue to maintain blood levels. The RBC test will give you a truer measure of your levels. He also recommends supplementing several different ways, trans-dermal via Mg oil, Epsom salt baths, and oral. The brand I take is by Jigsaw Health. It is a slow release formulation, so you can take heavy doses, and not experience the side effect of diarrhea. Morely suggests you aim for a dose of 5mg Mg/lb to get your RBC levels up to par. For me that works out to 1125 mg day. I take that with no adverse side effects. Would love to hear Paul comment on this if he is still on here and has any opinion on the Mg RBC test, dose or brand.

  58. Jane Karlsson on February 24, 2014 at 03:48

    The Wikipedia entry for manganese says the following:
    ‘Chronic low-dose manganese intoxication is strongly implicated in a number of neurodegenerative disorders, including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis.[citation needed]…’

    No citations. If you think they are in the entry for manganism you should point them out, because I can’t find them.

  59. DuckDodgers on February 24, 2014 at 07:59


    I think the part that you are overlooking (unless I’m just misunderstanding your argument) is that Manganese seems to exacerbate the toxicity of other metals. Manganese seems to make iron or aluminum or copper or other metal interactions in the brain much worse.

    For instance, here is a study tracking chronic Manganism in children and the ability for Manganese to exacerbate lead toxicity.

    From: Associations of Early Childhood Manganese and Lead Coexposure with Neurodevelopment

    We observed evidence of synergism between lead and manganese, whereby lead toxicity was increased among children with high manganese coexposure. Findings highlight the importance of understanding health effects of mixed exposures, particularly during potentially sensitive developmental stages such as early childhood.

    Many studies only try to look at a single metal — and they usually overlook that there is a synergism that tends to happen. But, as I’m sure you know, you will find plenty of hypotheses implicating Manganese plus other metals (iron, etc).

  60. DuckDodgers on February 24, 2014 at 09:20

    Scientists have tried injecting Mn directly into rats’ brains to solve this mystery, but unless the dose was extremely high the Mn was actually protective. Injected iron caused parkinsonism, and injected Mn prevented it. The authors were very surprised.

    Well, that “rat injection” model was done in 1998. Since then there has been a little bit of progress on understanding the role Manganese plays with other metals. For instance:

    From: Metal Ions in Neurological Systems (2012)

    Transport of manganese ions into the central nervous system as been directly investigated in a limited number of studies. It is generally believed that iron and manganese ions are able to be complexed and carried by transferrin/transferrin receptor, with iron being far more prevalent under normal circumstances [21]. Several authors suggest transport of trivalent manganese complexed to transferrin into the brain capillary endothelium, but the exact mechanism underlying the transport of manganese by transferrin to the brain has been elucidated very recently by us, which will be described below…

    You can read the rest of the hypothesis on the mechanism here.

  61. Jane Karlsson on February 25, 2014 at 04:40

    Groan. You really think I know nothing about this? What do you think I’ve been doing for the past 30 years?

    You may have noticed a reference in your link to the sheep disease scrapie. The authors think scrapie = manganism. I don’t expect they have read this paper showing that scrapie in Iceland occurs precisely where the forage is LOW in manganese and high in iron.

  62. DuckDodgers on February 25, 2014 at 05:31

    In any case, even if you could prove that supplemental doses of manganese is safe so long as no other toxicity is present, the evidence to support manganese supplementation appears to be pretty weak — though, admittedly, I haven’t been researching this for 30 years.

    From: (w/references):

    Manganese is needed to help multiple enzymes in a process called gluconeogenesis. This is the process by which we build non-carbohydrate food products—for example, digested fats—into sugars to burn as fuel.

    In animal studies, manganese-depleted diets can lead to high blood sugars similar to those seen in diabetics. Whether this is true in humans has not been determined.

    Either way, manganese deficiency is probably not a common contributor to human diabetes. Humans with diabetes do not reliably have lower manganese intake than people without diabetes. Also, supplementation with large doses of manganese—doses at the top end of what would be seen with plant-based diets—did not improve blood sugar control in diabetes. (link)

  63. Jane Karlsson on February 26, 2014 at 04:25

    In th paper you linked, Mn was measured in the blood but not in the environment, so we don’t know where it came from. It might have come from pollution, and it might have been released into the blood by the liver as part of a stress response. The older literature on Mn says glucocorticoids do this. Toxic metals can cause tissue damage, and Mn might be released to counteract it.

    ‘The possible endocrine regulation of Mn metabolism was investigated by studying the effects of ACTH or cortisol administration, and those of adrenalectomy, on the excretion and tissue distribution of radioactive and stable manganese (Mn54 and Mn55). Adrenal cortical stimulation with ACTH led to a shift of radioisotope from the liver to the carcass, similar to that described after administration of glucocorticoid hormones. …’

    Cotzias, G. C., 1966: Tissue concentrations of manganese and adrenal function. Amer J Physiol: 207-210

  64. Jon McRae on April 24, 2014 at 07:49

    Seems like a good point to ask this question, I just got blood work back that said my Glucose Serum was 101 with last year being 99, I am on 4 Tbsp of PS and taking a SBO probiotic, I am 6’5 310lbs, I work out everyday at lunch, Olympic lifts and fast pace. I just started adding in beans from Richards recipes. Any other tips for the group?

    • Pone on April 24, 2014 at 20:33

      Fasting glucose means almost nothing. Why they even bother to order this test by itself escapes me. The number that really matters is the A1C, which might show up as HBA1C. What is your value?

    • Richard Nikoley on April 26, 2014 at 10:22


      Those numbers are almost the same. For me, it took not only potato starch and the SBO’s, but also upping my carb intake to get down into normal ranges. Same for my wife.

      You didn’t mention what your carb/starch intake is.

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