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Second Meal Effect/Increased Insulin Sensitivity

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  • Second Meal Effect/Increased Insulin Sensitivity

    I've been reading about a well-known phenomenon called 'Second Meal Effect', as described here:

    The Second-Meal Phenomenon in Type 2 Diabetes

    The effect of a prior meal in decreasing the rise in blood glucose after a subsequent meal was first recognized almost a century ago (1). It has repeatedly been confirmed in healthy subjects...We recently observed that, in normal subjects, the second-meal phenomenon was associated with increased rates of storage of lunchtime carbohydrate in muscle glycogen.
    and here: http://images.abbottnutrition.com/AN...on%20Table.pdf

    Consumption of low glycemic-index (LGI) foods has been shown to attenuate blood
    glucose response during the postprandial period immediately following a meal. In
    addition, positive metabolic effects can persist well beyond this period. One of these
    extended effects, known as the “second-meal effect,” is the positive effect of the
    bioavailability of glucose on the glucose tolerance of the subsequent meal.

    This second-meal effect, initially observed in normal-weight, healthy adult subjec
    ts using glucose and guar, has also been documented in patients with type 2 diabetes.
    So, I'm thinking that the timing of carbohydrates could be manipulated to increase insulin sensitivity almost to the point of perfection.

    For instance, if one started the day with either no breakfast, or a breakfast of only protein and fat, and a lunch of mainly carb--no protein or fat--a vegan lunch if you will showcased by starch, such as potato or rice, then a normal dinner with very little starch/carb, and a serving of starch right before bed.

    This would make every second meal, a meal preceded by a known method of increasing insulin sensitivity.

    I think insulin sensitivity is one of the most important factors in any diet, particularly paleo. Insulin sensitivity means better muscle uptake of glucose, better liver function, better vitamin and amino acid uptake, and reduction of metabolic syndrome markers.

    What do you think?

  • #2
    Originally posted by otzi View Post
    I've been reading about a well-known phenomenon called 'Second Meal Effect', as described here:

    The Second-Meal Phenomenon in Type 2 Diabetes



    and here: http://images.abbottnutrition.com/AN...on%20Table.pdf



    So, I'm thinking that the timing of carbohydrates could be manipulated to increase insulin sensitivity almost to the point of perfection.

    For instance, if one started the day with either no breakfast, or a breakfast of only protein and fat, and a lunch of mainly carb--no protein or fat--a vegan lunch if you will showcased by starch, such as potato or rice, then a normal dinner with very little starch/carb, and a serving of starch right before bed.

    This would make every second meal, a meal preceded by a known method of increasing insulin sensitivity.

    I think insulin sensitivity is one of the most important factors in any diet, particularly paleo. Insulin sensitivity means better muscle uptake of glucose, better liver function, better vitamin and amino acid uptake, and reduction of metabolic syndrome markers.

    What do you think?
    So, are they saying there is a second meal effect in EVERYONE, or only in Type II diabetics?
    Rebooted Body -- Ancestral Health + Modern Psychology | The Rebooted Body Podcast

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    • #3
      It's for everyone. For a long time they thought it was missing in T2D's but now they see they have it, too.

      For a long time, low carb was used to blunt insulin, as part of the Carbohydrate-Insulin Theory of Obesity, but it turns out this leads to insulin resistance, high FBG, and other problems.

      Insulin sensitivity is the benchmark of health. Anything I can do to improve it seems worth a try.

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      • #4
        This sound like the same premise behind carb back loading.

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        • #5
          There is still a limit as to how much glycogen you can store and it is not that big.
          So if this second-meal-effect is true, then yes, you can have a carb'ish meal after a VLC one but I would not overdo it. What happens to the remaining glucose when the glyco stores are full ? ... I see carbs as "rocket fuel" so it's great to have when you have to produce a sudden bursts of effort but beyond that, not sure why I should increase my carb intake.

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          • #6
            Otzi, I hope you'll post your experience with this if you're going to experiment. I'll definitely follow this one.
            Life is not a matter of having good cards, but of playing a poor hand well.

            - Robert Louis Stevenson

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            • #7
              I knew you were Tatertot!

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              • #8
                This is rather interesting, being "former" type 2 having regained my sensitivity. I've been adding back in carbohydrate slowly, up to 125g a day and I'm STILL losing weight and have great glucose control. 150/day is coming soon, its been helping big time with my workouts. Getting in carbs 4 hours before my workout sound interesting.

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                • #9
                  Originally posted by otzi View Post
                  For a long time, low carb was used to blunt insulin, as part of the Carbohydrate-Insulin Theory of Obesity, but it turns out this leads to insulin resistance, high FBG, and other problems.
                  You need to back up this assertion.

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                  • #10
                    Originally posted by WeldingHank View Post
                    This is rather interesting, being "former" type 2 having regained my sensitivity. I've been adding back in carbohydrate slowly, up to 125g a day and I'm STILL losing weight and have great glucose control. 150/day is coming soon, its been helping big time with my workouts. Getting in carbs 4 hours before my workout sound interesting.
                    http://www.biomedcentral.com/content...3-7075-8-6.pdf

                    You may want to add a handful of almonds to your first meal, also.

                    Originally posted by Paleobird View Post
                    You need to back up this assertion.
                    When I first heard about LC, it was proposed as a mechanism to keep blood glucose low and prevent an insulin spike, since insulin in the blood prevents fat from being liberated from the adipose tissue for fuel.

                    This seems a reasonable theory, and is the backbone of the carbohydrate hypothesis of obesity as develed by Taubes in Good Calories-Bad Calories.

                    However, I have since learned that this thinking is a bit flawed. Protein ingestion also causes an insulin release. To preserve what glucose is in the blood and prevent hypoglycemia, glucagon is also released in response to protein ingestion. Glucagon acts as an inhibitor to insulin. It also turns out that in insulin isn't the enemy of fat, in fact it is needed to partition nutrients and has many other metabolic roles than simply putting blood glucose into glycogen stores and removing it from the blood.

                    Lyle McDonald, author of The Ketogenic Diet, puts it this way: Insulin Sensitivity and Fat Loss | BodyRecomposition - The Home of Lyle McDonald

                    As I imagine all of the readers of this know, insulin is a storage hormone released in response to eating with carbohydrates having the largest impact on insulin secretion, protein having the second greatest and fat having little to no impact on insulin secretion. Insulin sensitivity refers to how well or poorly the body responds to the hormone insulin. Individuals who are insulin resistant tend to have higher baseline insulin levels because the body is releasing more in response to try and overcome the resistance.

                    And while a great majority of insulin resistance is determined by lifestyle (training and diet play a huge role, as does body fatness), so do genetics. At the same bodyfat level, insulin sensitivity can vary nearly 10 fold for genetic reasons. So it’s possible that even lean athletes and bodybuilders could have some degree of genetic insulin resistant (I’ll talk about how to determine this at the end of the article). As it turns out, individuals also differ in how much or how little insulin they release following a standardized meal; some people release more insulin than others in response to a meal. While this can be related to baseline insulin sensitivity, it doesn’t have to be.

                    It turns out that both issue relate to fat/weight gain or loss (2). In contrast to what is generally believed, good overall insulin sensitivity tends to correlate with weight/fat gain and insulin resistance is thought to be an adaptation to prevent further fat/weight gain. However, some research suggests that a tendency to release too much insulin in response to feeding may predispose people towards weight/fat gain. One huge confound in all of this, mind you, is that high insulin secretion tends to make people eat more. Studies of diabetics find that decreasing insulin secretion with drugs tends to cause a spontaneously lower food intake (2).
                    For me, low carbing for 2+ years, I was able to lose about 80 pounds, reverse fatty liver disease, eliminate of gout, correct my high blood pressure, lower trigs from 1000 to 50. Raise HDL from 20 to 59. And maybe some other stuff, too.

                    But, most all of that occurred during the first 6 months, and the next 18 months I was stalled 20 pounds from my goal weight, was unable to progress in fitness, and fasting blood glucose crept up to pre-diabetic levels.

                    Adding carbs to the mix in controlled amounts was the finishing touch. I was able to lose the last 20 pounds and fasting blood glucose normalized.

                    Mark Sisson explained it well here:

                    However, going very low carb – to around or below 10% of calories, or full-blown ketogenic – can induce ”physiological” insulin resistance. Physiological insulin resistance is an adaptation, a normal biological reaction to a lack of dietary glucose. As I’ve said in the past, the brain must have glucose. It can use ketones and lactate quite effectively, thus reducing the glucose requirement, but at the end of the day it still requires a portion of glucose. Now, in a low-glucose state, where the body senses that dietary glucose might not be coming anytime soon, peripheral insulin resistance is triggered. This prevents the muscles from taking up “precious” glucose that the brain requires. The brain’s sensitivity to insulin is preserved, allowing it to grab what glucose it needs from the paltry – but sufficient – levels available to it.

                    It appears that weight loss is the deciding factor, and since low carb diets tend to be more effective at inducing weight loss in subjects, they also tend to be better at reducing insulin resistance in insulin-resistant, overweight people. Once you’re lean and weight stable, though, very low carb diets (less than 10% of calories from carbs) can reduce insulin sensitivity. This is normal and totally necessary in the context of a very low carb diet. If we didn’t become insulin resistant while eating very low carb, our brain wouldn’t be able to get the glucose it needed to keep us alive.

                    Read more: Does Eating a Low Carb Diet Cause Insulin Resistance? | Mark's Daily Apple
                    So, while some are doing just fine on a low carb, even ketogenic diet, others may find themselves struggling. I'm just exploring the aspect of regaining insulin sensitivity for those that are struggling.

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                    • #11
                      I'm glad you understand the difference between physiological and pathological insulin resistance. What you said earlier "it leads to insulin resistance and other problems", led me to question this.

                      Did you ever think that maybe your stall was because you were overdoing the protein? Perhaps the spuds just displaced some excess steak you didn't need from your plate. Just a thought.

                      The key phrase in the quote from Mark is : Once you’re lean and weight stable, though, very low carb diets (less than 10% of calories from carbs) can reduce insulin sensitivity. This is normal and totally necessary in the context of a very low carb diet. If we didn’t become insulin resistant while eating very low carb, our brain wouldn’t be able to get the glucose it needed to keep us alive.

                      This is why the young dude bros around here do better with more spuds. I never said otherwise.

                      This is a normal body adaptation, not something causing irreparable damage. Physiological insulin resistance goes away with the first plate or two of tators.

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                      • #12
                        This sounds similar in premise somewhat to the split diets like Sommers.
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                        • #13
                          Originally posted by Paleobird View Post
                          This is a normal body adaptation, not something causing irreparable damage. Physiological insulin resistance goes away with the first plate or two of tators.
                          I just get worried when I see my FBG hovering in the 110-120 range. Optimal FBG is said to be in the 85-95 range. I think for those of us who care about such things, finding out about the 'Second Meal Effect' and using that to our advantage could be wise.

                          I've been playing with my BG monitor for a couple weeks and find that the composition of my evening meal can cause a difference in FBG 12-18 hours later by 15-30 points. For instance, an evening meal with no starch but ample meat and LC veggies will cause an FBG of 110-120, but adding a potato to that meal, or eating a potato right before bed, will cause an FBG of 85-95.

                          Paleobird, I've read your posts and know what you eat. The difference between us is literally 1 or 2 potatoes a day. That's why I was very curious what your FBG was.

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                          • #14
                            Originally posted by otzi View Post
                            I just get worried when I see my FBG hovering in the 110-120 range. Optimal FBG is said to be in the 85-95 range. I think for those of us who care about such things, finding out about the 'Second Meal Effect' and using that to our advantage could be wise.

                            I've been playing with my BG monitor for a couple weeks and find that the composition of my evening meal can cause a difference in FBG 12-18 hours later by 15-30 points. For instance, an evening meal with no starch but ample meat and LC veggies will cause an FBG of 110-120, but adding a potato to that meal, or eating a potato right before bed, will cause an FBG of 85-95.

                            Paleobird, I've read your posts and know what you eat. The difference between us is literally 1 or 2 potatoes a day. That's why I was very curious what your FBG was.
                            How ample is ample? The higher than you would like BG may be due to excess protein. Are you only "adding" a potato or are you substituting it for having a second slab of beef?

                            When I did track it, my BG was consistently around 90 and always less than 100.
                            Last edited by Paleobird; 04-11-2013, 05:47 PM.

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                            • #15
                              The carb chapter in Perfect Health Diet mentioned something similar. Insulin sensitivity is a crucial signifier (whether or not its a determinant) and is much improved when going from 60%/300g carb to 20%/100g carb BUT we shouldn't assume that it's a linear function and that 5%/20g will be even better. They don't mention meal timing though. I kind of dread another layer of complication, especially when there seems to be a consensus that spreading carbs evenly reduces their hazards...
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