Are Fatty Foods Addictive?

Image Credit: Burger Austin / Flickr. This image has been modified.

How Fatty Foods May Affect Our Love Life

The food industry, like the tobacco companies and other drug lords, has been able to come up with products that tap into the same dopamine reward system that keeps people smoking cigarettes, using marijuana, and eating candy bars (See Are Sugary Foods Addictive?). New research, highlighted in my video Are Fatty Foods Addictive? suggests that fat may have similar effects on the brain. If people are fed yogurt packed with butter fat, within 30 minutes they exhibit the same brain activity as those who just drank sugar water.

People who regularly eat ice cream (sugar and fat) have a deadened dopamine response in their brains in response to drinking a milkshake. It’s similar to when drug abusers have to use more and more to get the same high. Frequent ice cream consumption “is related to a reduction in reward-region (pleasure center) responsivity in humans, paralleling the tolerance observed in drug addiction.” Once we’ve so dulled our dopamine response, we may subsequently overeat in an effort to achieve the degree of satisfaction experienced previously, contributing to unhealthy weight gain.

What do fatty and sugary foods have in common? They are energy-dense. It may be less about the number of calories than their concentration. Consumption of a calorie-dilute diet doesn’t lead to deadened dopamine responsivity, but a calorie-dense diet with the same number of calories does. It’s like the difference between cocaine and crack: same stuff chemically, but by smoking crack cocaine we can deliver a higher dose quicker to our brain.

As an aside, I found it interesting that the control drink in these milkshake studies wasn’t just water. They can’t use water because our brain actually tastes water on the tongue (who knew!). So instead the researchers had people drink a solution “designed to mimic the natural taste of saliva.” Ew!

Anyway, with this new understanding of the neural correlates of food addiction, there have been calls to include obesity as an official mental disorder. After all, both obesity and addiction share the inability to restrain behavior in spite of an awareness of detrimental health consequences, one of the defining criteria of substance abuse. We keep putting crap in our bodies despite the knowledge that we have a problem that is likely caused by the crap, yet we can’t stop (a phenomena called the “pleasure trap”).

Redefining obesity as an addiction, a psychiatric disease, would be a boon to the drug companies that are already working on a whole bunch of drugs to muck with our brain chemistry. For example, subjects given an opiate blocker (like what’s done for people with heroin overdoses to block the effects of the drug) eat significantly less cheese — it just doesn’t do as much for them anymore when their opiate receptors are blocked.

Rather than taking drugs, though, we can prevent the deadening of our pleasure center in the first place by sticking to foods that are naturally calorically dilute, like whole plant foods. This can help bring back our dopamine sensitivity such that we can again derive the same pleasure from the simplest of foods (see Changing Our Taste Buds). And this is not just for people who are obese. When we regularly eat calorie dense animal and junk foods like ice cream, we can blunt our pleasure so that we may overeat to compensate. When our brain down-regulates dopamine receptors to deal with all these jolts of fat and sugar, we may experience less enjoyment from other activities as well.

That’s why cocaine addicts may have an impaired neurological capacity to enjoy sex, and why smokers have an impaired ability to respond to positive stimuli. Since these all involve the same dopamine pathways, what we put into our body—what we eat—can affect how we experience all of life’s pleasures.

So to live life to the fullest, what should we do? The food industry, according to some addiction specialists, “should be given incentives to develop low calorie foods that are more attractive, palatable and affordable so that people can adhere to diet programs for a long time.” No need! Mother Nature beat them to it–that’s what the produce aisle is for.

By starting to eat healthfully, we can actually change how things taste. Healthiest means whole plant foods, which tend to be naturally dilute given their water and fiber content. Not only is fiber also calorie-free, but one might think of it as having “negative” calories, given the fermentation of fiber in our bowel into anti-obesity compounds (as well as anti-inflammatory, anti-cancer compounds). For this reason, those eating plant-based diets eat hundreds of fewer calories without even trying. (See my video Nutrient-Dense Approach to Weight Management).

-Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my videos for free by clicking here and watch my full 2012 – 2015 presentations Uprooting the Leading Causes of Death, More than an Apple a Day, From Table to Able, and Food as Medicine.


Michael Greger M.D., FACLM

Michael Greger, M.D. FACLM, is a physician, New York Times bestselling author, and internationally recognized professional speaker on a number of important public health issues. Dr. Greger has lectured at the Conference on World Affairs, the National Institutes of Health, and the International Bird Flu Summit, testified before Congress, appeared on The Dr. Oz Show and The Colbert Report, and was invited as an expert witness in defense of Oprah Winfrey at the infamous "meat defamation" trial.

165 responses to “How Fatty Foods May Affect Our Love Life

Comment Etiquette

On, you'll find a vibrant community of nutrition enthusiasts, health professionals, and many knowledgeable users seeking to discover the healthiest diet to eat for themselves and their families. As always, our goal is to foster conversations that are insightful, engaging, and most of all, helpful – from the nutrition beginners to the experts in our community.

To do this we need your help, so here are some basic guidelines to get you started.

The Short List

To help maintain and foster a welcoming atmosphere in our comments, please refrain from rude comments, name-calling, and responding to posts that break the rules (see our full Community Guidelines for more details). We will remove any posts in violation of our rules when we see it, which will, unfortunately, include any nicer comments that may have been made in response.

Be respectful and help out our staff and volunteer health supporters by actively not replying to comments that are breaking the rules. Instead, please flag or report them by submitting a ticket to our help desk. is made up of an incredible staff and many dedicated volunteers that work hard to ensure that the comments section runs smoothly and we spend a great deal of time reading comments from our community members.

Have a correction or suggestion for video or blog? Please contact us to let us know. Submitting a correction this way will result in a quicker fix than commenting on a thread with a suggestion or correction.

View the Full Community Guidelines

  1. This is the theory on “massive ingestion” of raw fruits such as dates and bananas, in that their such intense pleasurable effect (high-sugar) can take over the dopamine response. One can become less motivated. Basically, satisfied by the fruit, missing out on living. Any thoughts on this? Sort of like being drunk on fruit.

  2. Dr. G, I thought that marijuana activated cannabinoid receptors instead of the dopamine reward system. (Of course, now that I think about it, I’m sure there’s no reason it couldn’t activate both.) In either case, does marijuana’s activation of the dopamine reward system make marijuana harmful? I’m especially curious about this given the rise of medical marijuana and, frankly, the rise of legalized recreational marijuana. We all know that pretty much all smoke is carcinogenic, but is marijuana itself harmful, say if it’s infused into olive oil? I’ve heard that moderate use (1-2 times a month) is actually beneficial, especially to one’s psychology, and I’d really like to hear your thoughts on that.

    1. Nope. Not sugar alone. As I addressed in Dr. Greger’s previous blog post, no one binges on spoonfuls of pure white cane sugar.

      Disqus is not playing well with my cellphone right now, so I can’t copy and paste a link to my post (try my Disqus profile)…also…. Try Googling the title, “Cheesecake-eating rats and the question of food addiction “.

      1. Then the title of this article is misleading. That’s like smoking crack and eating an apple at the same time and then blaming the apple for the addiction. Why not study eating fat alone and see what happens?

          1. All you need to know is a can of Coke contains close to 40 grams of sugar. Find a study where fat was consumed with no sugar and no simple carbs.

                  1. What does this photo have to do with you not being able to find a study of fat consumption without sugar or simple carbs? And what about the misleading title in this post?

                    1. Anyone who writes books promoting damaging nutritional falsehoods, and lies about his own health and weight cycling, lies whicht contradict his own public blog posts deserves to be called out on that. It’s not fat shaming.

                    2. This post is not about him. You brought him into this discussion. You keep avoiding answering why the title of this post misleading. And?

                    3. I did not say the title of this post is misleading. That’s what you said. Answer your own doggone question. I’ve got a good night’s sleep to get. Over and out.

                    4. “Answer your own doggone question.” LOL I must’ve hit a nerve. Good night. I hope you toss and turn all night dreaming up an answer to my question.

                1. I didn’t say 40g of sugar aren’t a problem. I’m saying that isolated sugar is unpalatable and non-addictive unless combined with other agents. We tend not to eat plain sugar but use it to make other substances palatable. It’s the synergistic combinations that are the real problem.

  3. Okay, I’m confused. I have pre-diabetes from decades of following a grain-heavy vegan diet, so I now strictly limit my grain consumption, almost down to zero. I currently get about 35% of my calories from fatty plant-based foods (nut butters, avocados, etc.). This has helped me drop my high glucose levels well into the normal range, cause for celebration! But all these fats make me a bit nervous, especially given this post. Should I be? Am not overweight…

    1. Hi, Russell. Yes, you should be concerned … I can assure you that grains cannot and do not cause diabetes.

      Check out this excellent TED talk on diabetes, by Dr. Neal Barnard:

      In most people’s minds (including medical doctors), carbohydrate
      (sugar and starch) is the cause of blood sugar metabolic disorders like
      diabetes. However, although carbohydrate calories do count, in the sense
      that the blood sugar goes up right
      after eating a meal, this is
      actually normal … and it does not make the underlying disease of
      diabetes worse. Insulin is released from the pancreas after eating, and
      it causes body cells to take up carbohydrate and fat cells to take up

      When insulin doesn’t work well, the blood sugar rises,
      and diabetes is diagnosed. In type 2 diabetes, this ineffectiveness is
      caused by “insulin resistance” … which is actually caused by dietary FAT,
      not SUGAR. The video above explains how fat “paralyzes” insulin. Diabetics should actually be
      “fat-counting,” not “carbohydrate counting,” in order to improve their
      underlying disease.

      Almost all type-2 diabetics can REVERSE their
      disease by minimizing dietary fat. Type-1 diabetics will find
      their insulin needs decreasing by about 30% when they avoid the fat and
      add the carbohydrate.

      1. Thanks Laurie, you’ve sparked my interest. But here’s the thing — if I eat a normal sized bowl of rolled oats, my blood glucose shoots to about 180 and takes five hours to get back to 100. But if I eat a whole avocado with hemp seeds mixed in, I only spike to 125, and am down to 85 an hour later. So, you’re saying I shouldn’t be concerned about the grain-effect upon my glucose? There are many studies suggesting that any spikes above 140 are damaging to the internal organs. I should ignore those?

          1. And you “know” this how? I do not believe the saturated fat in nuts is any different than the one in red meat.
            If “fat” in the cell reduces the ability of insulin to take in the glucose where is your study that says it has to be saturated fat?

            1. I’ll work on getting you a reference tomorrow from a college prof.

              Meanwhile, keep in mind there are many different types of fatty acids which collectively compose fat, and there are a number of different saturated fatty acids, some of which are problematic and some which are not. Palmitic and myristic acids are considered the most injurious. The jury may still be out on Lauric acid.

            2. College prof refers me to a Google Scolar search of “saturated fat ceramides diabetes” which reveals a number of studies. Sorry Disqus isn’t accepting my attempts to C&P.

              1. Sorry, I am not impressed! You see many food items that people get addicted to like ice cream, red meat and many other items have high levels of saturated fats. Even if these things do lead to diabetes it does not mean that other type of fats would not do the same thing if consumed at the same levels. I did not say saturated fat was good nutrition but said there is no proof that it is not any type of fat in the cell that knocks off the insulin…

                  1. To be “heart attack proof”, low fat is ideal to maintain adequate cholesterol numbers. This 2 year study looked at coronary artery lesions of the heart after consuming different types of fat. Polyunsaturated fat, monounsaturated fat and Saturated fat. They looked at angiograms a year apart after intervening with increasing one type of fat in each group. All 3 fats were associated with a significant increase in new atherosclerosis lesions. Most importantly, the growth of these lesions did not stop when polyunsaturated fats and monounsaturated fats were substituted for saturated fats. Only by decreasing all fat intake including the polyunsaturated and monounsaturated fats did the lesions stop growing.


                    1. Interesting reference going back to 1990. I would love to see the same study done with IVUS.

                      Meanwhile, forgive my confusion. It’s due to other references I have come across.

                      For example, in Dr. Greger’s newest year in review video, he mentions a patient who resolved his angina with a vegan diet which was not, in fact, a low-fat vegan diet.

                      Also, in an interview on NPR, Dr. Steven Nissen maintained that a study demonstrated atheroma regression by means of a Mediterranean diet. Sorry I don’t know his source. (PREDMED, maybe?)

        1. Russell: If I may jump in here, I believe what is being said is that your blood spike is a symptom not a cause. When you eat a lot of those fatty foods, you are treating the symptom, not the cause. This may seem reasonable, except that the cause of insulin resistance is having a lot of fat in your cells. So, by eating all those fatty foods, you are continuing to make the disease worse. It’s not that your blood spike is good. It’s that you want to change your diet so that when you eat your bowl of oats, you do not have a dangerous level of blood spike.

          I think Laurie’s post was really great. In addition to her information and the video she listed, I recommend taking a look at the following book, which is as great for pre-diabetics as it is for people who already have it: “Dr. Neal Barnard’s Program For Reversing Diabetes: The scientifically proven system for reversing diabetes without drugs” Dr. Barnard’s diet is 3 times more effective than the ADA diet which counts carbs – I believe because Dr. Barnard is addressing the cause, not the symptoms.

          One of the reasons I recommend this book for you is not only because you can read the great information at the front of the book at your leisure, but also because there are recipes in the back of the book, plus meal plans. So, you can see for yourself exactly what a diabetes-healthy diet looks like. If you stick with it, your blood spikes should return to normal size.

          Please note: I’m not a doctor. I’m just a lay person explaining what I’ve learned – and so many people have reported experiencing. Plus, it’s not just anecdotes. Dr. Barnard has published clinical research on this. It’s worth checking out.

          1. Thea, thanks for your comments, and to others as well for jumping in. Just to clarify, insulin resistance is not causing my problems with glucose. My recent labs showed that my LP-IR score is only 25, which is in the bottom quartile of the reference range. In other words, I don’t have insulin resistance in my cells, so excess fats are not the cause of my problems metabolizing glucose. The issue is low insulin production. So, it is far more likely that I’m not treating a symptom, but the actual problem — the excess glucose. Also, a recent carotid scan shows no plaque buildup, so…. just saying… I’m concerned about the fats but I don’t think that blaming insulin resistance is always going to be the correct answer.

              1. And at the same time, I would surmise that reducing your dietary fat might yield superb results in any case. This is vitally important for blood-sugar metabolism and could be even more important in your case, because the last thing you want to do is CREATE insulin resistance … make sense? I’d be very interested to hear how it goes if you try this for a month.

                Just to blow your mind and bust your paradigms … check out this website from a type 1 diabetic (who obviously has the same insulin production problem) … you won’t believe what happened when SHE dropped the fat:

            1. Russell: Oh. Thank you for the clarification.

              Sounds like more of a typical Type 1 problem than at Type 2 problem??? I don’t have much to say on that one–other than, I don’t think there is any reason to believe this statement is true: “I have pre-diabetes from decades of following a grain-heavy vegan diet” My understanding is that type 1 is an auto-immune response that has nothing to do with eating grains.

              As for your question about eating a diet that is 35% fat – I think the worry would be that you might develop type two diabetes to compliment your type 1. ;-( I don’t know if we have any good data relating fat percents to diabetes. But is a thought: my understanding is that the typical American diet was at one point 40% and now has gone down some. And Type 2 diabetes is still on the rise. Does it matter that your fats are all from plant foods? I don’t know…

              Seems like you are in a tough spot. I’m definitely not one to give any advice for you. I was just trying to help out with some ideas/analysis that might help you figure out what to do or what questions to ask a doctor.

              Good luck.

              1. Thea, actually Type 2 diabetes doesn’t necessarily involve insulin resistance. Here’s what the Mayo Clinic says:

                “Type 2 diabetes, once known as adult-onset or noninsulin-dependent diabetes, is a chronic condition that affects the way your body metabolizes sugar (glucose), your body’s important source of fuel. With type 2 diabetes, your body either resists the effects of insulin — a hormone that regulates the movement of sugar into your cells — or doesn’t produce enough insulin to maintain a normal glucose level.”

                It would appear that I’m in the second category.

                As for diabetes relationship to fat, I just found that in Crete, the diet in the 50s was 37% fat, with stunningly low levels of cardiovascular events (for many reasons including only 15 lbs/yr/person of sugar intake, the lowest in the world, lots of anti-oxidant veggies, exercise, etc). So we know that high fat levels can be okay for the heart if other lifestyle factors are taken care of properly.

                And in this BMJ study below that I just found, it appears that a typical Mediterranean diet like Crete’s is associated with an 85% reduction in diabetes.

                So, I think I’ve answered my own question. It appears that a high-fat diet, and even more likely in my view, a high-fat vegan diet, should be extremely healthy for those of us with pre-diabetes, or vascular conditions as well.

                Last point, I can’t prove that my heavy grain-based diet caused my condition. Perhaps I have late onset Type 1 autoimmune diabetes instead. All I know is that I ate TONS of pasta, brown rice, quinoa, pizzas, etc., People were always amazed to watch me eat a 2 lb bowl of whole wheat spaghetti, or a whole pizza with fake cheese by myself. One can overdo anything and even a vegan diet isn’t bullet-proof, I believe, if grains or flours are excessive.

                1. I think you’ve got it exactly. Balance your healthy fats, lots of vegies, some whole grains but not too much,berries, some fruits, lots of legumes and some flavorful plant based sauces and you should be good. By the way, it also tastes better than heavy grain and carb.
                  John S
                  PDX OR

                2. I am in the same boat with you, Russell – approaching pre-diabetes despite following a vegan diet and being normal weight. In my case, the pre-diabetes is no doubt the result of decades of sugar addiction. Seeing my blood glucose levels shoot up was enough to motivate me to kick the sugar habit and go on the wagon. The higher GI index carbs, like whole wheat breads and potatoes, are also a problem for me. I replaced them with more nuts, seeds, flax, and avocados (35% dietary fat), and my total cholesterol dropped 60 points to 126, A1c is low, and blood glucose levels stay nice and steady. Following a vegan diet, exercise, and avoiding oils and high GI carbs seems to be a winner. I question whether the fats in nuts, seeds, and avocados are to be avoided. Maybe they have a different effect on our dopamine reward system and insulin resistance than animal fats.

                  1. Suepy, thanks for your feedback. It’s nice to know I’m not alone in my vegan, low-carb, high-fat diet :) What I haven’t mentioned yet is that my lipid particle sizes are in the ideal range, triglycerides are at 44, and HDL is at 90. These are better lipid values than anyone I know. And my A1C is down to 5.3. I’m beginning to think that ine day, this may be considered the most healthful diet in the world. Unfortunately, I am not aware of any studies being done on it yet.

                    1. Dr David Jenkins, aka the glycemic index guy, has been doing studies using added nuts in the diet and concluded that two ounces of nuts daily as a replacement for carbohydrate foods improved both glycemic control and serum lipids in type 2 diabetes.
                      He also tested a vegan, low-carb (Eco-Atkins) diet and found that it had lipid lowering advantages over a high-carb, low-fat weight loss diet.
                      I tried the Eco-Atkins diet and noticed that my energy level was lower, so I added back more healthy carbs – beans, lentils, barley, fruit – which gives me a ratio of 50% carb, 35% fat, and 15% protein. If I do eat some higher GI carbs, then exercising (fast walk, jumping jacks, stairs) within 45 minutes will reverse my rising blood glucose down to an acceptable range. Let’s raise a toast to nuts!

                    2. Dr. Greger has a recent video on LDL particle size. It’s mostly irrelevant. Large “fluffy” or buoyant LDL is not protective or benign. The current consensus is that it’s the particle number (concentration or LDL-P) in the blood that determines atherogenicity, not particle size.

                  2. Suepy, that’s so smart of you to notice that you can eater higher carbs if you exercise almost immediately. I do that too. But it takes me a lot of running to keep just one Cliff Bar from shooting me up to 150. My own diet is higher in protein — I rely a lot on seitan, and soy products like Tofurky — because lentils and chickpeas send my glucose up a lot too. But otherwise quite similar.

                    I love your thoughts about dopamine and am sure this must relate to the fats. I’m far less hungry now than at any other time in my life, and sometimes I just forget to eat. That NEVER would have happened to me when I was on a carb-rich vegan diet. My problem now is finding a way to keep my weight on. A BMI of 20.0 is just a tad too skinny! How’s your weight?

                    1. My BMI is 19.4, no problem keeping weight off. My metabolism seems to have sped up with this higher healthy fat, lower fast carb way of eating. Adding lots of fiber rich veggies and a shot of lemon juice while eating carbs also helps keep the glucose level down. Have you ever tried chana dal? It’s very low GI and a good substitute for lentils or garbanzos.

                      Seitan is great, handles any seasoning or sauce you throw on it. Since it’s low fat, that leaves more room for nuts!

                    2. So, based on a sample of two people, it seems that high-fat, low-carb vegans simply cannot get overweight. Sort of the opposite, actually! You would laugh to look in my fridge — I’ve got almond, peanut, cashew, walnut, and chia butter, and I eat them by the spoonful They are great snacks and protein sources!

                      I’ll give the chana dal a try. Thanks! And the lemon juice. You may want to check out Dr. Greiger’s video on Amla. I’ve been using it, but haven’t really done a comparison of before/after, so not positive its working, but I think so….

                      Btw, you’re not from the SF Bay Area, are you? Lots of progressive foodies here…

                    3. A caveat to eating more nuts, seeds, and avocado: they can’t be consumed in addition to crap carbs without causing weight gain. Also important is having a source of omega 3 fats, like 2T ground flaxseed, chia, or hemp seeds. I also use very little olive, canola, or whatever oils, instead making my own tofu mayonnaise and oil free dressings, and using water or broth for stir frying.

                      Hull-less barley makes a great breakfast cereal, although granted not a fast cooker.
             I boil a big pot of barley on the weekend, put half of it in mason jars to toss in the freezer, and keep the rest in the fridge. For a quick breakfast, add to a cup of cold (or heated) barley 1T chia seeds, a handful of raw pumpkin, sesame, sunflower seeds and walnuts or almonds, and a chopped apple or fresh berries. If blood glucose levels are not an issue, add currants, raisins, dried cranberries, or soaked goji berries. Yum.

                      Sue P.
                      sweet home Chicago

                    4. You’re a font of helpful information! I love these ideas, thank you. The only caveat — my dentist told me to stop eating so many nuts because they are grinding down my enamel, lol. So, moderate doses of whole seeds/nuts I guess, and will stick mostly to nut butters.

                    5. Russell, you’re welcome! Like you, I was cautious about upping my fat intake while reducing carbs to control glucose levels, especially after reading Dr Neal Barnard’s Program for Reversing Diabetes. Fats have had a lot of bad press! I also tried the Ornish method (vegan version), but found the very low fat part hard to maintain. Fortunately, Dr David Jenkin’s studies are revealing the value of healthy fats, and Dr Joel Fuhrman, although parallel to McDougall, Esselstyn, et al, differs from them in his support of nuts and seeds in the diet.

                      Definitely what we need are more studies that examine the health benefits of different whole food plant based diets, tailored to individual metabolisms. Meanwhile the proof is in the pudding, via good test results: lipids-check, A1c-check, weight-check, feel great-check.

                      Amla, flax, and turmeric took some experimenting to find a palatable delivery method. I don’t know if amla is helping – I trust the good Dr G’s recommendations. Isn’t there a test for antioxidant levels in the blood? And speaking of SF, it’s home to Robert Lustig and his great talk Sugar: The Bitter Truth, which points the finger to sugar as the real villain instead of fat.

                      Whether the fat in nuts and seeds are addictive maybe needs to be examined, but I must admit to a love affair with almonds and pistachios.

                    6. Suepy, the healthy fats issue is going to be controversial for some time. David Jenkins, for example, has been shellacked for his conflicts-of-interest, including Unilever, Bayer, and the Nut and Soy Industries. This link below on the fats issue is fascinating and lays out both sides pretty well (Jenkins’ conflicts are outlined in the second comment below the article). I’d love your thoughts on it.


                      Fyi, I spoke personally to Esselstyn this summer, and he remains adamant that eating nuts and avocados is a terrible choice even for diabetics. On the other hand, Denise Minger has a story online that seriously attacks his credibility, and it also happens to be quite funny and entertaining. She’s not a scientist, but is a young and original mind in the field:


                      I hope that Fuhrmann’s view is correct — thanks for sharing that.

                      As for sugar, I agree that minimizing it is important and I rarely eat cane sugar myself, but Lustig goes too far. Please check out Dr. David Katz’s takedown of Lustig in the Huffington Post. Katz is Director of the Yale Prevention Research Center:


                      There’s lots to chew on here!

                    7. Russell: Hi again. I just had to comment on one more thing. I recommend being very careful about Denise Minger. She may be young. And she may be “original”. But that doesn’t mean that she makes any sense, has any real science to back up what she says, or has integrity. To back up what I say: Denise also made an attack on Plant Positive. If you look at Plant Positive’s response to Denise, you will see what I mean in terms of my criticisms of Denise:
                      (Just scroll down until you find the link that starts with his first response and move on if interested.)

                      Just something to think about.

                    8. Thanks Thea. Yes, I see what you mean and am very disappointed that Minger is not speaking in an objective, intellectually rigorous, or impartial way. She appears to have failed to give appropriate credit as well. Sorry you’ve had to put up with that.

                      Nonetheless, her criticisms of Esselstyn’s original heart study are not completely baseless. In Forks Without Knives, for example, there was a patient with extremely high triglyceride levels, and yet that wasn’t considered a cardiovascular problem… why not? These are very dense, atherogenic particles. Easily controlled of course, by limiting carbs… there were also failures to account for patients who dropped out of the study. I’d love to see more detail, and explanation, on his studies to help guide our appropriate understanding. Do you know if his work was ever published in a peer-reviewed journal?

                    9. Russell: I don’t think Minder has very good objections. For example, the patients who dropped out of Esselstyn’s study were the patients who refused to follow the diet plan. And those patients *were* accounted for. Esselstyn takes great care to show that he followed those patients by showing the stats of those drop-outs compared to the stats of the patients who followed Esselstyn’s diet. (Those drop outs went on to have future heart attacks, including dying.) Those drop out patients were essentially the control group. It was great that there was drop outs so that we would have that comparison data.

                      re: “Do you know if his work was ever published in a peer-reviewed journal?” I don’t know the details, but the back of Esselstyn’s book includes a appendix titled “Publications on Heart Disease by the Author” and includes listings for The American Journal of Cardiology, The Journal of Family Practice, Preventative Cardiology, etc. I don’t know if those count or not.

                    10. Thanks Thea, that’s helpful information and I agree with your comment.

                      Btw, have you continued to follow this thread? Suepy and I are figuring out all the world’s diet problems :) Personally, I’d love to see Dr. Greger jump in with his thoughts on the high veggie fat issue, but if so, he should first look at the great study link that Suepy just sent. Someone reputable needs to blow the whistle on the high whole grain, low-fat vegan diet for people with diabetes risks. The data just isn’t supporting that approach. I think it looked good in the beginning because it helps lower BMI, but then the proponents became dogmatic. The fact is that higher MUFAs on a vegan diet will help A1c levels, not hurt them. And as for the heart data, well, I haven’t seen anything yet suggesting that high-fat vegan diets contribute to plaque formation or CVD. Thanks much.

                    11. Russell: I love your and Suepy’s enthusiasm for figuring out nutrition needs. I didn’t follow your discussion in detail. I just skimmed and decided that the best way to be supportive was for me to stay out of it. :-)

                      Except that I couldn’t resist commenting on the assertion that native Alaskans, etc are examples of people who eat high fat and manage to be heart disease-free. It’s just not true. If you missed my post on that topic and can’t find it, I’d be happy to repost for you. I think that accurate information on that point is important for the conclusions you are trying to draw.

                      Since you addressed me specifically, I’ll give you some more food for thought:

                      re: “Someone reputable needs to blow the whistle on the high whole grain, low-fat vegan diet for people with diabetes risks. The data just isn’t supporting that approach. I think it looked good in the beginning because it helps lower BMI, but then the proponents became dogmatic.”
                      This isn’t true. Dr. Barnard’s clinical, published research on live humans with Type 2 diabetes did a whole lot more than lower BMI. He was able to reverse the diabetes, getting most people off of their medications by following a low fat vegan diet that includes legumes and whole intact grains. And there continues to be success stories from person after person. The data is most definitely there – both clinically and anecdotally.

                      re: “And as for the heart data, well, I haven’t seen anything yet suggesting that high-fat vegan diets contribute to plaque formation or CVD.”

                      I’ll remind you that Esselstyn’s original study included one person who did not drop out, and who did go on to have another heart attack (or some kind of heart event). After looking into it, Esselstyn found out that that person had in fact strayed from the proscribed diet and started sneaking more fat into his diet. Everyone else in the study, everyone who stayed with the diet, but who had originally been giving up on by their doctors, did not have future heart attacks. (If memory serves.) This is not terribly strong evidence. But I think it is worth noting.

                      For some stronger evidence, I’m going to copy and paste a recent post from Toxins that begins to address this point:

                      To be “heart attack proof”, low fat is ideal to maintain adequate cholesterol numbers. This 2 year study looked at coronary artery lesions of the heart after consuming different types of fat. Polyunsaturated fat (omega 3 type of fat) Monounsaturated fat (75% of which makes up olive oil) and Saturated fat (the kind found in mostly animal products). They looked at angiograms a year apart after intervening with increasing one type of fat in each group. All 3 fats were associated with a significant increase in new atherosclerosis lesions. Most importantly, the growth of these lesions did not stop when polyunsaturated fats and monounsaturated fats were substituted for saturated fats. Only by decreasing all fat intake including the polyunsaturated and monounsaturated fats did the lesions stop growing.



                      I’m not necessarily trying to change your mind. I’m just explaining why I don’t buy your theories personally. At least you can see that it is not a cut and dried topic. In other words, “Someone reputable needs to blow the whistle on…” is too strong a sentiment at this point for what the data is telling us. That’s my opinion anyway.

                      I really do think it is great that you and Suepy have hit on a formula that you are excited about and believe in. For all I know, it may be just the ticket for your situations. I hope so!

                    12. Thea,

                      I very much appreciate your thoughts, as usual.

                      The study you cite finds that those with the best outcomes switched to low fat meat and dairy while those with poorer outcomes had switched to polyunsaturated or monounsaturated fats. My first concern is that the study isn’t based on those on a vegetarian or vegan diet, but on meat eaters, so I’m not sure it is entirely relevant; second, it sounds like the study doesn’t address the LDL issue that Dr Greger says is actually the most important factor. (I would read the full study but its not free online).

                      In his video this week, entitled “How to Prevent Heart Disease”, he says, “…according to the Editor-in-Chief of the American Journal of Cardiology, the only risk factor required for atherosclerotic plaques to form is elevated LDL, or “bad” cholesterol in our blood. Dr. William Clifford Roberts is the distinguished cardiac pathologist who doubles as the Editor-in-Chief of the American Journal of Cardiology…. To drop our LDL cholesterol, we need to drop our intake of three things: trans fat (found in junk food and animal foods – See Trans Fat in Meat and Dairy); saturated fat (found in mostly animal foods); and dietary cholesterol (found exclusively in animal foods).” He doesn’t mention reducing PUFAs or MUFAs….

                      As for the Inuits, I found this AJCN journal study below saying that Inuits have had very low ischemic heart disease as a result of their high omega diets, despite high levels of smoking and obesity. I’d appreciate your citation showing the opposite outcome, if you have one. Regardless, one cannot deny that there are populations who eat high fat diets with little or no heart disease, such as the Masai, and the Cretians. I’m curious if you think the studies are all poorly done, or if you have an alternative explanation for why this might be.

                      Fyi, here’s the Inuit study:


                      I think there’s enough strong evidence to support low LDL recommendations, perhaps LDL 100 is right, at least until we know more, but there are many other factors that indigenous studies are pointing towards that we don’t yet understand. Perhaps high levels of grains, or sugars, or daily exercise play a major role, and perhaps this is why some people with low LDLs still experience plaque build-up. Also, triglycerides are clearly being overlooked given their atherogenic potential. As per my former citation by Dr. Alex Sigurdsson, the Triglyceride/HDL ratio may be a more accurate predictor of heart attack risk than LDL.

                      We can probably develop a number of plausible theories why certain indigenous populations such as the Masai, Cretians, and others had high fat diets but low CHD problems. My speculation is that since they exercised prodigiously compared to modern populations, their TRIG/HDL ratios were superb, despite high fat intakes.

                      Anyway, I feel as though our western understanding of heart disease is in its infancy, and it will be another decade before we really begin to get more complete answers.

                      Until that happens, I don’t mind aiming for an LDL of 100 while continuing to eat plenty of nuts and avos. Suepy’s citations supporting nuts and seeds are pretty compelling and I encourage you to look at them.

                      Finally, as for Dr. Barnard’s diet, I respectfully must disagree with the statement that he (or anyone) “reverses the diabetes”. If that were the case, patients could go back to their former diets and not experience glucose problems again for years or decades, until their cells eventually became resistant again. But that’s not what happens. They must stick to the new diet, or they experience a very rapid reversion to their former diabetic conditions. So I believe this term is misleading, at best. To be more accurate, Dr. Barnard should be saying that his diet “reverses the symptoms and progression of the disease.” Yes, he can get people off their medications, and that’s entirely accurate, and wonderful, truly great news. But a reversal is suggestive of a cure, which just isn’t correct.

                      I’ll amend my comment about Dr. Barnard’s diet being inappropriate for those of us with diabetes or pre diabetes. What I should have said is that his diet is inappropriate for those of us who’s condition is related to insulin deficiency. We absolutely must limit carbs, and increase veggie proteins and fats, while keeping our LDLs within certain limits. Getting sufficient calories while keeping glucose and LDL low is a tough challenge.

                    13. Russell, I’m still chewing on all the good links you gave – thanks! Here is a link to Dr Joel Fuhrman’s comments on including nuts and seeds in the diet:
                      The 2010 study by Dr David Jenkins on adding monounsaturated fats (MUFAs) to a low cholesterol diet had some serious limitations. It was only for 2 months involving 24 people who switched to a cholesterol lowering diet that was hard to choke down. The MUFAs used were sunflower and avocado oil, so not exactly what ordinary people would eat! The diet itself lowered LDL levels in both the test and control groups, and the HDL did go up in the test group, but does that necessarily improve heart health? It made great news headlines, but wouldn’t a better test be to use vegans who already have lowered cholesterol levels and add MUFAs in the form of foods, like nuts, seeds, and avocado? Jenkins conflicts of interest also make one wonder.

                      Denise Minger’s critique of Forks Over Knives and Drs Caldwell, Esselstyn, and McDougall was amusing in parts, very detailed, but is not enough to negate the merits of a WFPB diet. Her beef was with some old studies that might be flawed or have ambiguous conclusions, and which helped launch the doctors’ inquiries into plant based diets. The correlations these studies show are another piece in the puzzle, and have been valuable in casting a light on the huge role that diet plays in health. What does seem relevant are the success these doctors have had in treating a variety of diseases, not the strength of the studies.

                      I noticed that Dr Barnard’s Power Foods for the Brain recommends one ounce of nuts and/or seeds daily as a good source of Vitamin E, the nutritionists Jack Norris and Virginia Messina in their book Vegan For Life suggest fat intake for vegans at 20-30% of calories, and Dr Andrew Weil’s diet for insulin resistance has monounsaturated fats at 30-35% and carbs at 40-45%. I doubt that Esselstyn et al have ever tried adding the healthy fats to their patients’ diets – Fuhrman has with great results. There should be a meeting of the minds; granted nuts etc have higher calories and saturated fat, but maybe their metabolism is different due to their high nutrient content. They could test this on a group of vegans who eat like squirrels by charting their lipid and A1c levels (us!).

                      Bottom line: we should test our own levels and follow the diet that works best. People are amazingly complex and there is more going on in our bodies than we’ll ever understand. I was cautioning a friend who has gone vegetarian about the high cholesterol in eggs, and she replied that her dad ate 3 eggs daily and lived to 102. Go figure.

                    14. Suepy, thanks for the Fuhrman piece. While obviously I hope he is correct and that one can safely and healthily eat over 2 servings a day of nuts, as I do. But I’m a bit put off by his fast and loose use of citations. For example, he cites a study that pumpkin seeds may prevent prostate cancer. But that’s not what the study that he cited said. It was testing the efficacy of pumpkin OIL, alone and in combination with saw palmetto, on BPH in men. First, the study wasn’t looking at cancer, only BPH; second, second, even if one makes the logical leap to assume that benefits to BPH extend to prostate cancer, the study itself shows that after 12 months, the pumpkin oil group’s PSA had reverted to their former values. In other words, no gain. The only group that actually experienced any 12 month PSA benefits was the pumpkin oil group combined with saw palmetto. So… gotta take Mr. Fuhrman’s conclusions with a grain of salt. Here’s the actual study if you want to see it:


                      I haven’t checked all of his citations but am concerned that he may not be 100% accurate on those either.

                      On a more positive note, I love this graph that I’ve posted below which shows almost no heart disease in the Inuit, Masai, Rendelle, and Todelau populations despite saturated fat intakes of over 60%. The Paleo crowd uses this citation to support their view on eating animal products, but the argument is germane to our community as well. Why are people from Crete (in the 1950s), and indigenous people from Africa and other areas not susceptible to heart disease despite the high fat intakes? Is it their daily exercise, low BMIs, and other lifestyle factors?

                      The recent meta study suggesting that saturated fats aren’t so bad after all has sent public health researchers into full defensive mode. See this statement from Harvard School of Public Health’s Chairman:


                      Harvard’s conclusion is that the substitution of animal products with refined starch or sugar does not create an improvement in public health or reduce cardiovascular risks. In other words, substituting a lot of processed grains for meat and dairy is simply maintaining the status quo.

                      Uh oh. This is disconcerting as most of my vegetarian friends eat a lot of bread, pasta, rice, and other processed grains because they believe those are safer, which may not be true.

                      Anyway, this begs the question as to whether perhaps all grains may lead to elevated CVD risks. I haven’t seen the data suggesting that someone who eats mostly whole grains has a reduced CVD risk versus someone, say, in Italy who eats mostly pasta.

                      To the contrary, grains directly elevate triglycerides. According to cardiologist Alex Siggurdson’s citations, the ratio of triglycerides to HDL is a far stronger predictor of future CVD risks than LDL itself or many other measures:


                      The best way to lower triglycerides? Cut out grains and sugars. Harvard’s Chairman may be on the right track with his statement, but perhaps he hasn’t gone far enough. What if the heart epidemic that we are experiencing today involves not just saturated fats but also all starches and sugars, refined and whole?

                      But how would that explain the Inuits and Masai? Just as you and I found that we can increase our carbohydrate intake if we immediately exercise, and our glucose won’t spike as it usually does (since we are pre-diabetic). Maybe because the Masai are moving their bodies all day long, these saturated fats aren’t stagnating and jamming up their cells. Instead, they are burning everything off immediately.

                      Maybe the problem is simply a problem of excess: excess grains, excess fats, excess sugars, excess proteins. And then sitting for 12 hours a day.

                    15. Good question, Russell, why don’t these indigenous people have heart disease on their high fat diets? Have their bodies adapted over the centuries, or is there something else in their diet that compensates, or is the fat not a problem in an unprocessed form? In our Western diet, food processing has probably caused the greatest harm, plus our excess consumption. We assumed that 100% whole grain breads were healthy, but grinding the grains into a flour changed their composition to a fast carb. Same with black beans – moderate GI until blended into black bean soup, then a higher GI. Centenarians around the world eat grains, but in Okinawa circa 1950 in much lower quantity, so grains per se might not be the problem.

                      I’m wondering how common insulin resistance and diminished insulin are among the US population? Few doctors seem to care about or measure insulin levels, just the fasting glucose. By the way, Dr Robert Lustig has amended his message to an anti-processed foods campaign. I think he needs to take a closer look at a WFPB diet for his overweight kids.
                      And I’ll take that grain of salt with Dr Fuhrman or anyone who might be too eager to make a point.

                    16. Suepy, I enjoyed reading your Okinawan diet link. Things the Okinawans seem to have shared with the Masai and Inuits — almost no sugar and dairy, and only a modest amount of grains (the Okinawans ate half the rice of their Japanese counterparts). The major difference appears to be that the Okinawans ate a lot of veggies and sweet potatoes, and very little fat, while the Inuits and Masai ate a lot of saturated fat and not so many veggies.

                      The Cretians ate a bit more dairy, sugar, and grains, but reportedly in low or moderate amounts. And they had plenty of vegetable fats as we discussed. Again, the fats appear not to have been an issue.

                      Another major common denominator between all groups was very high levels of daily exercise as part of their normal lives as is typical in these agrarian or hunter-gatherer cultures.

                      It’s still strange to me that meat/fish wasn’t a problem for the Inuits, Masai, and Cretians. It makes me wonder if perhaps meat and/or fish only becomes a problem once dairy and sucrose are added to a diet, especially in combination with an overabundance of calories and the failure to do rigorous exercise every day. Interestingly, in the 7th Day Adventist studies, the pesco-vegetarians did as well on overall mortality as their vegetarian counterparts. This site has a lot more info on vegan/veggie mortality data:


                      Totally agree about M.D.s testing insulin levels.

                    17. suepy: re: “why don’t these indigenous people have heart disease on their high fat diets?” Actually, they do. At least their blood work shows signs of antheclorsis (I know I spelled that horribly wrong). Even ancient mummies from those cultures show signs of heart disease. The reason they weren’t having heart attacks is that they weren’t living long enough (due to other reasons) to get to the heart attack point.

                      If this topic interests you, Plant Positive has some wonderful details and source materials on the topic. Search for words on the following link/page such as: masai, alaska, eskimo, etc. Then click the links to watch the videos. You can also click in his search box for “inuit”. Or even better, go to the top of the list of the “Primitive Nutrition” series and watch the whole thing. :-) It’s *very* educational.

                      If Plant Positive doesn’t interest you, here is a copy of a post from “xfjea” that is very helpful:
                      “the idea of excellent cardiovascular health among inuits is probably based on inaccurate data. See this review from 2003:

                      And here is what Graham wrote:
                      “Autopsy data on pre-westernised Inuit shows lots of data for atherosclerosis in the Inuit.

                      Personally, I think the evidence is pretty clear on this topic. Hope that helps.

                    18. Thea, Thanks for the links, and I agree with you that the Paleo diet is very troublesome. It looks like the large majority of studies done concerning the impact of fats on health have used animal products and oils, not whole food, plant based sources of fat like nuts, nut butters, seeds, flax, and avocado. The long term studies on unprocessed plant fats remain to be done, however the real-life and lab results for people using these foods in a WFPB diet show a very beneficial influence on their lipid and glucose levels. I know that Dr Barnard strongly endorses the science that fat clogs up the cells’ ability to respond to insulin, and he has had good success with his mostly overweight, diabetic patients. His book was written 7 years ago, and his comments about nuts are that despite their cholesterol-lowering effect, they make weight loss difficult and MAY interfere with insulin sensitivity. Dr Gregor has a video that challenges the weight gain effect of nuts:, and the science seems to be rapidly changing in our knowledge of fat metabolism. The majority of people who are pre-diabetic or diabetic are overweight, but what about those of us who are a healthy weight, exercise, follow a WFPB diet, and are still pre-diabetic? We have tried the low-fat, high-carb diet with limited success. Instead, reducing the carbs and increasing fat with the nuts, nut butters, etc have yielded much better test results: low total cholesterol, high HDL, low triglycerides, good A1c, and good FG. I don’t know the scientific reasons for that, and it contradicts the theory that all that extra fat gums up insulin’s action in the cells, but another mechanism must be going on with nuts, seeds, and avocado that produces these great results. I can’t say that it will work for everyone, but I think it should be seen as an option.

                    19. Thea, I just saw your reply to Suepy today, since it only appears on the Digest that arrives automatically every few days. Your links are interesting — thanks for sharing them. The Plant Positive analysis on Pygmies and Masai is compelling, and definitely alters my views of moderate or high intakes of animal fats. However, the Graham study concludes with this:

                      “The Eskimo diet was almost entirely meat, as attested to by their severe osteoporosis, while the Egyptian diet contained meat only at occasional festival times; yet the finding of atherosclerosis in both groups suggests that diet alone may not the critical factor…”

                      So, something else may have been causing heart disease even in ancient Egyptians who ate little in the way of animal products. Curious what that might have been….

                      The Pygmy diet was also interesting; high levels of trigyclerides from sweet potatoes, like the Okinawans, and yet very long life spans due to total cholesterols of only 130. That seems to contradict Siggurdson’s data citations on the TRGS/HDL ratio. Then again, his data is for Western populations, not people on anomalous ancient diets of sweet potatoes. Still, many researchers say that TRGS have been seriously overlooked as causes of heart disease. Perhaps that was an issue for the Egyptians. Just speculating.

                      But back to Suepy and my main point, where all this started: we are unaware of any studies on vegetarians or vegans that suggest that a diet high in nuts or seeds may contribute to plaque formation. There are a number of studies actually suggesting the opposite.

                    20. I was excited to find this intriguing study published in Nutrients journal on Dec 11, 2012, titled Monounsaturated Fatty Acids and Risk of Cardiovascular Disease, and which investigates the effect of MUFAs on CVS and diabetic risk factors.
                      It mentions that in 1999 the International Society for the Study of Fatty Acids and Lipids (who knew there was such an organization?) “agreed upon a recommendation table on daily intake of fatty acids as a foundation for further discussions.” The Dutch Dietary Guidelines set a range of 8-38% MUFA in healthy adults, 25% for obese, and the other international recommendations vary between 12% and 25% of total calories, while the recommendations for PUFA average 10%.

                      This is what the study found: in subjects with type 2 diabetes, “a significant decrease in TG values following a MUFA-rich dietary regimen could be observed when compared with a low-fat/high carbohydrate diet.”
                      ” Moreover, improvements in FG and pre-prandial plasma glucose were shown, while no significant changes in fasting plasma insulin concentrations, fructosamine and HbA1c were observed. The high MUFA protocols were accompanied with significantly lower values for TC and VLDL-cholesterol as well as increases in HDL-cholesterol, but were not correlated to changes in LDL-cholesterol. Comparison of high (>12%MUFAA) vs low (<12% MUFA) MUFA diets on glycemic control in subjects with abnormal glucose metabolism revealed improvements in HbA1c and fasting glucose in diabetic subjects, but no differences in blood lipids were found."

                      "There is strong evidence that by replacing SFA and carbohydrates with MUFA, various cardiovascular risk factors will be significantly improved. The results of the different meta-analyses addressed in this review point to a beneficial effect of MUFA-rich diets on systolic and diastolic blood pressure as well as parameters of glycemic control."

                      "Several studies indicated an increase of HDL-cholesterol and a corresponding decrease in triacylglycerols following a MUFA-rich diet. The effects on total and LDL-cholesterol appeared not consistent, but no detrimental effects on blood lipids were observed. Values for systolic and diastolic blood pressure were found to be reduced both during short- and long-term protocols using high amounts of MUFA as compared to low-MUFA diets. In type 2 diabetic subjects, MUFA exerted a hypoglycemic effect and reduced glycosylated hemoglobin in the long term. Although no detrimental side effects of MUFA-rich diets were reported in the literature, there still is no unanimous rationale for MUFA recommendations in a therapeutic regimen. Additional long-term intervention studies are required to characterized efficacy and effectiveness of recommending MUFA-rich diet among general and clinical populations."

                      The article also has a nifty table listing the fatty acid content of different oils, nuts, fruits, seeds, and animal products. So, more studies are needed to answer questions about how high MUFAs are advantageous, in which foods they work best, does saturated fat matter, are these benefits maintained long-term, are they applicable in only certain populations (healthy vs diabetic vs obese), can a healthy weight be maintained, and so on. If a diet has 25% MUFA and 10% PUFA, making a 35% total fat intake, then that might not be a bad idea after all.

                    21. Yes, great study! It’s strongly suggestive that you and I are on the right track with high-fat vegan diets. Nice find!!

                3. Russell: Thanks for the reply. That’s interesting. I’ve never heard of Type 2 defined that way. I’ll have to see how they define Type 1 to see if they think it is any different.

                  Sounds like you are happy with what you are doing. That’s great. I still don’t see how eating an over abundance of grains (while “over” is not good) would lead to your pancrease producing less insulin. But that’s neither here nor there if you feel that you are on the right track.

                  Good luck!

                  1. Thea, it’s based on the fact that a pancreas that overworks itself will begin to burn out beta cells. Fewer beta cells means less insulin production over time. And continuing to have big glucose spikes in one’s diet will cause further burnout or even the loss of virtually all insulin production. That’s why the gold standard for any diet, from a diabetic’s standpoint, is to carefully monitor one’s glucose meter post-meals. Anything that causes spikes over 140 is bad (for internal organs AND for further beta cell burnout). Anything under 140 is fine and shouldn’t cause any harm. This is why grains are so dangerous to anyone with diminished insulin production.

                    Interestingly, many of us have learned that whole grains carbs spike glucose as much as refined carbs. For example, I’ve tested and proven to myself that 50 grams of white flour has the identical effect upon my glucose as 50 grams of whole wheat flour. I was shocked when I saw that, but the effect was noticed and confirmed by Dr. Richard Bernstein in his book, The Diabetes Solution. Bernstein is renowned for having popularized the glucose strips that diabetics use today, and is widely respected in his field (Emeritus Albert Einstein School of Medicine).

                    Here’s the Type 1 definition for you, from Mayo:

                    “Type 1 diabetes, once known as juvenile diabetes or insulin-dependent diabetes, is a chronic condition in which the pancreas produces little or no insulin, a hormone needed to allow sugar (glucose) to enter cells to produce energy. The far more common type 2 diabetes occurs when the body becomes resistant to insulin or doesn’t make enough insulin.

                    Various factors may contribute to type 1 diabetes, including genetics and exposure to certain viruses. Although type 1 diabetes usually appears during childhood or adolescence, it also can begin in adults.”

                    1. Russell: Got ya. Interesting!

                      re: whole wheat flour producing same spike as white flour. I was actually aware of this since Dr. Barnard covers the same thing in his book–the one I mentioned previously. However, consuming intact grains – ie, not as flour is different. This is why I make a big point out of telling people in general (not your specific situation) that a recommendation to consume “whole grains” does not mean all those processed products with flour(s). It means *intact* grains – like barley, wheat berries, etc.

                      FYI: if you are a bread lover – they did find that for some reason pumpernickel and rye did not have as big an effect as other flours. I think pumpernickel bread even fell into the “low” glycemic index category, though just barely. You probably already knew that. I thought I would throw it out there in case anyone else reading this was interested.

                    2. Yes, I agree with you on certain grains, like rye and pumpernickel, but they still need to be used in moderation in their flour form.

                      But there is another problem. The most easy-to-make and accessible whole grains for vegans, I believe, tend to be rice, wheat, corn, quinoa, millet, and oats. Unfortunately, brown and white rice spike glucose equally so that’s not a great option (GI values both around 70). Wheat is not commonly used for cooking. Quinoa, corn (in whole grain form), and millet spike glucose very rapidly, so these aren’t good choices. And whole oats, although personally I love them, take forever to make in the morning, making them impractical unless you don’t have to rush out the door in the morning.

                      So unless I’m overlooking an important, low-GI grain that can easily and quickly be cooked, those of us with blood sugar issues are forced to keep them at very low levels in our diets. But we’d have better A1c levels if we eliminated them entirely.

                      Dr. Bernstein, who is a Type 1, has done that and is now in his 70s with no complications from diabetes. He has been a trailblazer. Unfortunately, I spoke to him this year and he is strongly against fats in the diet, for the same reasons as Dr. Barnard. Based on my previous citations, I think this position is a mistake. He is, unfortunately, also not vegetarian.

                    3. Russell: Either I’m not understanding what you are saying, or you and I have access to vary different data. In the table I’m looking at now, it shows a GI for white rice as 72 (high), but brown rice as 50 (low). Similarly, quinoa is 53 (still technically low). All of the legumes listed are below 40, with black beans at 30 and peas at 22. Of course, if your particular body reacts with a big spike, it doesn’t matter what the tables say. Maybe that was your point?.

                      I think someone already responded with this idea, but I wanted to share what I do for oatmeal, because I’m not a fan of the quick-cooking rolled oats myself. I make a big pot of whole or steel-cut oats on the weekend. Then all I have to do is scoop, heat and eat over the rest of the week. Works great. The oatmeal lasts at least a week. If you wanted to keep your meals fatty, you could add peanut butter for peanuty oats. :-)

                      Please note: I’m not arguing with you/trying to convince you of anything. Just exchanging information and ideas.

                    4. Hi Thea. That’s certainly a fair question. Here’s an Australian study on rice varieties that makes the comment that all “the results indicate that most varieties of rice sold in Australia, whether white, brown, or parboiled should be classified as high-GI foods.” There was one exception called Doongara rice that had a GI of only 64.


                      Here’s a diabetes site that says brown rice is 66-87, whereas white rice is actually the same or a bit lower.


                      Anyway, this discussion on GI is virtually irrelevant for those of us who lack a second-phase insulin response. I encourage you to read the following, which makes this abundantly clear:


                      I like your idea of keeping whole oats in the fridge. I’ll try that. I already put a big dollop of peanut butter in my occasional oats, and it really helps to slow down the glucose hit and allow me not to exceed my targets.

                      But the key thing for those of us with poor insulin response, or insulin resistance, is to strictly limit the carbs in the first place. Dr. Richard Bernstein’s formula is 12/6/12 carbs for breakfast, lunch, and dinner, totaling only 30 carbs a day! Basically impossible targets for a vegetarian or vegan and extreme of course, but he’s mostly talking to Type 1 diabetics with that advice, of which he is one himself. For the rest of us, its a function of what our glucose meters are allowing us to do. For me, I can get away with about 25/25/25 before going over 140 on my glucose meter.

                      Unfortunately, the differences between a serving of rolled vs. steel cut oats in a single serving is the difference between 27 and 32 carbs, not much. So, I can eat almost a full serving of one of them, but that’s less than 200 calories in total for my entire breakfast. I will starve to death! :)

                    5. Russell: Great info. I will take a look at your references/sources.

                      The only other comment I have is to the following: “But the key thing for those of us with poor insulin response, or insulin
                      resistance, is to strictly limit the carbs in the first place.”
                      I don’t know enough about poor insulin response to say anything about it. But for poor insulin resistance, I believe that was what was fully covered in Dr. Barnard’s book and clinical research. And that’s where we are going to have to disagree. Because Dr. Barnard has successfully treated, both anecdotally and in published clinical research, T2 diabetes without any strict carb limitations. He just encourages people to eat *low-fat*, low GI (no flours, sugars etc) and a whole plant food based diet. And that alone fixes their insulin resistance.

                      But that just brings us back to where we started the conversation. So, I’ll leave it at that. I’m glad you found a diet that you feel is healthy and will give you long results. That’s really great.

                    6. Thea, yes, I’m with you. I think many cases, if not most cases of insulin resistance are a function of people being overweight and having cells that cannot easily absorb the glucose. Once they lose the excess pounds, the insulin resistance dissipates and they can eat carbs with better glucose responses.

                      However, I believe that too many dietary experts, including Drs. Barnard, Ornish, Esselytyn, etc. have failed to acknowledge that there is an entire group of us who are diabetic or pre-diabetic, facing a different problem — insulin supply inadequacy. For us, the notion of reversing our condition is a fallacy, and eating more than modest amounts of grains may actually be harmful to our health. The American Diabetic Association is certainly culpable in this regard as well.

                      Dr. Bernstein, in my view, is a hero for finding a solution to this problem — low total carbs — even if he erred in thinking that animal-based proteins were superior to plant-based fats as the solution.

                      So… just saying… those of us with insulin inadequacy shouldn’t all be lumped together with those of us with insulin resistance.

                      That said, I hope I’ve made a reasonable case that plant-based fats may not only be a good solution for those of us in this category, but also that this may actually be a very healthy diet choice in general. Clearly more research is needed to distinguish health-related differences for those of us who eat high-fat, low-carb vegan diets, versus those who eat more carbs and fewer fats.

                      We didn’t get into it, but there’s also an argument to be made that lower carbs may also help to reduce IGF-1, and be associated with fewer primary cancers (higher IGF-1 appears to fuel tumor growth), compared to those who have higher average glucose levels, no matter what their diet.

                      With that in mind, I’m also happy to keep my glucose level as low as possible. Its hard to watch out for tumors, but easy to do annual carotid scans to insure that veggie fats aren’t plugging up our vascular systems. :)

                      Anyway, thanks for sharing your thoughts on this subject. The science obviously is far from complete, but perhaps we’ll know more in the next few years.

                4. Russell: FYI, the Mayo Clinic defines Type 1 this way: “Type 1 diabetes, once known as juvenile diabetes or insulin-dependent
                  diabetes, is a chronic condition in which the pancreas produces little
                  or no insulin, a hormone needed to allow sugar (glucose) to enter cells
                  to produce energy.”

                  I’m not necessarily making any point. Just sharing. :-)

        2. Hi, Russell. I think you will find that if you aren’t eating the high fat, you will be able to eat all the carbs you want (and need), without spiking your glucose levels like that. Here’s another piece by Dr. Greger:

    2. Nope. Nothing to worry about as long as you’re covering all your nutritional bases (proteins, vitamins, minerals) with the other 65% of your diet and are not in an excessive energy balance.

      However, it’s not carbs that cause insulin resistance but insulin resistance that causes problems with carbs.

    3. Please reference Dr. Joel Fuhrman’s (EAT TO LIVE author) new book THE END OF DIABETES. It will explain all. Meticulously supported by research as usual. Dr. Greger here is a fan.

      1. Thanks GardenGirl. From what I can gather on the web, Fuhrman’s plan is a vegan-based, nutrient dense diet, which is pretty much what I’m already doing. I’d love to know more and wish that he had further information publicly available without the need to buy a book who’s tenets I may already be following. Feel free to share any relevant details, if you like.

  4. I may be way off, but I am sure I read that because of the way cocaine screws up with the dopamine in the brain years of use can lead to neurological disorders such as Parkinson’s. If eating fatty or sugary foods screws with the dopamine in a similar fashion as cocaine, can eating fatty foods over a long period of time also leave you at risk of neurological disorders such as Parkinson’s?

  5. I wonder about the definition of “energy-dense”. Is just “sugar+fat” energy-dense, or would – say, a steak equally qualify as “energy-dense”? Surely there’s a definition for “energy-dense” including a kilojoule-per-weight-unit ratio?

  6. Should i moderate the amount of toasted rolled oats that i eat? People say we should aim for less than 10% of calories coming from fat. I think it’s 18% for oats…

    1. Also, should i stop putting soy milk on my oats and fruits? In one video dr greger says that soy milk may block the absorption of antioxidants..

  7. The “negative calories” concept for fiber is kool, although technically some dieticians consider soluble fiber as containing about 2 calories per gram ( ). So foods highest in zero calorie insoluble fiber might be best for weight loss, especially since that type of fiber speeds up intestinal transit time, and the faster food moves through, the less it has a chance of getting absorbed.

  8. This is hard to believe. And I think I am agreeing with this. In fact, not eating is even considered a mental disorder, right? Anorexia and obesity, are they just alike? Does craving for food have something to do with this? Perhaps, the first step is to admit that this isn’t normal anymore. I have to start eating healthy, otherwise I will gain weight instead. Being fat has a lot of drawbacks. is one.

  9. This discussion is really interesting to me–thanks, Russell, Sue P, Thea. I’m in a similar position with some differences; I’ve had “prediabetic” fasting glucose levels for at least 20 years–don’t have older records than that–but they were considered “normal” until a few years ago when the ranges were changed so “prediabetic” FBG was lowered from 115 to 100. I’m 72, have been a vegetarian (pretty much whole food, plant based) for 35+y, a vegan (WFPB) for 5, I’m underweight (BMI 17), exercise a lot (more since trying to manage glucose levels). My fasting glucose is upper 90s to mid teens, A1C is 5.5. Since my FBG was flagged about 3y ago, I’ve been really focusing on trying to lower it w/o losing more weight. I’ve read and tried to implement Barnard, McDougall, Fuhrman, and read as much as possible on the web. I’ve been following my diet and exercise carefully via Cronometer and fitbit and measuring glucose, had conversations with my doctor, with an endocrinologist, with a dietician in a diabetes center. My doctor and the endocrinologist say I don’t have a problem–I’m not diabetic, I’m stable, keep doing what I’m doing–it’s great, don’t “worry”. The dietician couldn’t find anything wrong with my diet and responded to my weight, recommending veggie protein powder, and (amazingly) a “blood type” diet (for me, type A, lots of meat!). These are all people at the nearest academic (and wonderful) medical center. However, they are not taking into account the fact that my tiny amount of body fat is slowly morphing from subcutaneous to visceral, and that the numbers of papers implicating “high normal” blood glucose with all kinds of ills, especially dementia, increases.
    It seems to me that the context of the current diabetes/obesity epidemic controls everyone’s understanding/research/recommendations about the disease. The WFPB doctors’ recommendations (and everyone else’s too) are based on the overwhelming numbers of diabetics who are overweight/obese (they so predominate that they skew the data and control the evidence for treatment); these people cure their diabetes by losing weight. The WFPB diabetes plans help these people do it in very healthy ways. But at 5’6″, I spent most of my adulthood weighing 125 and am now 105 and need to eat more than 2000 kcal/d to maintain it. So I need to do something else.
    I’ve switched all grains to their intact form, eating mostly whole oats, barley and long grain rice (lower GI for long than short grain. Russell, note that hulled barley’s GI is half that of all the other
    whole grains–27? cp to mid-fifties for the rest. It does need long
    cooking but that can be done ahead–this is a great grain for
    diabetics). Lots of beans, lentils. Lots of vegetables, especially non-starchy. Only low sugar fruits, no juice, no added sugars of any kind. I do eat seeds and nuts–flax, chia, almonds, walnuts, sunflower, a little cashew. No separated oils at all. Macronutrient kcals are 50% carbs, 35% fats, 15% protein, approximately, with energy about 2400 kcals. I am uncomfortable with the high fat levels (my husband would benefit from a straight Essylstein diet instead of his current approximation). I get enough calories by eating a large serving of whole grains at each meal, and I’m no longer losing weight.
    However, this diet has not had the effect I hoped for and I’m not sure it makes much difference in FBG. At least it’s not getting worse. And, visceral fat and all, I remain very healthy (always feel like the healthiest person in doctors’ waiting rooms!).
    I’ve felt like such an outlier. I’d love to get some feedback.

    1. Alice, It’s good to hear from another skinny vegan who’s pre-diabetic. What really works for me is testing my glucose levels after meals to determine how different foods raise it. I can’t handle too many carbs at once, even low GI foods, which can shoot my glucose up too high. Smaller meals more often have been a positive change, plus getting into motion after a meal. My diet is similar to yours, although most days my only grain is barley (does seitan count as a grain?). I’ve kept my fasting glucose in the 80’s and A1C at 5.2. Last year I switched out rice, white potatoes, and flour products for the nuts, seeds, and avocado, which gave me a fat ratio between 35-45% of calories. Worried about the higher fat, I had my cholesterol tested and it came back total 159, HDL 79, and triglycerides 28, so I decided that this diet looked like the right track. I hope so!

      1. Thanks so much for your reply. It sounds like you’ve solved it–fantastic numbers! FG in the 80’s and A1C of 5.2–you’ve become normal! Congratulations! You give me great hope that I can do it too. Can you give me more details? What number range 1h and 2h after meals do you work towards? How many kcals do you need in a day? How do you distribute them over the day? How much grain carbs can you eat without spiking high after eating and then eventually raising FG? Do you limit beans like chickpeas that have a lot of carbs?
        The best numbers I’ve had were when I was following Dr. Fuhrman’s plan–I ate a lot of soybeans and eggplant I remember, but I also lost weight, didn’t much like the soybeans, and had to cook 2 separate diets since my poor husband simply hated what I was trying to eat. Not sustainable.
        I have been eating rice and oats pretty much daily and I can easily switch over to barley which I love. Seitan seems a good solution–pretty much carb-less–but probably has zero micronutrients.
        I have not been testing glucose after meals–started today. Between 97 and 106 all day, walking after first meal and garden work after the 2nd. I need to start keeping good records again.
        Thanks again, Suepy. I’d like to keep asking you questions if you don’t mind. I’ll try to keep it minimal, but you’ve given me real hope after having pretty much given up.

        1. Absolutely there is hope! I would be happy to share with you some of my experiences and would be delighted if in any way this helped you achieve your quest for better health. It takes much trial and error in making diet changes, so proceed with care, testing often to see what works for you in your glucose control, lipid profile, and weight goals. Fortunately I have a local hospital which offers free cholesterol testing (non-fasting) every month, so I go every now and then to track my total cholesterol and HDL. I get the fasting cholesterol and A1c at my yearly physical, and test my glucose with a simple meter from Walgreens with test strips ordered online. It helps to keep a chart of my meals, or enter on cronometer, and I test 45 minutes after a meal to see how high my glucose is headed and if I need to get off my butt and exercise. A sandwich or veggie pizza will send mine to 170, but my goal is to keep glucose below 140, ideally 120, after a meal and below 100 after 2 hours. When I took the GTT test last year my fasting was 80, 1 hour 186, 2 hour 130, which makes me think that I’m insulin resistant. Smaller portions of carbs in a meal and eating/ snacking every 3 hours definitely makes a difference to me.

          I have great respect and admiration for Drs Barnard, Esselstyn, Ornish, and McDougall and basically follow their recommendations, but I seem to be having more success with Dr Fuhrman’s plan which allows higher nut/seed/avocado intake and stresses beans over grains. Of course, Dr Gregor is my favorite and I hope he looks more into the research on heart healthy fats. I’m almost embarrassed to admit that my fat intake has reached the 46% mark on occasion (love them pistachios!), usually it’s 30-40%, but that is when my lipids are best and glucose levels on target.

          I rely on beans, lentils, tofu, and seitan for my primary protein sources and have no limit on how much except as part of portion control in a single meal, keeping them between 1/2-1 cup. Same with whole grains, no more than 1/2 cup in a meal, but lots of veggies. My daily calories range between 1600-1800 and with moderate exercise that keeps my weight steady around 102 lbs (I’m 5’1″ tall). I make a meal out of a big salad every day, with 1/2 avocado, carrot, almonds, edamame, etc and use an Engine 2 recipe for no-fat salad dressing.

          I hope this has answered some of your questions and has been of help. Good luck with your awesome health adventure!
          Sue P.

          1. Thanks so much, Sue P. You’ve given me a very clear description of your pathway. Our diets are very similar (less fat in mine) but mine has not been controlled for quantity over time like yours. (I’ve been too concerned with adequate calories). This must be really important. You’ve convinced me that testing after meals is critical. I’ve started: 9 readings, very careful eating and 2 post-meal exercise sessions, with less relaxation after meals yesterday–and my FG this morning was 85! This is doable!
            I think I’ve been too frugal–unwilling to spend the expensive test strips densely enough to get their full information.
            Thank you for your guidance, friend. I’ll let you know how it’s going.

            1. Alice, I’m so glad to hear about your FG going down. Yay! Please do keep me updated – I’d love to hear about what’s working and what isn’t. I ran out of test strips last week, ordered more, but feel lost without that input on my glucose levels. Sore fingers are worth it!

    2. Alice, thanks for sharing your story. How many grain-based carbs do you eat every day? The lower the better as far as glucose goes — please see Richard Bernstein’s Diabetes book. It’s a brilliant read, though he’s not vegetarian. And do you know your triglyceride levels (they are usually in lockstep with your grain/sugar consumption)? My first thought is that your grain intake may be a bit too high… perhaps replace some of them with more salads with avocado? Fyi, I love my avocados and have a whole one for breakfast every day with hemp or ground flax seed and turmeric on top. I often have two a day for caloric content.

      1. Hi Russell. Thanks for responding. I’m so glad you started this discussion–I’m learning so much. I’ll look for Dr. Bernstein’s book. So far I haven’t paid much attention to anyone’s diet prescriptions that are not vegetarian/vegan.
        I have been eating a half cup (pre-cooking) of oat groats for breakfast cooked with tomatoes, shiotaki, turmeric, black pepper, kale, flaxseeds and soy milk. It’s a bit over 500 kcal and keeps me going for hours. Lunch is usually some kind of leftovers and a big salad. Dinner is some sort of stir fry with tofu and lots of vegetables, or dal and vegetables, or a stew or soup, usually with a cup or so of long grain brown rice. Then add calories as needed with nuts as dessert. I have fruit–maybe 2 apples–with lunch/dinner. I guess I get 250-300g of carbs a day–don’t know how much of it is grains–more than half. No added sugars or even high sugar fruit. No oils.
        My triglycerides were 68 when last measured, so haven’t been a problem.
        The thing is: you’ve got to eat something. (And I have to eat a lot.) Too much protein, IGF1 goes up. Too much fat, atherosclerosis, hearth disease and stroke. The evidence increasingly shows this. So the WFPB prescriptions emphasize carbs. This doesn’t work for thin “diabetics” like us. (Gabe Merkin, a mostly WFPB exercise physiologist MD with a blog, says that thin diabetics are “harder to treat”. Yes.)
        I like your explanation for what’s gone wrong with your metabolism–that your beta cells have been damaged and are unable to produce adequate insulin quickly enough. It makes good sense. I’m not sure it’s true for me–I have the additional metabolic disturbance of needing far too many calories to sustain life. This has been true for ~ 15y.
        We’ll see how many grain/legume carbs I can take in now without terrible peaks, and whether it will help to space meals differently. I can pretty easily lower BG 15 points or so by moving around vigorously. Fortunately.
        Suepy, I didn’t do so well today–93–but it’s a continuing project. I’m also away from home right now (w intermittent internet) and did a lot of driving yesterday. Does anyone have any experience with stress and BG? It has seemed to me sometimes that when I have a particularly “sweet” rewarding day my glucose drops to normal. (It’s hard to figure out a way to utilize that observation since my life is generally pretty stress-free these days.)

        1. Hi Alice. I’m also learning a lot from this discussion! First, I want to clear something up. IGF-1 on a plant-based diet isn’t a risk factor, according to Dr. Greger. See:

          So, I guess you can eat all the soy and seitan you want! And I don’t know if seitan affects triglycerides, but will try to find out from some self-testing as I’m raising my intake.

          I pay only modest attention to fasting glucose now because I’m far more concerned with the peaks. We should avoid any peaks, ever, above 140, from what I’ve learned. This will give us comparable values to those without glucose problems. A1c is only a partial measure — one can have a decent A1c and still have peaks in the 150s I think. So, after-meal testing is very important.

          Personally, I’ve found that avoiding all carbs except seitan, I can easily keep myself in the target range under 140, even under 130. But the moment I have a quarter cup of oats, rolled or steel cut, my glucose climbs right to my threshold. And a quarter cup is hardly enough for a breakfast. For me, carbs just aren’t an option. I wish they were. Funny enough, lentils and other beans have the same effect. I must try very hard not to eat more than about two or three big spoonfuls.

          1. Thanks for your links to Dr. Greger’s plant protein and IGF-1 videos, Russell. I agree with you about the importance of staying under 140 after meals, tho I’ve found it very hard to do–I’m experimenting now with immediate post-meal exercise as Sue and you described. Do you test at 1h and 2h after starting to eat a meal to best capture the peak?
            Seitan is interesting stuff. You can make it out of wheat flour by kneading the flour and water to develop the gluten–the protein constituent of wheat–and then washing out all the starch, fiber and fat in cold water, leaving nothing but protein behind. So there should be no carbs left in it. People sometimes refer to grains as “carbs” because they’re such a common source, but it’s confusing because lots of foods contain carbohydrates besides grains–such as lentils and beans, fruits and veggies. It’s not surprising that lentils and beans raise BG–they contain lots of carbs, along with their protein and fiber.
            I had your sort of lunch today–a whole avocado with a giant green salad–after a morning of outdoor work, and my “peak” if I measured it at the right moment was 97!

            Interesting about stress–I’m going to pay more attention to it.

            1. Alice, good going with that 97 post-meal glucose! That’s a great number. Yes, I test at around 1 hour and if its higher than I want, say 125-140, I’ll test it again around 2 or 2 1/2 hours because sometimes, especially with a carby meal like beans, I get a delayed peak. If I eat about 40 grams of steel cut oats, which isn’t a huge amount, my peak can be delayed for 3 hours. So, at one hour, it might be at 125, and its easy to get lulled into a false sense of comfort, but then at 3 hours, its at 165! On the other hand, if I have only 25 grams of oats, I may never go over 120. So portion size is critical. That said, I have trouble controlling my portions of carby foods, so that’s why I just decided one day — no more grains! Ever since then, its been a lot easier to manage my peaks.

      2. Russell, I looked up diabetes on Dr Fuhrman’s website
        and found these references for his article, so here are the links in case you’re interested in researching some more:

        9. Casas-Agustench P, Bullo M, Salas-Salvado J: Nuts, inflammation and insulin resistance. Asia Pac J Clin Nutr 2010;19:124-130.
        10. Martinez-Gonzalez MA, Bes-Rastrollo M: Nut consumption, weight gain and obesity: Epidemiological evidence. Nutrition, metabolism, and cardiovascular diseases : NMCD 2011;21 Suppl 1:S40-45.
        11. Jiang R, Manson JE, Stampfer MJ, et al: Nut and peanut butter consumption and risk of type 2 diabetes in women. JAMA 2002;288:2554-2560.
        12. Kendall CW, Esfahani A, Truan J, et al: Health benefits of nuts in prevention and management of diabetes. Asia Pac J Clin Nutr 2010;19:110-116.
        13. Li TY, Brennan AM, Wedick NM, et al: Regular consumption of nuts is associated with a lower risk of cardiovascular disease in women with type 2 diabetes. J Nutr 2009;139:1333-1338.
        14. Dunaief DM, Fuhrman J, Dunaief JL, et al: Glycemic and cardiovascular parameters improved in type 2 diabetes with the high nutrient density (HND) diet. Open Journal of Preventive Medicine 2012;2







        I’m convinced! A personal antidote: my vegan daughter is home for a few months and loves to cook gourmet, high-starch meals using olive and canola oil. Hard to resist, but after I have been eating small amounts of pasta-rice-bread, my glucose and weight have started to go up. Hence, more exercise, so I am now keeping my weight steady at 102, but I noticed that my waist has grown 1-2″. Insulin resistance?! It’s time to say no to the fast carbs and oil; I’m buying more pistachios.

        1. Suepy, thanks so much. Unfortunately, I probably don’t have enough time to look at those links, but I don’t think we have much alternative but to eat nuts and seeds. If you read my response to Thea an hour ago, if nothing else, please see my last two paragraphs about Dr. Barnard.

          The big question in my mind is how low can we get LDLs while getting sufficient calories and also maintaining low glucose? If you don’t mind my asking, what’s your LDL?

          As for your daughter’s great cooking, that’s tough to resist! But a bit of cheating is probably okay if you can still stay under 140 glucose at all times.

          1. Russell, I’m barely staying under 140 glucose and the exercise is vital, but I gave my daughter some different cookbooks to look at which don’t use cooking oils or processed starches. My LDL for the past year has been in the low 70’s, however when I had my non-fasting cholesterol tested in Aug and Oct, the LDL and triglycerides were too low to show on the nurse’s meter. She asked me if I took statins, and I said no, I’m a vegan. She asked me what that was, then said my low cholesterol must be genetic. I told her that on the contrary, both of my parents had heart disease, and my dad died from a heart attack at the age of 44, despite being slender all his life. That was my wake up call – food and lifestyle make the difference. My daughter has our fast metabolism and doesn’t gain weight, but cheap carbs can certainly catch up with you!

            1. Suepy, be sure to stick with VAP cholesterol, not the regular testing. Regular test results are significantly thrown off by low-carb diets because the LDL number is calculated, not measured. Also, non-fasting tests will throw off triglycerides a lot. You might want to re-test.

              I relate to having a fast metabolism. My cousin, my Dad, and I all have had hyperactive thyroids. Mine is fully controlled, but at times, I’ve had a massive appetite and couldn’t gain a pound. This might have contributed to my beta-cell burnout.

              1. Good advice, Russell. I am getting a fasting test in a few weeks and will request the VAP cholesterol. My last fasting trig was 48 and HDL 80, and that’s after 6 months of 30-40% fat from nuts, etc.

                1. Congratulations, those are incredibly impressive numbers for HDL, LDL, and Trigs!! You’re probably in the lowest 0.1% of lipids-based risk, and I doubt anyone could make an argument that your plant-based fats are causing one iota of additional risk! I continue to think that Dr. Esseltyn, Campbell, etc. are completely nuts (pun) on this point. You’re only a sample of one, but if you can get Trigs down so low while maintaining ultra low LDL, others can too. You are basically at the 60:60:60 levels. Of course, you could also check ApoB/ApoA1 ratio, which is a good telltale also.

                  Your glucose, on the other hand, shouldn’t be allowed to spike….

                  Last point — have you had a carotid scan? LifeLine Screening offers one for $150 in a mobile lab, and I think its really the gold standard. It will show whether you have plaque built-up or not. Way better than just measuring lipids.

                2. Suepy,

                  I just recalled a brief conversation I had this summer with Dr. Esselstyn, in which he said that eating plant-based fats increase our inflammatory markers and cardio risks. When I mentioned that my CRP was excellent, in addition to my lipids, he continued to highlight the dangers of fat despite my scores. So… I asked him isn’t there a viable measurement to find out if what you’re saying is correct? He said, “actually, yes, test for MPO”. I haven’t done that yet, but might ask my M.D. for a lab slip. Here’s what I found on the web about this. Given your family history, it may make sense to test it yourself — if you do, I’d love to know your results:


                  Elevated plasma free fatty acids increase cardiovascular risk by inducing plasma biomarkers of endothelial activation, myeloperoxidase and PAI-1 in healthy subjects

                  The novel finding that a mild elevation in plasma FFA may activate vascular MPO and tPAI-1 has important clinical implications. The mechanisms by which MPO may promote atherogenesis include conversion of LDL into more atherogenic oxidized particles (oxLDL), oxidative modification of apolipoprotein A-I that results in a dysfunctional HDL and reduction of EC nitric oxide availability resulting in endothelial dysfunction [21-24,26,53-55]. These multiple mechanisms help explain the strong predictive value of plasma MPO levels for acute coronary syndromes (ACS) in humans even after adjusting for traditional cardiovascular risk factors, Framingham risk score, or hsCRP [28-30].

                  (2) J Intern Med. 2012 Jan;271(1):43-50. doi: 10.1111/j.1365-2796.2011.02397.x. Epub 2011 May 30.

                  Myeloperoxidase is associated with incident coronary heart disease independently of traditional risk factors: results from the MONICA/KORA Augsburg study.

                  Karakas M1, Koenig W, Zierer A, Herder C, Rottbauer W, Baumert J, Meisinger C, Thorand B.

                  Author information



                  Oxidative stress plays a critical role in the initiation and progression of atherosclerosis. Myeloperoxidase (MPO) is a marker of oxidative stress. We prospectively investigated whether an increased serum concentration of MPO is associated with an increased risk of incident coronary heart disease (CHD).


                  We conducted a population-based case-cohort study in middle-aged, healthy men and women within the MONICA/KORA Augsburg studies. Serum levels of MPO were measured in 333 subjects with (cases) and 1727 without (noncases) incident CHD. Mean follow-up time was 10.8 ± 4.6 years.


                  Baseline concentrations of MPO were higher in cases compared with noncases (P ≤ 0.001 in men; P=0.131 in women). After adjustment for major cardiovascular risk factors, the hazard ratio (HR) with 95% confidence interval (CI) comparing the top with the two lower tertiles was 1.70 (95% CI, 1.25-2.30). After additional adjustment for markers of inflammation and endothelial dysfunction, the association was attenuated (HR 1.50; 95% CI, 1.08-2.09). There were no significant interactions of MPO with sex or increased weight on CHD risk.


                  Elevated concentrations of the oxidative stress marker MPO were independently associated with increased risk of incident CHD. This finding deserves detailed evaluation in further studies.

                  © 2011 The Association for the Publication of the Journal of Internal Medicine.

                  1. Interesting, I’ll see if my doctor will order a test for MPO. I’ve never heard of that test before and looked it up on the Cleveland Clinic website
                    I’ll be sure to let you know the results if I can get the test. The more information we have to evaluate our diets, the better, and it would be reassuring to know that the higher fat diet is not creating hidden CVD.

    3. Alice,

      You have a very interesting story. It’s interesting, because you have been eating right for so long, but now you feel that you have a big problem. On top of eating right, it sounds like you are exercising quite a bit. My guess is: for a 72 year old, I’m guessing that you are doing better health-wise than many (most?) of the 30 year olds in America.

      I’m not a doctor, but I think you are asking for my take on what you wrote. Here’s my take:

      I keyed in on these parts of your text: “My doctor and the endocrinologist say I don’t have a problem–I’m not diabetic, I’m stable, keep doing what I’m doing–it’s great, don’t “worry” … I remain very healthy (always feel like the healthiest person in doctors’ waiting rooms!).” And yet you are certain that you have a problem, because, “…the numbers of papers implicating “high normal” blood glucose with all kinds of ills, especially dementia, increases.”

      My thought is that those associations that are being drawn between high glucose and ills are probably being drawn on people who eat poorly and/or are overweight. As you have pointed out, the results of such research may not apply to your situation. In fact, we have absolutely no idea whether or not such an association would apply to someone who has been eating incredibly healthy for at least 5 years and who exercises more than most people. We have plenty of examples where we know that the bodies of whole plant based eaters are different than the bodies of SAD eaters. So, it stands to reason to me that the numbers of various indicators for “normal and healthy” would be different compared to the numbers for SAD eaters. Plus, we know that what counts as normal numbers for a 70 year old is often different than what is normal for a 20 year old. My point is: I don’t think your concern about your current numbers is all that well founded.

      I’m not a doctor. So, what do I know. But your doctors are telling you that you are fine… Maybe they are right? I’m concerned that you may be so worried about hitting an arbitrary number, that you change your diet in such a way that ultimately does hurt your health. Consider that for a moment.

      Another thought for you: You say that you are under weight. Who says? I understand that you weigh less now than you used to. But does that mean that you are underweight – in the sense of “your health is at risk because of your weight” – right now? Maybe your current weight is what is healthy for this stage of your life? I don’t mean to imply that underweight is OK. I know that underweight can be as big a health risk as over weight. I’m just questioning whether or not you really are underweight. (I don’t know. It’s just a question.)

      Similarly, you are concerned about your fat type. How do you know this is not normal for someone of your age? I truly hope I don’t sound like someone who is brushing off your concerns as, “oh, she’s just a senior and you should expect poor health.” I don’t think that AT ALL. What I am thinking is that it is appropriate to acknowledge that body composition does naturally change somewhat with age. So, it is *possible* that the changes you are seeing are perfectly normal and healthy for your stage of life. Again, I’m no doctor. So, I don’t know. I’m just believing you when you say that you are the healthiest person in the doctor’s waiting room. So, maybe you really don’t have anything to worry about.

      It sounds like you already know what to do in order to gain weight if that is your goal – eat more calorie-dense foods. I thought I would point out that gaining weight is usually done one of two ways – by gaining more fat and/or more muscle. You say that you have lost weight. Do you have a sense of whether or not that loss was muscle, fat or some combination? If you can gain weight by gaining more muscle, that seems like a good idea to me. You mention doing more exercise, but not which kind. If you can work in the kind of exercise that will build up muscle, some safe weight-bearing exercise that will be intense enough to build muscle, that might help you feel like you are more on track health-wise.

      While I don’t expect that I will have changed your mind on anything, I hope that I at least gave you some food for thought.

      1. Thank you, Thea, for your
        very detailed response. I have admired the kind way you moderate this
        discussion site. The points you raise are ones I have thought deeply about over
        a long period of time. I know that I am not typical of the population the
        statistics are derived from; however it seems to me that I have to operate on
        the assumption that some things are true and apply to me: that glucose peaks
        over a particular level are damaging to cells throughout the body, that A1C
        measures actual damage to red blood cells that has occurred over the previous 3
        months, and that it’s reasonable to try to lower these measures thru diet,
        exercise, lifestyle, as possible. I have never come across differing ranges of
        healthy glucose levels intended for “elderly” people.

        I think assuming that
        less-than-good health outcomes are the inevitable result of “aging”
        is a logistic mistake.

        Something else I would like to say is that glucose measurement is sort of
        miraculous–it’s one of the few instances where people can easily get immediate
        hard information about themselves and how they’re doing, in an area,
        “health improvement”, that tends to be very theoretical, with people
        arguing from authority–so-and-so-says…–rather than experience/knowledge,
        which is hard to come by and where “facts” are frequently not all
        that clear. It’s a mistake to discount it.

        My description of myself as
        among the healthiest people in the waiting room was merely to say I’m not very
        “sick”. Certainly not in the range for my doctor to want to treat.
        Fortunately. I basically believe that if I were eating the SAD, I would have
        diabetes and she would have to treat it. I credit my WFPB diet for my current
        not-terrible values, and I’m certainly not willing to change it more than

        My “underweight” has been well checked to rule out dreadful
        causes. It’s a practical problem mainly because anytime I’m away from my own
        kitchen, visiting family for instance, and don’t have pretty complete control
        of my food, I lose weight, several pounds a week, and it takes a long time to
        regain it.

        It is also a big constraint
        in tweaking the diet to improve glucose control–if I’m losing weight my
        glucose improves. But I mustn’t lose weight so I can’t really cut carbs much
        which is the thing, of course, that would help.

        It’s not clear to me what range of fats that are unrefined, plant based,
        minimally saturated, and balanced between omega 3s and 6s, are healthy and
        good. The nominal 10% levels seem impossible for me to achieve–oat grains
        themselves are 15% fat. These low levels seem to be very important for anyone
        with heart disease or increased risk for heart disease, but, thankfully, I
        don’t think that includes me. I’ve been following more of a Fuhrman approach
        and eating nuts, seeds, avocados, etc. as needed to maintain weight.
        So sometimes fat has made up 40% of daily calories. I truly don’t know what the
        cut off value should be. I’d love to have some new good ways to think about
        this. It seems the central question of this discussion. We “know”
        that 40% of animal based/processed SAD fat is terrible, but what about the
        healthiest plant based fats?

        Exercise really helps blood glucose. I walk, jog a bit depending on the state
        of my knees, and do some weight lifting. I’m very interested in increasing
        muscle mass, especially since that’s what is removing the glucose from my
        blood! It seems very difficult for my body to increase muscle, and I think that
        is the result of aging, since it wasn’t true a few years ago. I continue to
        work at it.

        1. Alice, I love your reply to Thea, considerate and thoughtful. Since you are interested in increasing muscle mass, maybe you could try replacing more of the carbs with protein. As Russell pointed out, IGF-1 shouldn’t be a problem with plant based protein. Dr Gregor has a number of videos about IGF-1, and he observed that what matters most on all-cause and cardiovascular disease mortality rates isn’t the ratio of fat to carbs to protein, but the source, whether from plants or animals.

          Dr Fuhrman has an article linking higher animal and concentrated soy protein to increased IGF-1along with suggestions for building muscle mass.

          A new study published in March suggests that animal proteins have a different effect on IGF-1 than plant proteins, but they used soy protein and want to test the other plant sources.

          Another advantage to including more plant proteins and fats in you diet are that they are easy to eat while on the road and visiting family. Bean burgers are everywhere, bean salad and lentil salad are easy to make, and scrambled tofu, steamed edamame are simple. I snack on the White Wave seitan right out of the box and always have a supply of nuts and fruit for those between meal snacks. Traveling does upend our routines!

          1. Thanks, suepy. I’m sorry it’s taken me so long to reply–I’ve wanted to accumulate enough results under my new regime to see what’s happened. It’s all good. By exercising right after each high carb meal 20-30m, and including one low carb/ high kcal meal (salad with avocado ) each day, my postprandial peaks have mostly been under 120, a few ~130, only 3 above 140 (when I hadn’t planned enough time for the necessary immediate postprandial exercise) during the past week. And FG has all been under 100; it’s less predicable–2d in the 80s, then a couple in the 90s, back to the 80s. It’s harder to understand–maybe reflecting accumulated effects of more, or more vigorous exercise, or less obvious differences in dinnertime meals (more fiber, resistant starch, etc). Some days my measurement have been completely normal.
            I’m very happy and relieved. And I’m so glad this topic came up, and you and Russell pursued it, and I happened upon it.
            Thanks very much for your links as well. It only makes sense that there are reasons besides sheer Virtue that animal protein is so bad for us–that an amino acid profile dissimilar from ours might be healthier. Dr. Greger has a nice article about it too, trying to establish where the limit on soy should be:
            The Cell article is particularly interesting and apropos to me–how much protein forms how much IGF1 and how harmful is it, but it’s different in the “elderly”, and an attempt to discover at what age the trend reverses. I’m an admirer of Valter Longo’s work.

            1. Alice, I’m happy to hear that you are maintaining good control of your blood glucose. I am having more success, too, at keeping my postprandial peaks below 120, but it’s a challenge, so I am trying a few new tactics. Since fiber and acidic foods slow the glucose response,
              I have been adding lemon juice and flax to my higher carb meals: 1 tbsp lemon juice, 1 tbsp flax, 2 tbsp erythritol (or Truvia packet), and 1/2 cup water for a modified lemonade. Exercising before a meal also seems to lower the BG spike, and I keep the low GI carbs below 45g in a meal for a daily total under 200g. Not low carb, but careful use of moderate carbs. Dr Gregor recommends 2 tbsp of flax daily, which is even more important for those of us increasing our healthy fats in place of carbs. We need those omega-3’s!

              1. Hi Suepy. My update is for you too. I like your method of limiting carbs at any one meal and spacing them out. Do you count all carbs in your 200g limit including fiber, or is it “net” or “active” carbs minus the fiber?

            2. Alice, thanks for your thoughtful comments to both Thea and Suepy, which I learned a great deal from. All three of us are very much on the same track. Maybe we should set up our own website specific to low-glucose vegan diets! Hahaha… okay, that sounds like a lot of work, so forget that. :) Anyway, I’m going to try hull less barley, and reduce my soy intake, based on the Greger video link, which may be over 5 portions a day currently if you include soy milk in my tea and coffee. Looks like three portions is in the safe-zone. Thanks for the info!

              Its funny also to see that we eat the same things when traveling. I put plastic bags of organic walnuts and peanuts in my travel kit, and an avocado. And when I arrive, I hit the grocery store and get more avocados, tofu, seitan (if I can find it). Still, I tend to lose about 2lbs a week when I’m away from home.

              Btw — just learned my recent LDL is 132, despite my replacing all olive oils (I had about 8 tablespoons/day), with more avocados (probably went from 1 to 2 a day) in addition to my steady diet of two to three servings of nuts and two to three servings of soy meats, which I haven’t changed. My LDL actually went up 9 points from 123 to 132 once I quit olive oil and added more avos. Any thoughts on this? Ideally, I’d like to get it down a bit. Fortunately, HDL is 77 so its not all bad news.

              My first thought is it must be the saturated fat content of my foods. But the web is filled with data showing that nuts lower LDL even for those on a vegetarian diet. So…. perhaps the oils in the soy products? Or the high saturated fats in avocados? This study suggests avocados lower LDL vs a vegetarian diet:


              So I’m stumped.

              On the other hand, there’s lots of data that also indicates that the LDL relationship with all-cause mortality is a J- or U-shaped curve, and perhaps 100-136 is ideal, especially for older adults. See this:


              Anyway, don’t feel the need to respond. Just thought that given both of your great analytical minds, you might clue me in to something that I’m missing to lower LDL a bit. Thanks!

              1. Russell, maybe a missing element in our discussions of a higher fat vs low fat diet, to eat nuts or not, might be the vital role of omega-3’s and soluble fiber. I’ve been looking again at Dr Gregor’s past videos and the following comments concerning fats, oils, and omega-3’s. Thea gave a good link to a talk Dr Gregor gave in 2003 about surprising research on omega-3’s and B12. Within a few years of each other two prominent men with heart disease died: Dave Thomas, the founder of Wendys died at the age of 69 with advanced heart disease, and Jay Dinshah, founder of the American Vegan Society died from a heart attack at the age of 66. Dr Gregor puzzled over why studies show that meat-eaters, vegetarians, and vegans all have the same mortality rate, and in the category of degenerative brain disease (i.e. Alzheimers), we non-meat eaters have 2X the risk. Possibly the reason is that vegetarians/vegans are known to have deficiencies in omega-3’s and B12, which have a strong influence on heart and brain health. Since the ideal ratio of omega-6 to omega-3 is 1:1, with a 4:1 ratio good enough, what would it take for vegans to improve that ratio, especially those of us eating extra nuts, seeds, and avocados? I checked my Cronometer diary and if I eat 3 oz of nuts and seeds daily plus 1/2 avocado, but no flax or chia, then my ratio is 8.3:1. By adding 2T of flax and 1T of chia, the ratio becomes 2.3:1, and then I take a supplement of 300 mg algal DHA for extra. Flaxseeds also are great in the soluble fiber department, so maybe a higher fat diet could use a little more, since a low carb diet can be lacking fiber without ample veggies and fruit. My daily fiber intake is between 50 – 60mg, and with daily apple, barley, carrots, that might be what keeps my cholesterol and LDL low.

                1. Thanks for the great link, and your ideas about fiber, which make a lot of sense. Strangely enough, I’d never thought about this! I did some calcs and am probably getting about 12-15 grams/day from veggies and beans, 20 from two Haas avocados, and about 10 from almonds, walnuts, chia, and my Italian seitan. Total around 42. My other thought is to experiment with reducing high saturated fats sources like peanut butter, walnuts, tahini, and getting rid of one avocado, and replacing with lower saturated fat sources with similar or better fiber, like whole hemp seeds (not hulled). So… this would raise fiber and lower saturated fats. If that doesn’t bring down LDL, I don’t know what will! I also find that I can eat a half-cup of oatmeal with two tbsps of almond butter and it only take my glucose to 120, but has 10 grams of total fiber.

                  On another matter, Dr. Greger says we can have 3-5 servings of soy a day. Do you have any sense of what that means? For example, one serving of Tofurky sausage is 280 calories, and 30 grams of protein, but one serving of soy milk is just 70 calories and one gram of protein. Does each qualify as one serving? Just wondering because tofu is a very high source of calories relative to saturated fat…

            3. Alice, I wanted you to know that I just did some calcs to figure out which foods have the highest calorie-to-saturated fat ratios, and I also made a note of calories relative to carbs. Top of the list are seitan and tofu. Anyway, I’m going to experiment to try to gain some weight. Thought you’d be interested.

              Hmmm…. it seems I can’t upload this though…. if you can’t see this, let me know. On the far right, I started to add some info on fiber, but that part isn’t complete yet. Draft form….

              1. Hi Russell and Suepy. I’m sorry I’m so slow
                responding. It’s such a pleasure to share these “conversations”.

                I’m back to struggling—FG in the high
                90s—yesterday 107!—as I have to focus on other areas of my life and branch out
                to other foods, and I make mistakes, only some of which I understand. So much
                to learn. I’m back to using cronometer again despite the time it takes, and
                trying record activity and glucose measurements.

                I came across a study on postprandial
                exercise, which had prediabetic older healthy adults as subjects
                (unfortunately, heavier than we are). I think we might be similar (sorry,
                Russell, I don’t know your age—don’t be offended) since their impaired glucose
                was assigned to low insulin production, ascribed to aging.


                “Three 15-min Bouts of Moderate Postmeal
                Walking Significantly Improves 24-h Glycemic Control in Older People at Risk
                for Impaired Glucose Tolerance”

                There’s quite a bit of information here. Especially look at the graph
                of meals, exercise and glucose (fig 1). My readings are very similar; if I can
                catch the rise before it peaks (30m after starting meal) and jog/walk 15-20m,
                it goes down but then rebounds to a smaller peak once I stop moving as
                digestion continues and adds new glucose into the bloodstream. Do you notice
                that too? I am following this plan, at least after breakfast and dinner, tho
                frequently more that 15m. (I’m eating Russell’s avocado lunches and there’s
                almost no peak, so no walk then.)
                I had an interesting dinner jog tonight: I had made one of my favorite
                tofu dishes, and my husband had provided a sweet Riesling white
                wine that he wanted to try with this favorite dinner. It was all really good
                and I ate more than usual. When I measured at 30m, it was 173. I jogged 1K
                steps (7m) and it went down to 149. I walked another 1K (10m) and it went up
                to 152. My dinner was feeding glucose in faster than walking was removing it. I
                jogged another 3k steps and it went down to 129. I think it might have been the
                sweetish wine, not something I have much experience with; maybe equivalent to a
                glucose solution!

                Sue, I like your lemonade—do you drink it before the meal? I think I
                remember someone (probably David Mendoza) recommending red wine vinegar in
                water before a meal for glucose control.

                Russell, I’m sorry your LDL increased—mine is not very
                different at 90 something. My doctor thinks it’s great (she’s Very Positive)
                since my HDL is high too.
                American Heart Association recommendations (lower than USDA) are to keep saturated fat under 5-6% of daily calories–about 11g for someone on a 2000kcal diet. I went over that today just with oats, flax, avocado and tofu–12g. I like your chart; it looks really useful to compile one of just your foods.

                Do you use cronometer? I think it’s the easiest clearest way to examine
                foods. It’s free and you don’t have to enter your diet, you can just look at
                an individual food. What I do is to use the Search Foods button to select a
                food, establish a quantity that’s reasonable, and it provides a complete
                nutrient data set for the food, including carbs, fiber, “net carbs” (that’s
                carbs minus fiber, the glucose-active carbs), starch, and all the sugars, etc,
                etc. The only problem is you can’t print it out, so I end up laboriously
                writing it out so I have it to hand. It’s easy to set up the quantity so foods
                are comparable by energy or by some other characteristic. (There are multiple
                data sets for some foods, sourced from different food analyzing agencies, and
                you want to use the one that has the most complete information.)

                It’s very hard to make sense of all the studies and their differing
                recommendations about cholesterol. You have to look at who the study subjects
                are and what they ate before the intervention. Jeff Novick has some wonderful
                comments about this. Here’s one about nuts (You have to read to the bottom,
                despite its initial repetitiousness.):


                It seems to be true in a lot of cases that study findings don’t apply
                to us because we don’t have the deficiency or imbalance that people who eat the
                SAD do, so the intervention doesn’t help us. As Thea was telling me.

                I’ve been making more measurements—before, at 30m, at 60m, usually with
                some exercise at the 30m mark—for each meal and I’ve been surprised how fast my
                glucose rises, even with very low GI (supposedly slow digesting) foods, to at
                least 140 something 30m after starting breakfast and dinner, the meals that
                include significant carbs. I’m also noticing (I think) how affected glucose
                peaks are by the background context; if I’ve had a really high peak one evening,
                FG and the next day’s values seem to be raised, and maybe the next day’s. As
                tho it comes in waves. If it’s been unusually low one day it will tend to stay
                that way. I sure wish I understood. It seems something more than just the sum
                of the diet and exercise. I’ve been amazed at how high my peaks have been—I had
                no idea when I was measuring at 1h, or even 30m after finishing the meal. The
                15m bout paper says something about how the peaks are the cause of
                microvascular damage, but the reference they supply doesn’t really address the
                subject. Have you seen any studies of this?

                Good luck gaining weight, Russell. I’ll be very interested in what you
                find helpful.

                Sorry this is so long…and looks so bad. (I wrote it in word because sometimes discus has lost it before it gets posted. Aack!)


                1. Alice & Russell, thanks for your informative posts! Balancing carbs-fats-protein is sure tricky when our postprandial glucose likes to soar too high in response to those carbs. My 200 daily carbs are total, so minus my 50-60g fiber, that should put me near the recommended daily 130 carb amount. My BG usually peaks 45 minutes after breakfast at 110-120, but if I try adding any dried fruit or extra tablespoons of erythritol (4g carb each T), or had a late carby meal the night before, then it will rise to 150-180. I need to get moving 30 minutes after a meal to lower it, so I put my little cycle machine under my desk to make exercising easier.

                  I am sold on the benefits of flax, at least 2T-3T daily, and have found several ways to include it in my diet. The easiest is adding it to a smoothie along with 1t alma, but I don’t have a smoothie every day. This is good: mix 1T flax, 1T erythritol, 1t chai spice mix (cinnamon,ginger, cardamon, cloves), and 1 cup soy or almond milk, and stir while drinking. If I add 1t alma, then it needs another 1T erythritol. Sometimes I just mash 1T flax with ripe or defrosted raspberries and 1T erythritol. In a tribute to omega-3’s, studies have shown that they have a beneficial effect on dopamine, opposite the effect that “fatty foods” have. Dr Pamela Peeke had an interesting analysis, “Food and Addiction: The Dopamine Made Me Do It”, which points to the addictive effect of hyper palatable foods – sugary, starchy, fatty, and salty foods.

                  Flax is great because it has the omega-3’s, fiber, and lignans. Russell, I like your plan to lower your saturated fat and raise the fiber. Beans and lentils are undoubtedly one of the best sources of fiber and protein, but maybe best 2 or 3 times a day in smaller amounts to limit the carb overload. A serving of soy is:

                  WHOLE SOY FOODS one serving is equal to ½ cup tofu or tempeh, 1 cup soymilk, ½ cup cooked edamame, 1 ounce of soynuts. Healthy choices: Tofu, tempeh, edamame, soy nuts, soy milk Why: Soy foods contain isoflavones that have antioxidant activity and are protective against cancer. Choose whole soy foods over fractionated foods like isolated soy protein powders and imitation meats made with soy isolate.

                  1. Okay, I’m going to have to chastise both of you for eating too many carbs… its just not okay to be up there at 150-180! Some thoughts from Dr. Bernstein — don’t subtract the fiber — just stick to your glucose meter to figure out how many carbs, in total, you can have at each meal. One of his patients substituted oat bran for protein in her diet thinking that high fiber would be beneficial, “…and her A1c became elevated and her cholesterol to HDL ratio nearly doubled.” So subtracting fiber may not be particularly useful and may serve to overcomplicate a relatively simple glucose test. As Bernstein points out, the GI test also has a number of problem inherent in it for diabetics, namely, that it only measures out three hours, and it doesn’t account for impaired insulin production (meaning diabetic peaks could be MUCH higher), among other things.

                    Thanks for the link to the exercise bike for under-desk use! I may get one too.

                    As for whole soy, where I get confused is that some products like Tofurky sausage are listed as “one-serving” at 3.5 ounces (100 grams). But the web sites I’m looking at list a half-cup of tofu anywhere from 125 to 600 grams! That’s a big range which is why I’m confused. There must be a clearer definition somewhere of what Dr. Greger’s recommended daily amounts are.

                    1. Russell, I had to laugh at your admonition to watch my carbs – I’ve been good! Well, pretty good. My postprandial glucose has only gone over 140 3X in the past few weeks, and cycling right after eating seems to really make a difference. My daughter has flown the coop, so I am renewing my commitment to an ideal diet and exercise with vigor. I wonder if the low fat, high carb doctors like McDougall can keep their patients’ postprandial readings under 140, or are they even concerned about that? If you ever meet Dr McDougall, I’d love to hear the gist of that conversation! What I find exciting about this 2003 study that I mentioned to Alice was the conclusion that isolated postprandial hyperglycemia (IPH) is very under diagnosed, pervasive, and a high risk factor for CVD independent of all the other risk factors. Could IPH be the smoking gun behind so much of the heart disease in people with normal cholesterol and nondiabetic? Intriguing.

                    2. Suepy, I’m glad to hear that you are keeping your postprandial excursions limited to just occasional trips to the wild side. :) Thanks for the study — Thea needs to see this one as it confirms exactly what we were trying to tell her about grains/carbs and the associated risks. Would you consider sending it to her, or if not, may I do so?

                      It underscores the importance of getting our A1cs as low as possible. I’m wondering if there’s some way to get to 5.0… if anyone figures out a good vegan formula for that, please let me know. I’m going to try to push mine down since I’m usually 5.3-5.4. Anyone care to join me in this little experiment? It might mean even more nuts and seeds… but perhaps worth the fat risk.

                      Also, thanks to Alice also for turning me onto the Cronometer. It’s a pain — who has the time? But I’ll keep at it a few more days to help dial me in. I’ve already learned that my sodium intake is double the recommended amount, from all the fake meats. Guess I’ll have to make my own seitan from now on :(. I’ve also learned that I’m getting too much iron and calcium from food on top of my multivitamins, so I’ll back off on the multis. And now I see why its so hard to maintain weight. Most of my calories come from tofu, seitan, nuts, seeds, and a daily glass or two of red wine. I didn’t know that the wine was so important! Obviously, I will have to force myself to drink more.

                      Btw, I have a new breakfast cereal mix — three tablespoons of oatmeal, three tablespoons of almond butter, and one tablespoon of flax meal/chia meal (yes, you can ground chia in the coffee grinder just like flax seeds). Its about 16 carbs and 350 calories total, and when added to my soy green tea, with erythritol, my glucose barely creeps over 100 and I get around 400 carbs. Love the taste, too.

                    3. Russell, Since you and Thea have been exchanging ideas, why don’t you give her a heads up about that article on postprandial hyperglycemia. David Jenkins published a study last February about a 6 month trial of a low carb vegan diet vs a high carb lacto-ovo vegetarian diet. The conclusion was: “A self-selected low-carbohydrate vegan diet, containing increased protein and fat from gluten and soy products, nuts and vegetable oils, had lipid lowering advantages over a high-carbohydrate, low-fat weight loss diet, thus improving heart disease risk factors”. He probably should have made both diets vegan for better comparison. PubMed has 36 related articles published in the last 5 years, with several showing improved results on LDL and insulin resistance from soy products. I’m plowing through them to see if there is anything relevant. Here’s hoping that there are some ongoing studies which will shed some light on this low-carb vs low-fat debate.


                      I’ve been using the under desk cycle or other exercise after each meal and snack, starting at 30 minutes after the first bite and continuing for 15-20 minutes. It keeps my postprandial glucose under 110 at the one hour mark, and I have a sufficient second insulin response to keep glucose no higher at the 2 or 3 hour mark. Also I’m trying to build more muscle mass by following the super slow weight training and HITT. Russell, Since you and Thea have been exchanging ideas, why don’t you give her a heads up about that article on postprandial hyperglycemia. David Jenkins published a study last Feb about a 6 month trial of a low carb vegan diet vs a high carb lacto-ovo vegetarian diet. The conclusion was: “A self-selected low-carbohydrate vegan diet, containing increased protein and fat from gluten and soy products, nuts and vegetable oils, had lipid lowering advantages over a high-carbohydrate, low-fat weight loss diet, thus improving heart disease risk factors”. He probably should have made both diets vegan for better comparison. PubMed has 36 related articles published in the last 5 years, with several showing improved results on LDL and insulin resistance from soy products. I’m plowing through them to see if there is anything relevant. Here’s hoping that there are some ongoing studies which will shed some light on this low-carb vs low-fat debate.


                      I’ve been using the under desk cycle or other exercise after each meal and snack, starting at 30 minutes after the first bite and continuing for 15-20 minutes. It keeps my postprandial glucose under 110 at the one hour mark, and I have a sufficient second insulin response to keep glucose no higher at the 2 or 3 hour mark. Also I’m trying to build more muscle mass by following the super slow weight training and HITT.

                      However, I’m losing weight, down to 100 lbs, BMI 19.0. Since my fats are already in the 40% range, I’ll increase protein through soy and seitan, keeping carbs around 40%. Probably changing snacks from fruit and nuts to soy and nuts will help and would eliminate the need to exercise off those extra snack carbs. Postprandial goal is under 120 mg/dL and Never Ever Over 140 (that could be a website!). The chronometer diary is good to use because it has the calorie breakdown wheel which you can click on to show percentages, but it IS time consuming.

                      BTW, your breakfast cereal mix looks good – is the oatmeal cooked or raw? Isn’t it interesting being a guinea pig – lab rat?

                    4. Btw, here’s a graph from Bernstein’s book that you and Alice may appreciate. We’re all probably at the bottom of this scale. It’s amazing that others continue to lump us together with the high-insulin people. That’s why we’re being told to go to a high-carb diet, which obviously cannot work for us based on this chart.

                    5. Russell, thanks for the note to Thea and this chart. It clearly shows how carbohydrates would be a problem for a thin type 2 diabetic because of low insulin levels. Google “thin prediabetic” and you’ll find several forums discussing this plus some interesting magazine articles. We have company, although it seems that we are in the small minority of pre-diabetics treating it with a vegan diet.

                    6. Russell, your page from Bernstein’s book is really informative. I’ve bought his book– it vastly simplifies my view of my glucose. It’s so obvious I’m amazed I hadn’t seen it before. I was told (w/o testing) that I made plenty of insulin, so I’ve had trouble accepting that I didn’t. Also I’ve been a pretty happy vegan for a long time, and a gardener growing a lot of what we eat, and I have real trouble believing that the wonderful stuff coming out of my garden isn’t what I’m supposed to eat. Butternut squash, red potatoes. Arrrg!
                      But now that I’m testing more often and can see the shape of the peaks in response to the grams of carbs I eat, and the possibilities of modifying them with immediate exercise, it’s really clear.
                      So I do need to modify my diet. I’m starting with the hope that I can manage 40g of carbs at a meal if I can walk afterwards, and I’m choosing them carefully for low GI and nutrients, and my 40g covers only “net” carbs, so I’m not counting fiber, which is pretty high in my diet. If this doesn’t work I’ll have to lower it.
                      I also read recently that caffeine decreases insulin sensitivity, so I’ve switched to decaf, and my postprandial peak is possibly a little lower, but does seem to occur a little later.
                      I think it’s important not to include fiber in your carb count, Russell. It will skew your choice of foods–like avocados. What cronometer gives me for a ~100g avocado is ~9g of carbs but ~7g of fiber, making it a really low net carb food.
                      It’s hard to get enough calories with lower carbs and I make them up with almonds.
                      I hope this will work–it’s so much easier to think about than to do–but I now have a pretty reasonable understanding of it I think.
                      Thanks for you Bernstein post. He’s right I think. Are we going to invent the new WFPB SOS paleo diet?

                    7. Alice, I’m so glad you bought the book! Yes, it makes a lot of sense. I’m grateful for having spoken to him on the phone earlier this year. Such a trailblazer… we basically owe glucose test strips to this man since he popularized them immediately after finding them in an obscure journal before they were known.

                      I hadn’t been aware of the caffeine link — I’ve been increasing my caffeine due to its effect upon lowering LDL. Sheesh, I guess I need to revisit that now.

                      As for carbs, I always use the gross amount, never the net amount after subtracting fiber. I think that’s what you meant. Bernstein uses gross as well which makes it very easy to make calculations. I basically ignore the fiber count as I find on cronometer that I’m always fine on this.

                      Yep, almonds are my favorite, though my dentist is telling me that I have to stick to almond butter since they wreak havoc on enamel! :)

                      If you ever want to test your insulin, you can buy tests on for $24. Some generic doctor signs them digitally. Then you can print it and go to LabCorp and get them done. Cheap and easy.

                      The Diabetes Director for the Center for Responsible Medicine looked at the Bernstein graph I sent her and admitted that we thin diabetes/prediabetes people are very rare and really not studied in any of the literature. But I’ve also read that we represent 5-10% of the whole group, so why not? We could certainly use more dietary studies along the lines of what we’re all doing now.

                    8. Alice and Russell, I’ve been reading Dr Bernstein’s book, and it’s new territory for me to be counting the carbs in each meal, yet that seems to make the difference in preventing BG spikes over 140 after meals. I’m safe if I keep under 30g of mostly low GI carbs per meal, and can go to 40g with exercise soon after. I never realized how much fruit I eat, with daily banana, pomegranate, and dried fruit, but am now much more judicious with the fruit and generous with the low-starch veggies. My excursions to the wild side (high carb!) leave me hungry 2-3 hours later and require so much exercise to bring glucose down. After trying to work off a slice of Chicago deep dish pizza (veggie, no cheese please), an hour of exercise got my glucose down to 120, but the next morning fasting was 68, lower than normal. What I’ve realized is that a high carb meal can cause my BG to swing between too high and too low. Two years ago I had a much higher carb diet and first started testing my glucose, but knew little about what the normal readings were. I found that some of my glucose levels had dropped to 62-68 after several hours postprandial, and it was common to go over 140 an hour after a meal. That would explain how I can have an A1c of 5.2 or 5.5 with normal fasting, because the too highs and too lows got averaged out. Proof that A1c and fasting glucose don’t always tell the whole story. So in my case, it might be insulin resistance and not insulin deficiency that is the problem. I’m really hoping I caught it in time, didn’t burn out too many beta cells, and will keep to smooth sailing on the glucose sea.

                      I’ve checked with Labcorp and Quest Labs to see if they offer the insulin response test, but they only do fasting insulin with the 2 hour Glucose Tolerance Test., which costs out of pocket, does have it: “Insulin response test—fasting, 1-hour, and 2-hour glucose and insulin levels after a 75-gram glucose load. This is like a glucose tolerance
                      test but measures both glucose and insulin. Your blood sugar can be
                      normal but your insulin can be sky high.” Russell, they are a bit cheaper than (your link was for walkinlabs, which is something different). I had a good conversation with the ClevelandHeartLab and they have both MPO testing and an Inflammation Panel
             for a very reasonable cost if your insurance doesn’t cover their lab (they aren’t in my insurance network). Your doctor would requisition their supplies, draw your blood, then mail it to them for no extra charge – they provide all the materials. I believe the MPO would cost $14.40. They aren’t the same as the Cleveland Clinic, which also tests for MPO, but maybe only onsite.

                      I think we are starting to figure this out! It takes a willing doctor to get the testing, or order online and pay a bit extra. Alice, have you ever tried a rebounder (mini trampoline)? It is good for lowering blood glucose, building bone density, and easy on the knees. I am on my third rebounder and found that it’s definitely worthwhile to pay extra for a good one – I use the Rebounder Air, which can fold in half for storage or transport. Between my rebounder and my under-the-desk cycle, I don’t need to venture out into the cold for exercise as much. A trip into the carb wild side requires the jump rope, (sorry knees!).

                    9. Alice, wow it is rare for me to fall under 80-85, so I’m not sure why that happened in your case. This seems like a huge insulin response, but that seems counterintuitive for someone with such a low BMI. Have you done the test for insulin resistance? I seriously doubt you have it… But you didn’t say if you still have hypoglycemia now that you’ve adjusted your diet.

                      Another option, I think, is just meter error. My experience is that even the best meters will be off by up to 25% (despite the claims of only 15%).

                      Anyway, I’m very glad to hear that Bernstein’s book has been helpful. Honestly, someone needs to do a veggie/vegan version of it!

                      I don’t think I’ll ever do a 2-hr glucose/insulin test, because I’m quite frankly scared of EVER letting my glucose go above 140, even for a test. Maybe one incident is inconsequential… I don’t know… but I’d rather not burn out even a single beta cell unless there is an upside to the risk.

                      Thanks for the info on SaveOnLabs, and on MPO. I’ll look into both of them.

                    10. I had a fasting BG of 68 four days ago, after my fling with a slice of pizza (it was yummy, but not again!), retested and it was 70. The 2 or 3 hour insulin response test suggests eating high carb for the previous 3 days, so I am hesitant, like you Russell, to let my glucose go high for that amount of time. Regardless of the results, I would continue with my current lower carb, higher fat and protein vegan diet and exercise. Possibly the serum C-peptide test would give, as Dr Berstein says, “a crude index of the amount of insulin you’re producing. The level is usually zero in type 1 diabetics, and within or above the “normal range” in mild type 2 obese (insulin-resistant) diabetics. If your serum C-peptide is elevated, this would suggest to your physician that your blood sugar may be controllable merely by diet, weight loss, and exercise.” Hypoglycemia was a problem for me when I was in my 20’s, so I’m familiar with the lightheaded/fuzzy feelings that accompany it. Normally I don’t drink alcohol because more than a glass of wine gives me a headache, but 2 years ago I had one margarita with lots of chips and salsa. An hour later I got very lightheaded, dizzy, queasy, and ended up briefly passing out – I would make a cheap drunk! I thought it was from alcohol intolerance, but now that I think about all those carbs I consumed, I bet it was hypoglycemia. My poor pancreas has obviously been overworked all these years; time to make amends.

                      Some interesting information about the MPO test and why our local labs don’t offer it:
                      “Research shows that a large percentage of people who have a heart attack or stroke don’t have high cholesterol or high blood pressure. That fact sent a team of Cleveland Clinic researchers in search of a better predictor. They found it in the enzyme myeloperoxidase. We all have myeloperoxidase, known as MPO, in our bodies. But as plaque inside our blood vessel walls becomes more likely to rupture, we produce more MPO. Increased amounts of MPO can cause erosion of artery walls, too. When a blood vessel erodes or plaque ruptures, a clot forms to patch the weak spot. If that clot blocks blood flow to your heart or brain, you’ll have a heart attack or stroke. So a high level of MPO is a sign that you’re at a higher risk of having a heart attack or stroke. That’s true even if your cholesterol levels are normal, your blood pressure perfect and you’re running marathons. After the discovery, the Cleveland Clinic, through Cleveland Clinic Innovations, launched ClevelandHeartLab, one of 33 companies the Cleveland Clinic has spun off in the past 10 years. What ClevelandHeartLab does is test blood samples, mailed from across the country, for high levels of MPO, then sends those results back to doctors so that they can pass the information on to their patients. Cleveland Clinic has a patent on using MPO to predict cardiovascular disease. But it has licensed that patent to ClevelandHeartLab, on the Cleveland Clinic campus. That doesn’t mean that no other lab can conduct the test, it just means they have to work through HeartLab to do so because the testing method is protected. And labs around the world are doing that.” The Inflammation Panel, with MPO, costs $189 without insurance. This looks like a good test for those of us with good cholesterol, blood pressure, and weight, but maybe have hidden inflammation. I will definitely pursue this and the C-peptide test with my (hopefully willing) doctor, who will give me the NMR results today – finally! BTY, what percent protein do you eat? I’m now at protein 20%, carb 35%, fat 45%, but am thinking of increasing protein – soy and seitan, and lowering fat from nuts.

                    11. Suepy, good to have that info from the Cleveland folks. You’re good at this! Was your night job doing medical research for a living? :)

                      My protein is 20-25%, carbs 10%, wine 6-10% (lots of calories!), and 60% fats. But watch out for the commercial soy and seitan varieties… lots of iron and salt. Must be a bit cautious.

                    12. Ha ha, I wish I had some experience in medical research – I’m flying by the seat of my pants! My doctor was very interested in the Inflammation Panel offered by the Cleveland HeartLab, and agreed to order the test for me. The lab called today and said my cost would be $32 since I have insurance but they are not a preferred provider. I’m envious of your wine consumption -fun way to get calories.

                    13. Here are some thoughts about insulin resistance in thin people. I’ve found 4 factors mentioned in the literature that could cause it: genetic link, hidden visceral fat, sleep disturbances, and hypothyroid. People who work the night shift are at greater risk, and voila, I worked nights for 31 years – definitely sleep deprived. I happily retired not long ago at age 60, but still rise before the rooster. According to Dr Neal Barnard, increased dietary fat can cause insulin resistance, and glucose spikes caused by too many carbs can cause it, so that leaves us with increasing protein as an option (and exercise), back to the Eco-Atkins diet. How much soy to safely include in our diet is a very good question.

                    14. You realize that you can test for insulin resistance, right? But I’m very dubious about the dietary fat link. My own fat intake is currently running at about 60% of calories. And my insulin resistance score is unmeasurable, below the scale. I shared your seitan and soy protein intake concerns, so I tested my IGF-1. The score came back this morning at the midpoint of the reference range so I am officially less concerned about this now. The great news though is that my A1C is 5.1, the lowest I’ve ever had! The less than great news is that my LDL is still hovering around 136, even though I reduced my vegan saturated fats from 16g to 10g a day. so it appears that it is total fat content that drives up cholesterol, not just saturated fat. Unless I am an anomaly. I’d love to cut out all fat to test this theory, but I’m afraid I would lose 10 pounds in 10 days to do so. I suppose I could live on salads and homemade oil-free seitan for 10 days… Might be a bit tough! And probably pointless too.

                      Trigs at 66, lower than HDL, at 75, which is also good news.

                    15. Russell, congratulations on your A1c dropping, looks like low carb is working! I got my CardioMetabolic lab report today and am trying to analyze it all – any input you want to give would be appreciated. The pre-diabetes risk factors were mostly good, except for a troubling c-peptide of .64, which is low enough to put me near the high risk zone. I think my beta cells are burned out, but fasting insulin was OK at 5.7. Glucose was 67, which is in the caution zone for too low, and A!c was 4.8 (thanks to watching those glucose peaks). Lipids were: cholesterol 182, trig 49, HDL 73, LDL 101, so I haven’t figured out why my total cholesterol went up along with the LDL since this summer, when total was 125 and 136. Maybe the little meter the hospital used to test lipids then was not very accurate? I’d like to know what makes the readings climb. Total LDL and HDL particles were just above normal, as were ApoB and homocysteine, and CRP was 1.0. Not the stellar numbers I was hoping for, although not bad. I think reducing carbs more and spreading them out in smaller meals would be prudent. These diet changes are an experiment in progress – I have never read so many scientific papers in my life!

                    16. Its all quite a mystery, isn’t it? Also, we’re looking only at the dietary component. Complex as that is, the genetic element is even more so. I have polymorphisms on my CETP chromosomes — about a third of the population does — and it reduces cholesterol metabolism. So… just sayin’…. we’re not really even looking at those things.

                      Oh and btw, are you getting sufficient B12? It plays a huge role in bringing down some inflammatory markers. It was either homocysteine, or CRP I believe.

                    17. There seems to be a sweet spot in the fat/carb balance where the lower carbs improve A1c and glucose, but not too much fat to increase cholesterol, and I think you’re right, it’s the total fat content and not just the saturated. Which test did you take for insulin resistance? My B12 is high, as is folic acid – no problem there.

                    18. The NMR Lipoprotein Test, aka The Particle Test, includes insulin resistance. On, it is $117, unless you can get your physician to order it.

                      Yes, you’re probably right about the fats/carbs thing. Saturated fats may not be any different to our LDL than mono or polyunsaturated fats. So, I will have to experiment with finding the right sweet spot with fats/carbs. The only other alternative is to increase proteins further, as I mentioned. Basically, that would mean a lot more low-fat seitan, I guess. I have about 150 grams of protein/day, so I was relieved to see my IGF-1 score be only 121. Reference values for my age are 78-222, so it seems that high plant proteins are not affecting it much, if at all.

                      Btw, have you ever done the ApoB/ApoA1 ratio? Just found a study saying this is the best measure for predicting MI events. The control group was at 0.74. The MI patients were at 1.34. In addition to MPO, this seems like a worthwhile thing to test.

                    19. Hi Suepy. Your numbers look good–esp A1c. And Russell, congrats on yours. From the amount of testing you’ve had can you tell whether you are more likely to be insulin deficient or insulin insensitive? How would you know?
                      I have never had c-peptide, homocysteine, CRP or ApoB tested, or insulin. I live near Seattle and go to a UW clinic for healthcare. I expect that they’re the best in my area, but testing seems to be on some sort of evidence-based schedule–lipid panel every 3y for people whose lipids are OK, for example. Haven’t decided what I want to do about it…
                      Suepy, are you concerned about you glucose going too low? I remember a magazine article among the items that came up on your google search for “thin diabetics”, where the author figured out that he was having very low overnight glucose levels, from the disparity between his fasting glucose readings and his A1c. His doctor thought it was serious enough to treat.
                      I’m as mystified as ever. I tried your plan of keeping carbs under 30g per meal this morning by reducing the amount of oat groats in my usual breakfast to bring it under 30. Instead of walking at 30m I sat there and at 40m I was at 148 (at which point I walked as fast as possible). If I eat carefully and start walking at 30m I can usually keep it from going above ~135 or so, and I can get it down pretty fast, but I have to keep moving for at least 25-30m or it will head back up. It usually lands in the mid-100s and stays there.

                      I love your indoor exercise solutions. I do have a rebounder and I’ve hauled it out and started using it.
                      The things I’ve tried that seem to help w peaks: switching to decaf (min difference but feels good), something acidic before meals–diluted vinegar or lemon juice, something fatty at the beginning of the meal. Macronutrient levels now are usually 35-40% CHO, 16-20% P, 40% fats.

                      I need some good seitan recipes!

                    20. What I found out about insulin resistance is that, according to “There is no one test that can directly detect insulin resistance”, but there are some complicated procedures which can help determine it, and some mathematical calculations based on lab results. Commonly used is a formula called the homeostatic model assessment, HOMA2 which uses fasting glucose and fasting insulin or c-peptide to calculate beta cell function and insulin resistance. The formula is set up so that normal IR is 1 and normal %beta and % insulin sensitivity is 100%. Usually an IR above 2 is considered resistant, but normal varies depending on ethnicity and gender, with the average IR in healthy humans at 1.7-2. Liposcience Labs has developed a score (LP-IR) using lipid count and size to estimate insulin resistance and offer it with their NMR test. They found that “”Insulin resistance is accompanied by alterations in lipoprotein metabolism that result in distinct changes in the lipoprotein profile detected by NMR.” Recently they announced a Diabetes Risk Index stating: “Many clinicians are challenged about how to effectively manage patients with ‘intermediate’ blood glucose levels ranging from 90 to 110 mg/dL, as within this range there is often ambiguity as to whether a patient will progress to type 2 diabetes. The ambiguity is particularly pronounced in normal-weight individuals, who do not typically present with overtly visible risk factors.” Spectacell Labs, which my doctor used, has a CardioMetabolic Risk Score to determine the chance of developing diabetes and has a bit different presentation of the lipoprotein particle numbers than the NMR. I couldn’t find their apoA1.

                      I used the HOMA2 calculator and my IR is 1.11, so Russell, you’re right that I am not insulin resistant but instead am insulin sensitive. Maybe I have a low insulin reservoir, aka the California Syndrome :), which causes my postprandial to spike too high.

                      Speaking of meter error, when I had my blood tests last month, the routine tests were done by Labcorp and the lipid numbers were done by Spectracell, both drawn at the same time. Labcorp said my FG was 79, Spectracell said 67, and my home meter read 76. The previous day, my fasting at home was 80, and usually my meter is a bit lower than the labs, so I’m tending to believe the higher FG since I’ve only gone into the 60’s postprandial after a load of carbs. Could my insulin have surged between tubes to cause glucose to fall? Perplexing.

                      Alice, what I think is also helping me to lower fasting and A1c has been increased intensity when I do strength training 2-3 times a week. If I put more effort into the weights, my glucose levels are lower for the next day or so. While counting the carbs in meals, I realized that erythritol has 4g of not so innocent carbs. The lemonade that I suggested with 1T flax, 1 lemon, 2T erythritol has 14g carbs! Even 1 tsp of alma has 3g of carbs, so when I mix 1cup soy milk, 1t alma, 1T flax, and 1T erythritol, that gives me 14g carbs. How fast it all adds up.

                      I’ve found some good seitan recipes on the web:
                      My favorite vegan cafe, Native Foods, has 2 cookbooks, a website, and a newsletter with great recipes – their seitan is delicious.

                      Good luck!

                    21. Thanks for the seitan recipes. They look great. Thanks for all your other useful suggestions too–I’m paying more attention to intensity in weight workouts, and the main reason I’m so slow in adding to our conversation is that I’m trying to correct my life-long miserable sleep habits. This cuts into my late-night reading/computer time too much! It’s a struggle, but has to be done.

                      I did some reading about the HOMA2 test, and it’s supposed to give you a value for %beta cell function as well as insulin resistance. Did you get such a value? This seems the important result. Here’s an article comparing tests of beta cell function:


                      And another article on an improved test, iHOMA2:


                      The newer test works better for people who are being treated with various drugs, maybe to improve beta cell function, so I guess it doesn’t apply to us.

                      I’m continuing to try things–starting each meal with a vinegar “cocktail”, adding avocado or almonds to each meal. I’m impressed with how time-specific my exercise has to be, and I’ve wondered if timing (e.g., at the beginning of the meal) of these other modifications might also be important. I tried amla quite a while ago, before I was taking many postprandial readings, and didn’t see any difference in my FG. Do you see any difference in peaks?

                      We’re all quite different aren’t we–my peaks seem to occur so quickly–I sometimes don’t have time to finish eating before I have to start exercise (30m after starting, and sometimes sooner). It must have to do with differences in insulin availability over time–insulin signaling?

                      A question: would it make any difference in how you would treat it to know whether you’re insulin deficient or insensitive?

                      Hope you’re having a wonderful holiday. I’m going to a neighborhood Christmas brunch potluck tomorrow, which will have vegetarian options, but they’ll all be cheesey quiches and fancy fruit salads and desserts. This will be a dietary challenge, which I’ll fail, but I can’t eat by myself all the time…. Doesn’t happen very often.

                    22. Happy holidays, Alice! I’ve been tracking my postprandial peaks more carefully, and with a lower GI meal it peaks at 30-35 minutes, while a high carb meal will keep my glucose rising up to an hour later. I’ve been trying to exercise at the 30 min mark, but can get indigestion if I’m too active, so am taking care with the amount of carbs per meal. I hope you can get tested for fasting insulin and c-peptide. I used the HOMA2 calculator for % beta cell and it was 102 by using the c-peptide, which I read is better than using the insulin if you are not insulin resistant. I think our diet plan would be the same whether insulin resistant or deficient, but it would be helpful to know the status of our beta cells and how careful we need to be with carbs. Probably the insulin response test would indicate insulin resistance best and is the test recommended in The Blood Sugar Solution. That book is really aimed at people who are insulin resistant, and I haven’t found a book that talks much about pre-diabetics who are not. They forgot about us!

                      I don’t know if amla makes a difference in FG since I never tested my FG before starting amla. I also wonder if the timing of an acid with a meal makes a difference in glucose rise – adding lemon water before, during, or after eating? Exercise and low GI, low carb seem to make the biggest difference for me. I lament having to restrict my pomegranate intake – last year I was eating one a day, but they are high in sugar, so no more than 1/4 cup now at a time.

                      Since my cholesterol and LDL went up so much in November, I’ve been scratching my head trying to figure out what caused the change from my low readings in summer. My basic diet didn’t change much all year, but over the spring and summer I ate more beans, along with lemons and greens in order to become more alkaline since a doctor told me I was testing acidic. I also added 2 tsp of Natural Calm magnesium daily, and I wonder if this made a big difference? In the fall my garden went kaput, so I slacked off on the greens and got lazy with the lemons and magnesium. It’s an easy theory to test – I’m adding them back and will test my cholesterol periodically. Maybe it will help with blood sugar control, too.
                      Have a great new year!

                    23. Happy New Year! I too have been trying to track postprandial glucose carefully.

                      This last holiday week has been particularly difficult, with several lovely social occasions organized around food, annual things I really look forward to, pretty much spoiled by my sense of having to Minimize the Damage, then coming home hungry and upset, perhaps overeating my own “safe” food and seeing enormous peaks. Probably cortisol as well as carbs. Dinner with dear friends and facing the choice again of eating their carefully prepared super healthy food, organized especially for me, or protecting my carb level. I found an OK compromise and of course loved seeing them, but I feel so cut off from normal human means of socializing. It’s been discouraging. Not sure what I’m doing is sustainable.

                      I’ve also had particularly high peaks after what I thought were manageably low carb meals. Once to 217 an hour after one of Russell’s avocado/greens lunches. Another time to 157 at 30 min which stayed there at least half an hour while I jogged/walked my heart out for 5000 steps. It may not seem likely, but the change I had made was adding 1t amla to my mid-day meal. I continued it for 6 days, then quit and my peaks have gone down–I think. Maybe amla’s effect is on insulin resistance–can’t think of a likely mechanism. It certainly didn’t help me. Maybe I’m wrong and simply connecting 2 separate concurrent factors. (But check it with your own experience.)

                      I’m feeling better now–back to working on the old high nutrient density/low carb/optimal exercise combination that will allow a long, high-function life–as possible. I’ve got an appointment next week with the endocrinologist I saw 2y ago and have been trying to clarify exactly what it is I need from her. Here’s what I’ve been thinking:
                      1. I’d like to dismiss the problem of whether I have diabetes or not, and what type. Those are her markers, her problems. Since I don’t want or need treatment, I don’t think it matters. She can categorize it as she wants.
                      2. I do want to establish benchmarks for my current state of (let’s call it) impaired glucose tolerance. I’ve been doing that with FBG, which hasn’t changed, and 2 years of annual A1c tests. These are helpful but inadequate–probably miss the important numbers–peak height & frequency.
                      3. A1c levels will be misleading for her, because I’m pushing “lifestyle” corrections as far as I know how, to normalize A1c.
                      4. When I look at the shape of the peaks I’ve mapped over the last few months, like you, I see a fast rise starting at 20-25m after starting to eat, which peaks at 45m to 1h and comes down to 130’s – 120’s – 110’s by 2h. I’m thinking that indicates inadequate insulin in the 1st phase–i.e., no stored insulin, but eventually plenty. If not an insulin production problem, maybe a signaling problem?
                      5. What I would find helpful is some way of testing the patency/effectiveness of my beta cells, that would provide an indicator of where I am now in the spectrum of normal to insufficient insulin production, and a benchmark for comparison in the future. (First priority–preserving the beta cells and ability to measure success over time.)
                      6. Her judgement of best testing method. (I’m thinking HOMA2 with fasting PG,
                      insulin, C-peptide. But she’s the expert.) She may not be willing to order the tests due to institutional limits on testing for “non-diabetics”. If she can’t, where does she recommend I go.
                      7. Her take on effective target peak limits to prevent tissue damage at any level. As I’ve thought about this I’ve wondered whether peak height and frequency; time per incident over some threshold (e.g., 140), cumulative; or sheer glucose instability is the most damaging factor.

                      Can you add anything to this, Suepy?

                      Much appreciated!


                    24. Happy New Year Alice! Yes, I’m with you 100% on the challenges of holiday meals. I’ve got a reputation among my friends for spurning all their great dishes, or only having a bite, and then diving into my home-made salads and stir fries. Anyway, they get over it eventually. And my will power is pretty strong to avoid those things that will harm me. I’ve got a young son and I want to be healthy for him as long as possible, so the will power part is easy.
                      Your 217 after a salad meal is concerning — Bernstein recommends no more than (if I remember right) about one cup of salad at a time. I find I can eat about three cups safely but if I go to four or five, my peaks go crazy. I’m pretty careful about limiting the amounts. You probably had way too much at one time. Also, it depends on how much exercise I had before the meal (not just after).
                      I just got back from a ski vacation and I found that I could eat tons of salads and other foods and all my glucose numbers were superb. But this morning, a big handful of oats and walnut butter sent me over 150 at 1-hour. Sheesh.
                      So many people with our conditions just don’t pay attention. We may not be perfect, but we’re clearly doing all we can to control and aid our future health. Its a constant mindfulness practice, isn’t it?
                      Sorry I can’t help on the test methods you mention, but perhaps Suepy will have guidance. In any event, please keep me updates on your progress and findings.
                      best —

                    25. I really sympathize with your frustration when eating with friends who eat far more carbs than you can handle, and with not wanting to be antisocial by refusing or eating little of their carefully prepared food. I have to eat before I get into that situation and have nut snacks to keep myself fortified. I wonder if you could bring a big dish of veggies or salad to share, and eat just a bite of your host’s food? I feel so limited when eating at a regular restaurant – just salads or grilled veggies, and even vegan restaurants can go heavy on the carbs and oils.

                      I have experimented with bigger meals, up to 48g of carbs, and then exercising from 20 minutes post meal to an hour later, which does keep my BG down but the indigestion is not comfortable. Back to frequent smaller meals, every 2-3 hours, of 20 – 30g without the need to exercise right away. I’ve read that taking vinegar or lemon juice before a meal works best when it is a high carb instead of low carb meal, and optimum is 2T apple cider vinegar 2 minutes before the meal. I can’t tolerate acid on an empty stomach and have found that it works while eating my meal, either 1T lemon juice or ACV, which slows the glucose peak to 50 minutes instead of 30 min, giving me time to digest more before exercising.

                      I am curious now about your BG reaction to the amla, because all the studies have shown that it has a beneficial effect on fasting, 2 hour post-prandial, and lipid levels.

                      There are so many variables that affect our BG that it is hard to pinpoint one item as causing the result, because it can vary according to exercise and diet the day before, sleep, stress, etc. I am going to pay more attention to my glucose readings after adding alma and see if I notice a difference.

                      With a post-prandial reading of 217, some sources would qualify that as a diabetes diagnosis, but most official guidelines for diabetes specify a random reading over 200 with symptoms is diabetic.

                      “Regardless of when you last ate, a random blood sugar level of 200 mg/dL (11.1 mmol/L) or higher suggests diabetes, especially when coupled with any of the signs and symptoms of diabetes, such as frequent urination and extreme thirst. Without intervention, prediabetes is likely to become type 2 diabetes in 10 years or less. If you have prediabetes, the long-term damage of diabetes — especially to your heart and circulatory system — may already be starting.”

                      Whatever your doctor wants to call it, you certainly should get more testing, at the minimum a fasting glucose, insulin, C-peptide and A1c. I think the insulin response test is even better and would give you a good measure of your beta cell and insulin resistance status, with insulin and glucose measured at fasting, 30 min, 1 hour, and 2 hour. A funny coincidence is that I also have an appointment with an endocrinologist (first time) this month for the same reasons as you, not wanting any drugs or treatment but for further testing and an experienced analysis of the test results. Regardless of what they say, I think we should give a wholehearted effort to normalize our blood glucose levels with diet and exercise.

                      Getting to the source of our impaired glucose tolerance is the real goal, and it isn’t easy, like with overweight people, to just say the cause is insulin resistance and losing weight will cure it. An interesting study was done, the Counterpoint study, which duplicated the diabetes reversal experienced by people who undergo bariatric surgery by reducing a group of diabetics’ calories to 600 cal/day for eight weeks, concluding that type 2 diabetes was reversible at least in the early years of diagnosis. f

                      Of course that’s not an option for someone who is thin, but they also concluded that if a person has type 2 diabetes, they have more fat in the liver and pancreas than they can cope with.

                      “Reversing Type 2 Diabetes
                      Our work has shown that type 2 diabetes is not inevitably progressive and life-long. We have demonstrated that in people who have had type 2 diabetes for 4 years or less, major weight loss returns insulin secretion to normal.

                      It has been possible to work out the basic mechanisms which lead to type 2 diabetes. Too much fat within liver and pancreas prevents normal insulin action and prevents normal insulin secretion. Both defects are reversible by substantial weight loss.

                      A crucial point is that individuals have different levels of tolerance of fat within liver and pancreas. Only when a person has more fat than they can cope with does type 2 diabetes develop. In other words, once a person crosses their personal fat threshold, type 2 diabetes develops. Once they successfully lose weight and go below their personal fat threshold, diabetes will disappear.

                      Some people can tolerate a BMI of 40 or more without getting diabetes. Others cannot tolerate a BMI of 22 without diabetes appearing, as their bodies are set to function normally at a BMI of, say 19. This is especially so in people of South Asian ethnicity.”

                      If in fact we do have too much fat in our liver or pancreas which inhibits beta cell function and insulin resistance, how do we get rid of it? That’s a question for further investigation. Keep testing, stick with what works, get your sleep, and don’t stress (easy to say!). I can hear Russell advising now to lower your carbs and eat more nut butters/nuts and proteins – don’t worry about the higher fat or IGF-1 levels. I’m with you in this journey.
                      We can do it!

                    26. Great comments, Suepy! And just to add one minor thought — my IGF-1 levels are on the bottom third of the scale, and that’s with about 150-160 grams of protein a day! That’s just not a concern. Still a bit uncertain about the higher fats but homocysteine, CRP, both low. Haven’t tested MPO yet….

                    27. Thanks for your very helpful comments, Sue, and yours too Russell. The link to the counterpoint study–brilliant–thanks. Did you see a further paper by the same group–“T2 Diabetes, Etiology & Reversibility”?

                      Lots of new ideas–I’ve never seen fat described in the pancreas before.

                      Can I possibly be insulin resistant tho…?
                      I appreciate your comment about my 217 peak–it shocked me and I’ve had trouble even thinking about it.

                      Our situations seem so similar and our conversations here have helped me enormously. This may not be the right format for them–it gets harder and harder to locate the last post. Do you know of any protected/private way to share email addresses among the three of us and not burden NutritionFacts any further? Or are we maybe helping some other thin prediabetics and should feel right at home?

                      I’m off to the Big City tomorrow. I’ll keep you posted about the appointment.

                    28. Alice, while you are at your doctor’s office, there are two more tests that you could request that would ve very helpful in accessing both your cardiac and diabetes risk. The NMR LipoProfile is available through Labcorp and would indicate your insulin resistance and has a new Diabetes Risk Index.
                      The Inflammation Panel from Cleveland HeartLab would also be very good to indicate any cardiovascular risk.

                      You have a legitimate reason to be concerned about these health dangers, and I hope your doctor agrees that it’s good to monitor them. Thank you for the link to the paper on T2 Diabetes Etiology – it isn’t easy to understand all the details, but I gained a better knowledge of how diabetes develops and can reverse. The more we understand about how our bodies work, the more steps we can take toward vibrant health.

                    29. I’m not concerned about putting my email out there… if you want to write, I’m at If I see a strange email address, I’ll open it and hope it is you. :)
                      Btw, I’ve been making my own seitan lately, and it is chewy and delicious. 45 minutes at 325 degrees, let it sit after in the oven or each piece will sort of collapse. Also, add spices and soy or tamari sauce to the gluten dough. When its done, you can dip in olive or canola oil — fantastic treats that you can eat all day long. Also, its about 16 carbs for each 500 calories. Great weight-gaining food.

                    30. Hi Russell and Happy New Year! My post to Suepy is for you too–and I’d appreciate anything you can add.

                    31. Okay, I shared the link with Thea, as well as an email colleague who runs Dr. Neal Barnard’s diabetes program. Not sure if she understood though (or read it), because she replied that Brenda Davis is a great authority on diabetes and I should read her book. Unfortunately, Brenda’s diet has a high level of carbs!

                      Glad to hear you’re dropping or reducing dried fruit — that made a huge difference for me in my controls. Bernstein actually says to give up all fruit and sweets. which strangely enough has not been a problem for me to do. It seems that a single glass of evening wine seems to satisfy my sweet tooth.

                      I use rolled oats, and just pour hot water over the whole concoction from my filtered hot water dispenser. Works like a charm.

                      Thanks for the Jenkins study. He is funded by some questionable sources, but otherwise it is very compelling.

                  2. That recipe for chai flax milk should read 1t amla optional, and stir slowly since flax will clump. My computer keeps correcting my spelling when I write amla to alma – guess spell check doesn’t know those Indian fruits.

                2. Alice, so many good thoughts…

                  Yes, I agree about the peak… got to keep them down. Sometimes I don’t peak for over 2 hours. Reisling wine is a no-no! I actually find most white wine is a no-no and stock to reds. But like you, I experimented recently and had a shot of slightly sweet tequila for a friend’s 50th (I’m 58), and the next morning I was at 111! No more sweet tequilas! Anyway, I’m less concerned with morning glucose levels since the real concern is avoiding EVER being over 140.

                  I’m not sure how you get so high… perhaps too many grainy foods?

                  Yes, last time I had 3/4 cup of oatmeal as an experiment — my glucose quickly shot up to mid-170s and I went on a one-hour walk and it dropped about 50 points. But then it bounced up again about 20 points so I had to walk some more to reduce it again. That slow-moving glucose is a gift that keeps on giving!

                  I”m trying out the chronometer– thanks for the tip.

                  Btw, don’t put too much stock in the readings. I sometimes take two measurements and get readings about 15 points apart. During my 2-hour challenge test at Labcorp, I took my meter and grabbed a reading at the same time as their reading (at 2 hours) and got a 50 point difference!!

                  Dr. Bernstein’s book discusses why glycemic load and indexes are relatively useless. He thinks counting carbs is the ultimate guide. 30 carbs a day for a Type 1! Anyway, there’s no doubt in my mind that if you want to avoid those peaks over 140, that’s the only formula that truly works. Not sure how many carbs that would be for you based on your insulin production, but its not hard to figure out with a few days of testing.

                  Last point — yes I also noticed that there is a carryover from the day before in my readings. So if I’m high in the morning, I might reduce my breakfast carbs to compensate. It seems to work to equalize and rebalance things.

                  1. Russell, I’ve also noticed some variations in my glucose meter readings, wondering what causes that? I had a lipid profile test last week, NMR and MPO, so I’ll let you know the results when I get them. The day before the test I ate over 45% fats from nuts, seeds, avocado and will see if that makes a difference, or my daughter’s tasty cooking! I’m going to read Dr Richard Bernstein’s book like you recommended, and am aiming to keep postprandial glucose under 140, relying more on beans, lentils, and barley for protein and carbs.

                    1. Yes, keep me posted. That will be very interesting to see the results from. by the way, I just noticed that Bernstein has a chart showing insulin production for obese people with normal glucose, versus obese people with diabetes, as well as thin people with normal glucose, and thin people with diabetes.The levels of insulin for thin diabetics was far below obese people with either impaired or normal glucose. This explains the discrepancy that we discussed with Thea!

                    2. A funny thing happened on the way to the lab: my doctor had never heard of the MPO (myeloperoxidase) test for cardio risk, and ordered for me the only MPO test which her lab offered, called the anti-MPO. It appears that only the Cleveland HeartLab tests for MPO, and this is what they say about the anti-MPO test:

                      Is the p-ANCA test (anti-MPO antibody test) the same as the MPO test performed by Cleveland HeartLab?
                      No. The p-ANCA test primarily measures the amount of antibodies directed toward the MPO protein whereas the MPO test performed by Cleveland HeartLab directly measures the amount of MPO protein. The p-ANCA test is useful for identifying systemic inflammation and vasculitis. In contrast, the MPO test performed by Cleveland HeartLab is useful for identifying cardiovascular risk.
                      CPT Code 83876 Sample Type EDTA Plasma Order Code C133 Tube Type Lavender Top

                      I checked the labs in my area using the CPT code, and none perform this test, and I don’t know if my health insurance would cover using the Cleveland lab by mail. I’m still waiting on the NMR results, but am confident that following a WFPB diet, maintaining a healthy weight, and keeping blood glucose at normal levels will provide cardiac protection, regardless of higher fat intake.

                    3. That’s funny… I guess MPO is still a cutting edge tool that labs don’t really offer yet. I checked with Labcorp and they also don’t offer it either. But they do have the anti-MPO test. I wonder if that would still be useful for inflammation-related issues, much like CRP? Esselystyn was the guy who recommended MPO to me, because I told him my CRP was normal — 0.8 actually — and his reply was that CRP was not useful and that a high-fat vegan diet was unhealthy. When I countered that there must be a way to determine whether a high-fat vegan diet was causing actual CV damage, he mentioned doing an MPO test.

                      Why MPO would be superior to CRP, I have no idea. He said he had to go to an appointment so I didn’t get to ask further questions.

                      Anyway, I think he’s off-base, but will continue to do annual carotid scans to be sure. And if I could get the MPO here in SF, I would do it.

                3. Alice & Russell, the link Alice gave to the study on postprandial 15 minute exercise was a goldmine of links to other studies that are relevant to our discussion: do post meal glucose levels below 200 matter and if so, how to reduce them, which stemmed from our original discussion on the amount of fats and carbs to include in the diet. Now we have a medical term for those after meal glucose spikes- isolated postprandial hyperglycemia. Following that, I found an interesting article published in the Archives of Internal Medicine on June 9, 2003
                  which concluded: “Recent studies indicate that elevated plasma glucose concentrations are an independent and clinically significant risk factor for cardiovascular disease in nondiabetic and diabetic individuals. Thus, isolated postprandial hyperglycemia (2-hour postprandial glucose level >140 mg/dL in the face of normal fasting plasma glucose <110 mg/dL and normal hemoglobin A1c <6.1%) values is associated with a 2-fold increased risk of death from cardiovascular disease." Another study of concern to older women found: At baseline, 70% of 125 women and 48% of 133 men with previously undiagnosed diabetes had IPH. Over the next 7 years, women with IPH had a significantly increased risk of fatal CVD and heart disease compared with nondiabetic women. This increased risk was not observed in men with IPH. This association was independent of age, hypertension, central obesity, cigarette smoking, HDL cholesterol, and triglycerides (multiply adjusted hazard ratio and 95% CI: 2.6 and 1.4-4.7 for CVD; 2.9 and 1.3-6.4 for heart disease).

      2. Thea, Suepy and I wanted you share this study link with you. It suggests that it is essential for those with pre-diabetes or diabetes to keep glucose below 140 at all times. It appears that even occasional excursions above 140 double the risk of CVD. If so, then Alice is correct about maintaining tight controls on glucose even at older ages.

        Thanks for your open mind and support on this issue.

Leave a Reply

Your email address will not be published. Required fields are marked *

Pin It on Pinterest

Share This