Tuesday, March 26, 2013

True or False? Adding Fat to A Carby Meal Lowers Insulin Response. Muscle Hypertrophy Impairs Oxygen Diffusion. Reducing Carb Intake Improve Muscular Insulin Sensitivity

Will the additional butter on top of the potatoes reduce the insulin response? You can find the answer to this and the other questions in today's episode of "True or False?"
If you are a regular here at the SuppVersity you should by now recognize the "True or False" part of the headline of today's SuppVersity article. Therefore it's probably unnecessary to say this explicitly, but this is a new series, where I could use a little help from your side. Well, ... I should say, I believe it would become even more fun, if you lend me a hand and send me short pieces of wisdom or idiocy like "Adding fat to a carby meal reduces the insulin response"  you deem worthy of being addressed in the True or False series. I cannot, or rather will not promise that I will address each and every of your suggestions, but if it interests me and can be tackled in a 2-3 paragraph text, your chances ain't bad to get your suggestions dealt with - if you got any ideas, just post them in the comment section of one of the previous installments (including today's, obviously).

Adding Fat to A Meal Will Ameliorate the Insulin Response

False. When you are browsing the Internet it is easy to get the impression that what is wrong or right is not determined by scientific evidence, but by the number of people who repeat it in their blogs, on their facebook walls and in their bulletin board contributions. The common "wisdom" that it would be a good idea to add some fat to a meal to reduce the insulin spike it will give you is one of those paradigms that remain intrinsically flawed no matter how often they are repeated.
Figure 1: Althoug the glucose AUC drops after the addition of fat (slowed absorption of glucose from the intestine), the amount of insulin (2ndary axis) that is needed to stash the glucose away is 8.5x higher (on a per unit base; cf. violet bar) and the absolute insulin response does not decrease at all in lean healthy men and women (Collier. 1983)
If you do take a look at what actually happens, when you add fat to a meal, it is yet not difficult to understand how that myth came about. Just like people don't understand that the GI of a certain carbohydrate source doesn't tell you much about it's effect on insulin, the fact that the addition of fat ameliorates the postprandial spike in glucose gets misinterpreted as "fatty meals are less insulinogenic than low fat meals". In fact, the addition of 50g of butter on top of the 50g of carbohydrates the 8 lean, weight stable men and women (N=4, each) consumed in form of potatoes, did not have any effect on the post-prandial insulin release at all.

GIP Or Not GIP - That is the Question: "Fat intake, in addition to ingestion of carbohydrate, stimulates GIP release. Therefore, during a mixed meal GIP might act to promote the storage of both triglyceride and glucose indirectly via the release of insulin." (Kieffer. 2003)
The amount of the fat storage peptide GIP (learn more), on the . Therefore, Collier and O'Dea are 100% right, when they state in the conclusion of their 1983 paper that...
"despite the apparent improvement in glucose tolerance when carbohydrate is ingested together with fat, the accompanying potentiation of insulin secretion could form the basis of long-term changes in insulin sensitivity which accompany alterations in dietary fat intake." (Collier. 1983)
You may want to remember that, whenever you feel inclined to add a ton of bacon on top of your sweet potatoes in the false believe that this would "mitigate" the effects of the carb-laden tubers the insulin response.

This obviously does not change the fact that having some fat in a meal does have the added benefit of increasing GLP-1 and PYY levels and thus contributing to a longer satiety effect (eg. Knut. 2008)

 Skeletal Muscle Hypertrophy Impairs Oxygen Diffusion

"Some HIIT For Life & Less LISS For More!" As the study at hand shows, this mantra is all the more important for the more muscular SuppVersity readers - that does not change that exercising longer to burn more fat won't work for anyone, muscular or not (learn why).
True! Contrary to the previous myth about the beneficial effects of adding fat to a high carb meal, which was not just totally messed up, but also pretty well-known the physical necessity that marked skeletal muscle hypertrophy will have a negative effect on he O2 diffusion of the "balooned up" musculature is something I would guess few of you have ever heard about before.

I have to admit that the 15-20% reduction in maximal oxygen consumption per kg of quadriceps mass a group of researchers from the University of Udine observed in 11 young athletes with marked skeletal muscle hypertrophy induced by long-term resistance training (body mass ~103kg), when they compared their them to 11 normal controls (body mass ~77kg) looks scary at first.

If you do yet also take into consideration that this decrease in oxygenation was accompanying improvements in ADP-stimulated mitochondrial respiration (+59%; takes place, when the ATP stores are used up) and a tighter coupling of oxidative phosphorylation, it becomes evident that the training induced enhancements in mitochondrial respiration seem to compensate for the hypertrophy-induced impaired peripheral O2 diffusion.
"The net results are an enhanced whole body oxidative function at peak exercise, and unchanged efficiency and O2 cost at submaximal exercise, despite a much greater body mass." (Salvadego. 2013)
In other words, despite "suboptimal" oxygenation of the musculature a bigger metabolic engine will still burn more fat... but only when it's working at peak intensity. It won't do so at submaximal intensities, where the O2 costs are "identical" (statistically). So, what does that tell us about the usefulness of training in the non-existent fat burning zone for advanced, heavily muscled trainees? Yep, it's even smaller than for the average sedentary housewife.

Low Carb High Fat Diets Lead to Acute Improvements in Muscular Insulin Sensitivity

False. Although the slowly abating low-carb craze does still make it appear as if "just eating less carbs" was the solution to everything, it is only logical that low carb dieting leads to changes in skeletal muscle insulin signaling, i.e. decreases in insulin-stimulated tyrosine phosphorylation of IRS-1 and PI3-kinase activity, which reduce, not increase the ability / willingness of the musculature to suck up glucose from the blood stream within no more than 5 days (cf. Pessin. 2000; Reusch. 2002).
Figure 2: Changes (before vs. after 5-day intervention) in fasting glycemia and lipidemia and glucose rate of appearance and disposal during euglycemic clamp conditions (Wang. 2013)
So even in the absence of significant effects on the body composition or signs of full-blown whole body  insulin resistance, the changes Cecilia C.L. Wang and colleagues observed in muscle samples that were taken from their insulin tolerant, but overweight subjects are identical to those you would observe in the early stages of diabetes, and do thus predate "changes in whole body insulin sensitivity" (Wang. 2013).

"But that ain't low carb!" Certainly a valid critism w/30% carbs and 20% protein in the diet it is practically impossible to reach ketosis, but - believe it or not - this is representative of the "low carb" diets you will usually see in the pertinent literature.
Wang et al. base their conclusion on the results of a recently conducted weight loss intervention that involved 18 obese individuals without diabetes who underwent euglycemic-hyperinsulinemic clamp and skeletal muscle biopsy after:
  • 5 days of eucaloric diet (30% fat, 50% carbohydrate), and 
  • 5 days of a 30% calorie-restricted diet, containing either...
    • LF/HC: 20% fat, 60% carbs
    • HF/LC: 50% fat, 30% carbs.
As mentioned in the introduction it's only logical and not necessary a bad thing that the skeletal muscle of the LF/HC group reacted with favorable changes in inulin receptor phosphorylation and lead to improvements in the IRS-1-associated PI3-kinase activity, which also figures in the exercise and nutrient induced increase in skeletal muscle protein synthesis (its among others the main target of IGF-1, of which keto dieters are known to have significantly reduced levels, anyway; cf. Fraser. 2000; Glass. 2003).

In other words, "No, 'just eat no carbs' is not the solution to everything", but will lead to certain metabolic adaptations which are not exactly conducive to returning to a normal carb diet afterwards. Plus, if you are a lean gymrat striving to to maximize your lean mass gains the full-blown hepatic growth hormone resistance and corresponding -50% drop in hepatic IGF-1 mRNA expression Bielohuby et al. observed in a rodent model of ketogenic dieting in 2011 probably won't come handy in the long run (on a side note: The "keto rodents", with their 92.8% fat diet also had a 5% reduction in lean mass and 46%, 56% and 223% higher relative amounts of visceral fat in the inguinal, epididymal and perirenal fat pads; cf. Bielohub. 2011)

Keep in mind this is a physiological form of insulin resistance

Learn how Adelfo lost his carbophobia and saw nothing but benefits from it (read more). That someone in the >30kg/m² BMI region with type II diabetes should keep a close eye on carb intake is a whole different story.
That being said, it is at least in part due to this mechanism that this type of diet works so well for highly insulin resistant individuals. It does not require the body to become insulin sensitive to work, but provides your body with a substrate that would - in and out of itself - require a certain degree of insulin resistance to make sure your muscle don't suck away the little glucose that's floating around and make you feel miserable and hypoglycemic. That you cannot observe those changes with a glucometer at home should be obvious. After all you are not eating carbs, are you?

Would the effect have been different with a true keto diet? The weight loss? Maybe. The transient insulin resistance? More pronounced, if anything. If you are already obese and freakin' insulin resistant to begin with, this does yet hardly matter. Low fat, high fat, keto - I don't care! The weight loss, the ensuing reduction in chronic inflammation and the new room to actually stash away superfluous energy alone will sooner or later also help you to reduce your insulin resistance.

Suggested read on physiological (=adaptation to diet / exercise) insulin resistance: "The Marathon Paradox - How Temporary Exercise-Induced Insulin Resistance Paves the Way for Fat Burning Machines" (complete article)

  • Berk ES, Kovera AJ, Boozer CN, Pi-Sunyer FX, Johnson JA, Albu JB. Adiponectin levels during low- and high-fat eucaloric diets in lean and obese women. Obes Res. 2005 Sep;13(9):1566-71.
  • Bielohuby M, Sawitzky M, Stoehr BJ, Stock P, Menhofer D, Ebensing S, Bjerre M, Frystyk J, Binder G, Strasburger C, Wu Z, Christ B, Hoeflich A, Bidlingmaier M. Lack of dietary carbohydrates induces hepatic growth hormone (GH) resistance in rats. Endocrinology. 2011 May;152(5):1948-60.
  • Collier G, O'Dea K. The effect of coingestion of fat on the glucose, insulin, and gastric inhibitory polypeptide responses to carbohydrate and protein. Am J Clin Nutr. 1983 Jun;37(6):941-4.
  • Fraser DA, Thoen J, Bondhus S, Haugen M, Reseland JE, Djøseland O, Førre O, Kjeldsen-Kragh J. Reduction in serum leptin and IGF-1 but preserved T-lymphocyte numbers and activation after a ketogenic diet in rheumatoid arthritis patients. Clin Exp Rheumatol. 2000 Mar-Apr;18(2):209-14.
  • Glass DJ. Molecular mechanisms modulating muscle mass. Trends Mol Med. 2003 Aug;9(8):344-50. Review.
  • Kieffer TJ. GIP or not GIP? That is the question. Trends Pharmacol Sci. 2003 Mar;24(3):110-2.
  • Knuth ND, Shrivastava CR, Horowitz JF. Reducing dietary fat from a meal increases the bioavailability of exogenous carbohydrate without altering plasma glucose concentration. J Appl Physiol. 2009 Jan;106(1):122-9. doi: 10.1152/japplphysiol.90404.2008. Epub 2008 Nov 13. 
  • Pessin JE, Saltiel AR. Signaling pathways in insulin action:molecular targets of insulin resistance. J Clin Invest. 2000;106(2):165–9.
  • Salvadego D, Domenis R, Lazzer S, Porcelli S, Rittweger J, Rizzo G, Mavelli I, Simunic B, Pisot R, Grassi B. Skeletal muscle oxidative function in vivo and ex vivo in athletes with marked hypertrophy from resistance training. J Appl Physiol. 2013 Mar 21.
  • Reusch JE. Current concepts in insulin resistance, type 2 diabetes mellitus, and the metabolic syndrome. Am J Cardiol. 2002;90(5A):19G–26G.
  • Wang CC, Adochio RL, Leitner JW, Abeyta IM, Draznin B, Cornier MA. Acute effects of different diet compositions on skeletal muscle insulin signalling in obese individuals during caloric restriction. Metabolism. 2013; 62:595–603


  1. T or F? The elderly need more recovery time when strength training.

    1. *lol* good question, but I am not sure whether I can come up with a good answer - will look into it anyway.

  2. To make sure that I am understanding "during a mixed meal GIP might act to promote the storage of both triglyceride and glucose indirectly via the release of insulin" from the Adding Fat to A Carby Meal Lowers Insulin Response article, is it best not to mix fats and carbs in a meal so there is less GIP and less of a chance of storing carbs converted to glucose into fat cells?

    1. I am curious to this as well. From that article it appears that separating your macros (fats and carbs) is better for body composition. If this is true, then my theory would be to eat carbs around training and at night, and eat fat at the other meals. Protein with every meal obviously.

    2. It would be important to at least have another test with an isocaloric addition of protein, carbohydrate, or even a different type of lipid composition to really determine if GIP response is due to the fat intake, or just increased energy.

    3. in theory that is right, mixing fat + carbs = potentially fattening. Whether this does make much of a difference in practice... or rather whether having it seperately makes much of difference is yet questionable.

      JP also makes a valid point, it would be interesting to compare the effects of PUFAs or MCTs to those of SCFA and SFA (in butter, which was used in the study at hand)

      what I still feel can be said for sure is that adding fat to a meal just do reduce the potentially fattening effects is absolute BS. What remains to be seen is whether eating carbs and fats seperately makes a difference.

      On a side note: Not eating any fat makes a difference on a bulk - a beneficial one; I have written about that here => http://suppversity.blogspot.de/2012/03/if-you-go-high-carb-you-better-go.html

    4. Dr. Andro,

      Would adding 4 tablespoons or another amount of Apple Cider Vinegar to a meal of high or low GI carbs help lower the release on insulin?

    5. Apple Cider Vinegar has been shown to lower the glycemic index of starchy foods, yes.

    6. To confirm, does Apple Cider Vinegar act like a meal with fat and carbs as above and lower the glucose but the insulin response of Apple Cider Vinegar with carbs the same as a meal with fat and carbs?

      Also, are there any side effects of using Apple Cider Vinegar with a meal?

    7. The antiglycemic property of vinegar is related to the inhibition of starch digestion. No side-effects except that it might burn your throat. Drink it with fizzy water, that's what I do.

    8. In the article, "Adelfo Cerame: Is Intermittent Fasting 'Bulk-Compatible'? Plus: Adelfo's 3-Months Intermittent Bulking Plan With Macronutrient Ratios, Meal-Timing and Sample Plan" at

      Adelfo Cerame used this combination "Intra workout: BCAA’s + 5g Creatine + Braggs RAW apple cider vinegar + Thermicarb + 4-8 oz of tart cherry drink."

      Do you know why he added vinegar to his Intra workout?

    9. Also,
      "Vinegar lacks antiglycemic action on enteral carbohydrate absorption in human subjects." at

      "The oral octreotide/insulin suppression test suppressed endogenous insulin secretion for the first 100 minutes of the study. During this time, the rate of rise of glucose was modestly but significantly (P = .01) greater after vinegar ingestion compared to placebo, suggesting that vinegar does not act to decrease glycemia by interference with enteral carbohydrate absorption."

    10. cooling works better than vinegar => http://www.nature.com/ejcn/journal/v59/n11/fig_tab/1602238t3.html

      2h AUC for insulin with
      fresh potatoes (warm): 16.1
      same potatoes after cooling: 12.2
      cooling + vinegar: 11.7

      ^ at least it does not make it worse ;)

    11. The subjects in that study consumed the vinegar before the meal, not with it.

      More recent research by Johnston "Suggest that the antiglycemic effect of vinegar is best realized when ingested with foods composed of complex carbohydrates and that vinegar may not attenuate PPG following the consumption of foods sweetened with corn syrups or dextrose, as is the case for many processed beverages and foods."

      Johnston, C. S., Steplewska, I., Long, C. A., Harris, L. N., & Ryals, R. H. (2010, January 4). Examination of the Antiglycemic Properties of Vinegar in Healthy Adults. Annals of Nutrition & Metabolism, 56(1), 74-79. doi:10.1159/000272133

    12. In the article, "Adelfo Cerame: Is Intermittent Fasting 'Bulk-Compatible'? Plus: Adelfo's 3-Months Intermittent Bulking Plan With Macronutrient Ratios, Meal-Timing and Sample Plan" at

      Adelfo Cerame used this combination "Intra workout: BCAA’s + 5g Creatine + Braggs RAW apple cider vinegar + Thermicarb + 4-8 oz of tart cherry drink."

      Do you know why he added vinegar to his Intra workout?

    13. I have no idea, but my guess would be help with the Thermicarb or give a slight alkaline effect to the drink (similar to lemon juice).

    14. he added the vinegar because he fell for the health community scam that this was what you are supposed to do. If you asked me - for a healthy person it does not make any difference (even if it works)

  3. T or F? Glucosamine Sulphate accelerates cartilage regeneration.

    1. You could add to that T or F a few others, such as: glucosamine hydrochloride is more effective than glucosamine sulfate; or chondroitin sulfate mitigates cartilage cell death; or orally ingested hyaluronic acid increases the concentration of hyaluronic acid in synovial fluid in people with osteoarthritis.

    2. *lol* I guess since they are often used in concert it will be difficult to pick that apart anyway. Also MSM, which has GH boosting effects => http://suppversity.blogspot.de/2012/10/low-vitamin-d-insulin-resistance.html

  4. Interesting as always !

    Reminds me of some weird experience I had.

    I did one month on a VLC/Keto diet.
    During that time, my FBS were pretty good : steady at 4.8mmol. Before it used to be around 5 any time I did some blood test.
    Aside from that, it actually didn't go that well...

    The first surprising thing is that I didn’t experience any weight loss while on Keto…
    (I am 178cm tall and weight 77Kg. I workout 2/3 a week, mainly doing resistance training)
    My digestion also slowed down seriously.
    On top of it, I also experienced a severe mode disorder : Big melancolia and sadness…

    After one month, I found it to much of a cost for no results, and introduced more carbs again. The first few days, I did it in a reefed/backload fashion and ate tons of high GI carbs.
    For 10 days my glycemia went completely out of whack, my mood was also not extraordinary and I gained 3kg and 2cm of waist… Not that great.

    I’ve read about Physiological/Peripheral Insulin Resistance which is supposed to be a normal adaptation while on ketosis. But I understood that it is supposed to to go back to normal within few days of eating carbs again…

    My blood glucose stayed between 6.5/7mmol all day long for almost a week, and for quite a while my best reading has been 6.1 for FBS and 5.3 during the day.

    anu idea why it went SO BAAAAADDDDD ?

    Thx :-)

    It sucks :-/

    1. why on earth did you eat HIGH GI carbs in the transition phase? There is nothing that could be "more wrong" than that. You need a slow transition back to eating carbs gradually introducing them back in and starting with low GI carbs if you want to avoid your BS blasting off the charts.

      I hope your blood sugar is now back to normal!? Also, what's your HBA1C and did you ever get a hs-CRP reading?

    2. Dr. Andro,
      What is your opinion on a diet which involves eating only fat and protein and under 30 grams of carbs a day for 6 days then on the 7th day a carb refeed of 6 to 8 hours of high GI foods to spike insulin to restore hormones. Then on the 8th day going back to eating only fat and protein and under 30 grams of carbs a day for 6 days then repeat the refeed on the 7th day?

    3. possible, while you are dieting, probably not optimal when you are not. Carl and I have actually planned to talk about a related issue with Intermittent fasting on the SuppVersity Science Round-Up tomorrow. You may want to listen to the show (1PM EST live or download the podcast from the "Seconds" I'll post on Friday)

    4. Dear Adel,

      Thx for your answer. I know now that the high GI thing was complete non sense...
      At first, I thought a big glucose and insulin spike might better because "quicker".
      But that was before I read about physiological insulin resistance...
      Stupid me !

      By FBS is ok now. But I'll do a a blood test soon and will check what you suggested.


  5. What is the biochemical/health significance of the insulin:glucose ratio? I.e. why should we care about it per se?

    1. it's a rudimentary, but very straight forward mesure of insulin sensitivity. The more glucose you got floating around at a given level of insulin the less insulin sensitive you are

    2. Could you please give ranges for interpreting this ratio ? Thx ;-)

    3. I wish I could, but this is a meal dependent thing. It's not useful unless you use a standardized meal and measure both insulin and glucose in a group of people.

  6. Interesting in the Collier 1983 study that protein + fat induced a much lower GIP response than carb + fat. I think we have all noticed that foods that are high in both fat and carbs ( chocolate and ice cream ) are the most fattening, and this further confirms my belief that we shouldnt have meals that are both high in carbs + fat.

    1. yeah the insulin spike by protein is not mediated by GIP (this requires the activation of the sweet taste receptors in the gut)

  7. So, what's your opinion for a clean bulk while hitting the gym for heavy training ~ 4 times/weak.

    I've read so much information and am more confused about the right nutrition when keeping up on reading.

    I'd been doing DC Training for quite a time. It's about splitting your nutrition into carb+prot and fat+prot and going really high with protein/day. After that, I tried low carb. But seriously, after about 8 months on low carb, I felt pretty messed up.

    Currently, I'm trying to eat 30% prot, 30% fat and 40% carbs a day with just whole foods.

    I know it's really hard to speculate about the right personal nutrition, but could this 30/30/40 split be the right way for a clean bulk? Or should I lower fat or carbs?

    My weight gain / month is ~ 1kg and I'm able to lift heavier stuff each training.

    Thanks in advance, Prof

    1. Have you read part II of my interview with Sean Casey? I give some very concrete advice there. Also, make sure those percentages are in calories not in grams. Because eating 30g of fat for 30g of protein and 40g of carbs will pretty certainly not allow you to gain LEAN mass.

      here is the link to the interview => http://www.caseperformance.com/145/interview-with-the-expert-adel-moussa-part-ii

    2. thanks adel, going to read it!

      haha, sure,% of my 3000 kcal's. but thanks for the reminder ;-)

  8. Hi Adel,

    Just stumbled across this page disputing baking soda as an ergogenic aid:

    Could make in interesting true or false since I know you've advocated baking soda usage in the past.

    1. don't know when this pamphlet was written, but with the latest citation being from 2004 some of the most significant studies are missing. That being said, there is no question that it is ergogenic. The question is only: For which athletes?

  9. I never understood the fuss about insulin resistance. It's just a mechanism, can be good, can be bad. If I don't eat carbs or don't eat, I want my muscle tissue to become insulin resistant. Failure to develop insulin resistance in such circumstances would be very bad..

    And regarding the carb + fat = more insulin topic, can't say I'm surprised by that either (sorry for the smartassery). If we make the highly likely assumption that palmitic acid is a signal for insulin resistance (highly available during fasting and after high fat meals) it's pretty clear that there should be a signal so you could overcome the insulin resistance if you also eat carbs -> GIP!

    I generally thought that GIP was a Good Thing, as it is present in lean individuals and either absent or fails to affect insulin release in obese individuals. It's not that clear though, you can do all sorts of stuff with GIP receptor knockout mice. (From the abstract of the following paper, while knocking out GIP receptors seems to result in a lean phenotype, they were able to make their GIP deficient mice fat with a high fat diet, but they got fat without increases in lean mass..)
    This seems to be a nice overview of GIP, the full text is free, if anyone is interested: http://www.ncbi.nlm.nih.gov/pubmed/22142579

    Which brings me back to wondering: Do postprandial insulin levels matter? I mean, if your fasting insulin is low enough you'll have no trouble accessing it, and you gotta store what you eat somewhere..

  10. T or F? Proteolytic enzymes reduce inflammation.

    1. without having looked into it another time, I remember that back in the day when I was interested in this myself I hit an "advertisment wall" with little to no independent research being available, but I will take a look at it again

  11. Hmmm. Seems like insulin on a per calories basis is much better with fat. Doubt you can more than double your total caloric intake and not expect to generate some insulin

    1. This is a good argument and part of the reason "we are getting fat" the fat + carb binges people call "meals" these days are simply freakin' calorically dense and unsatiating

  12. T or F, the following are good for tendonitis:

    Eccentric exercises

    Currently suffering from "golfer's elbow" and achilles pain myself, but not convinced many of the treatments above are worthwhile besides maybe ice and eccentrics. Would be interested if you have any thoughts on the best ways to heal tendonitis.

    1. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1122566/


      These are worth a look, but eccentric cable extensions worked a wonder on my elbow tendinopathy's.

      Heat > Cold

      Cross friction is great.

      Cortisone and Anti inflammatories are awful and actually worsen the condition by inhibiting healing.

  13. "the GI of a certain carbohydrate source doesn't tell you much about it's effect on insulin"

    Could you say more about this--it seems like it has to tell you something about effect on insulin. E.g., for average athlete in a rested state, wouldn't you expect eating high GI carbs to quickly raise insulin and have potential negative hormonal effects?
    Thx, Jon

    1. Most people eat mixed meals, which can influence the insulin response. Also, the glycemic load matters more. Take carrots for example. They have a high GI but so little carbs per serving that they don't influence insulin significantly.

      For completeness, carbs aren't the only stimulators of insulin. Protein does as well (whey is a perfect example).

  14. I don't understand this. Theres a video on youtube of a guy drinking a small cup of olive oil, and then eating some pizza. And he became temporarily diabetic for a few hours. His blood sugar shot up because the fat was blocking the cells at the insulin receptors an spiking his sugar. I'm so confused

  15. Nice blog comment Inulin used in medicines and the leaves are not medically used. The chief constituents of Inulin,

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    resin, with Inulin (a sort of sugar which replaces starch in many of the Dandelion family,Compositae), gluten, gum and

    potash.Dandelion Root provides vitamin A, vitamin C, vitamin D and vitamin B complex, as well as zinc, iron and

    potassium. Because of its iron content, it is widely used as a remedy for liver ailments, and has a diuretic effect that

    can help rid the liver of toxins.