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Fats and Insulin Resistance

Discussion in 'Low-carb Diet Forum' started by Sean_Raymond, Jan 6, 2021.

  1. kokhongw

    kokhongw I reversed my Type 2 · Well-Known Member

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    Not sure if you have ever considered Dr Joseph Kraft's study on hyperinsulinemia. But I think that is central to understanding the conflicting low cal/carb results that is often generated. While some takes fasting insulin measurements, almost non seems to document the post meal insulin response in the detailed way that Dr Kraft had.
    https://denversdietdoctor.com/diabetes-vascular-disease-joseph-r-kraft-md/

    And what may be insightful is that a person with normal fasting glucose/insulin level may have post meal insulin response that is many times the baseline. Resulting in extended high level of circulating insulin levels that goes unaccounted for.

    [​IMG]

    Perpahs this is the elephant in the room and fills many gaps.

    If the low cal diet is predominantly carbs based, patients with excessive insulin response will have much more difficulty losing fats.

    Which brings me to the next point that we often consider weight loss without factoring changes in body composition, thinking there's no apparent success. Yet we frequently find people on low carb diet with little weight loss, yet could see inches melt away...

    If it is already known that the predominant function of insulin is to inhibit lipolysis, then there will be a level where lack of insulin will allow lipolysis to occur. The challenge is to find that level for the individual and if there are other hormonal conditions that interfere with this... Carbs/Insulin model may not explain everything, but appropriately applied, via low carbs/keto/fasting... it has proven to be successful and sustainable for many...
     
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  2. Sean_Raymond

    Sean_Raymond HCP · Well-Known Member

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    That is an incredible story, a lot of hardship but many triumphs too. I think it is a testament to your character and that you kept going and found a way - many may have become angry and or given up. You worked it out for yourself, and regardless of how - the point is it does and it has made you much better. This is incredibly helpful and rewarding to me because either I do what many do and disregard such experiences because they do not fit the text book theories of what should happen or try to find out why and convince others in these fields.

    As I have said, I have no doubt low carbohydrate works for people, I just struggle with the explanation which as a clinician is important for me for many reasons - such as being able to justify why I might use them. Thankfully, incorporating low carbohydrate diets (not ketogenic ones) into a dietary plan isn't quite as difficult as it was even 5 years ago. However when I work for a particular trust they will have programmes for weight loss, diabetes etc and I have to stick with these broadly speaking. Luckily I can justify adapting the approach if their programmes do not work - there is no clear evidence reduced carbohydrate diets are risky, unhealthy etc (some argue they are). The issue is explaining to peers how it works to convince ha ha.

    To you I say well done on doing what top medical practitioners in their respective fields could not do and thank you for sharing it with me and others.
     
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  3. Sean_Raymond

    Sean_Raymond HCP · Well-Known Member

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    Hi.
    Thank you for sharing your personal experience with me. Yes, it still boggles my mind that a diet of 1000kcals did not cause weight loss (not as much as used too though). Given your weight and activity, I roughly worked out your calorie requirement and in 'theory', we should have seen weight come off. I understand how frustrating it would have been having many 'professionals' not believing this and probably saying maybe that you were not counting accurately or not remembering everything you ate because we mindlessly consume food etc etc.

    I can see how serious you take this and how vigorously you would have monitored your diet. This is what happened - we need to accept that regardless of whether it fits our understanding or not. I know you believe you have the answer ask to why it worked and disagree with my difficulty with the insulin idea. You're the one that achieved what specialists couldn't so I have to take your lead here. As I said, I am going back to a few sticking points which convinced me it wasn’t insulin to see if I have missed something because what I was taught isn't answering these results and or lack of.

    I hope I am not coming across as patronising and my messages are received in the spirit I send them. I take these things seriously and hope to learn, improve - ultimately so I can help people.

    Something is happening here that I know certain Professional circles believe with certainty cannot happen so I need to get this out there more and also ensure I do not ever subject any person I work with to the frustrating unhelpful experiences you have had. Part of the issue for me is that to be listened to, I have to show the how which I struggle to explain meaning its hard to convince people who make policies and programmes.

    Thank you.
     
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  4. Sean_Raymond

    Sean_Raymond HCP · Well-Known Member

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    Hi. Great post.

    Yes, I have heard of Dr Kraft but it was many years ago since I looked or considered the implications for his findings. I had tried to address this with colleagues at the time but it fell on silent ears. Thank you for jogging my memory on this.

    I completely agree. Loss of insulin sensitivity may have been going on for years but taking blood sugars will have made it remain silent because the extra insulin was keeping the blood sugar normal. It does make sense to test for insulin levels which would help reveal the beginnings of the disease earlier.

    I’ll post the main issue I have with believing insulin is the sin que non of lipolysis/lipogenesis.
     
  5. Sean_Raymond

    Sean_Raymond HCP · Well-Known Member

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    I have previously watched a few lectures by Dr Bikman, the author of the book a poster previously recommended, and I revisited a random one yesterday. I find him very professional and he puts together some very plausible and interesting ideas. However I have seen a potential issue with part of his hypothesis and I'll share it for information and potential discussion purposes rather than as a sort of 'take down' of him. He is clearly very learned and so I will be contacting him directly with a few questions for more details

    The lecture is titled Insulin v Glucagon: the relevance of protein. Dr Bikman puts forward the idea that in the fasted state, when blood sugars are euglycaemic due to a low insulin to glucagon ratio, if we give protein we do not see an insulin response. Essentially he is saying proteins insulinaemic properties should not be feared by those on low carb diets as the response is not relevant in certain glycaemic conditions. He says this happens because the body cannot shut down gluconeogenesis in the fasted state as a hypo will occur. This is true.

    The issue is numerous studies clearly demonstrate that if a fasted person consumes protein we will see a rise in insulin. We do see a rise in glucagon (which is already raised due to the fasted state) so essentially we see a hyperinsulinaemic hyperglucagonaemic state to maintain the blood sugar/euglycaemic state. I accept that he describes just one study in humans in the video and perhaps he has more in his book. But these potential sticking points are what I find difficult to move past because if he can put forward an idea that, from the literature appears to be incorrect, then the whole hypothesis crumbles even if the actual end point is correct.

    I am aware I am going around in circles - I see something working but just can't get to it with the paths science or explanations offer. I put this out there to see if I have interpreted this incorrectly. I will also try to view the study Dr Bikman used in that video,
     
  6. Sean_Raymond

    Sean_Raymond HCP · Well-Known Member

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    I'll quickly explain why I came to the conclusion that Insulin could not be the ultimate cause of fat storage/burning. At this point I am putting the brakes on my view of this until I review a few aspects of this. But this was my thinking prior to having the conversations I had over the past few days.

    Putting the studies which lower insulin but don't show fat loss aside, quoting Dr Bikman - he says "insulin has a direct effect on how every cell uses energy”. Dr Fung says similar things. Insulin seems to be portrayed as being the ultimate determinant of energy storage/energy burning. Yet the effects of insulin are regulated at hormonal, biochemical and allosteric levels.

    Energy homeostasis is a complex system made up of peripheral signals from organs and fat tissue and muscles integrated with cellular signals to orchestrate hunger, satiety and whether the body uses or stores energy. Yes, a role of Insulin is to signal to the body to stop fat breakdown (inhibit lipolysis) and promote fat storage (lipogenesis) but it is a signal which the cell is not obliged to follow - insulin is important in energy metabolism but it is just one of the players involved in the burning or storing of energy.

    The cell is the energy consuming unit of the body and it is here where we can better understand how the decision on what to do with the energy we consume is made. I won't discuss the specific allosteric regulation that occurs at the cellular level as it is very technical but when a cell receives an instruction from Insulin the cell will first look to its energy status before acting on insulin’s directions.

    That energy status it looks to is made up of a complex ratio of elements and their levels together act as a kind of thermostat to inform the cell of its energy status and whether it needs to store or burn energy. It is this Enzymatic control that ultimately determines the fate of energy not insulin.

    So it is at this cellular level of control which tells the cell if it should listen to what Insulin is telling it to do or not. If the answer is to burn energy it is the detected ratio of the mentioned elements not insulin that will determine to switch on catabolic pathways whilst switching off fuel utilising pathways to burn fuel. Whilst Insulin does promote fat storage or fat breakdown, it can be thought of as posing a question from which the cell will decide if the answer.

    It is at this level I never see Dr Bikman or Dr Fung or Dr Watson or anyone else describe - let alone explain how Insulin overcomes this control step for energy metabolism. The release of Insulin is not the be all and end all of fat burning because the body hasn't evolved direct fat burning/storing pathways that simply say yes or no. If Insulin was then the argument is that with the presence of insulin we are unstoppable fat building machines (protein causes insulin release).

    This is a very basic explanation of how Insulin may tell the body to do something but this order can be overridden if this instruction opposes what is happening at the cellular level . Fatty acid synthesis is tightly regulated and responsive to physiological needs.

    And if we think about it – this makes sense if we consider the fundamental survival of an organism. In order to survive energy is needed – it makes little sense that the body could then afford to decide to store energy when there is an energy deficit and energy is needed - just because a hormone told you to. Made worse by the fact energy will also be expended creating/storing that fat.

    I am going back to the mechanisms behind this to see if I can find a way that Insulin (or another mechanism) actually does override allosteric control of energy use in the cell . I accept that I may have something wrong here.
     
    #126 Sean_Raymond, Jan 14, 2021 at 11:37 AM
    Last edited: Jan 15, 2021
  7. Lamont D

    Lamont D Reactive hypoglycemia · Master

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    I hate to use a saying, but with calories, what goes in, must come out, sadly it doesn't come with the details. Most people struggle on such diets. With low carb the success a lot of people have to help lose weight and improve their life, have a look at the success stories in the forum.
    A lot of people nowadays are finding ways dietary to improve their health.
    You only have to look at allergies, and see that some people are risking their health by ignoring that there is a reason why you have the allergy. One that is usually not thought of is wheat and how the grain has been changed in the last century, tolerance to grains is a relatively new problem. And yet, it is a staple dietary necessity.
    It is as an impact on your blood glucose as bad as glucose itself. 100% carbs!
    Dieticians say and still say that I have to eat bread, why?
    Probably because of the fibre, but why should I?
    A lot of people have digestion and metabolic conditions that they don't know they have. Gluten for instance.
    You are what you eat! No I'm not!
    People are going vegan etc.
    How do they know, if they have an intolerance to certain things in that diet or they need micronutrients from meat, that they have always had.
    It is a minefield.

    As I said, I went through my young days, being told to eat vegetables and milk.
    Why couldn't I just eat it, why did it make me ill?
    Imagine a baby spitting out food because he didn't like it. He is hungry but would rather do without, that eat what is in front of him.
    Is this telling the parents, not to feed him that or persist with the same in case, he was not well or teething etc.
    So a mother will find what the baby does like and make sure he is not going hungry.
    How many mothers use convenient tasty food? Just to get the baby to eat.
    What can be missed, is that some foods like some green vegetables, some of them are liked by the baby, but some are not. They (I'm told) the taste, texture and smell are similar but the baby will have favourites. Why?
    Again the baby is hungry and needs feeding, but what is happening with his preference to eat or not eat? Vegetables are really good for (so called) normal healthy humans. And when growing up, the information overload on vegetables, he still won't put a sprout anywhere near his mouth, inside his brain and the gut are having a conversation back and forth, don't eat that!! Again why?
    The child knows why but cannot explain it!
    As in my experience, if I had known that I had as well as my lactose intolerance, that I had a wheat intolerance, a grain intolerance, a rice intolerance, and to a certain extent other food that makes me ill!
    Does the body know why it won't eat certain foods, is the likes and dislikes of food, the body telling you, you don't have to eat that food?

    When I was a teenager into my twenties and played cricket and football, this is in the sixties and seventies, I was told often enough, by coaches, the way to stay fitter was to not eat spuds, bread and beer, this was common knowledge in the day.
    Why has this great advice been ignored?

    I thank you for seeing that my metabolism works differently (I am weird) and realising to think about the diversity of people and the reason why our dietary requirements are different and should be tailored to the individual.

    I have learned through experience, to keep an open mind and be proactive, rather than reactive (see what I did there?) to get real control of my condition, if I can get my head right, I may have a much better retirement! (Ha!)

    Stay safe, best wishes.
     
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  8. zand

    zand Type 2 · Master

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    I apologise for taking so long to reply to this. My brain is still struggling with long covid and the article was too difficult for me to read again until now.

    I am not sure you read the link properly.

    The reduction in calorie intake was BECAUSE insulin was suppressed. There was no dietary intervention. We often say that carbs are addictive and make you hungrier, but maybe it's the insulin that makes us crave the carbs. A true vicious circle then. The easiest way for us to break this vicious circle is to reduce carb intake.

    From the 2nd link I posted:-

    "Subjects were allowed to eat ad libitum, and neither dietary nor exercise interventions were recommended.

    Concomitant improvements in body composition occurred with insulin suppression. Weight and BMI decreased during the 24-week study period.

    Both leptin and fat mass decreased, consistent with changes in weight and BMI. Total caloric intake, carbohydrate intake, fat intake, and protein intake decreased despite the absence of a dietary intervention. Carbohydrate craving was also significantly decreased in the entire cohort. Self-reported physical activity was unchanged during the study period.

    This study supports the primary role of insulin in the genesis of obesity in some individuals.

    A previous study reported the efficacy of insulin suppression in promoting weight loss using diazoxide. However, the magnitude of the effect of insulin suppression on weight loss was confounded by the concomitant use of a low-calorie formula diet in all patients, limited period of insulin suppression (8 weeks), and failure to examine insulin dynamics. This is the first study that prospectively evaluated the effect of chronic insulin suppression on fat mass and body weight in severely obese adult subjects without dietary or exercise intervention.

    We found that insulin suppression for 24 weeks was associated with marked weight loss (mean 12.6 kg) in 18% of an otherwise healthy subpopulation of adult obese subjects, and a small but significant weight loss (mean 3.6 kg) in another 57%. This weight loss occurred without dietary or exercise intervention, and occurred slowly but without asymptote.

    The role of increased carbohydrate craving and intake has been previously suggested to play a contributory role in the development of obesity. However, the connection between insulin and carbohydrate craving and intake is less clear. The frequent intake of highly refined carbohydrates may induce weight gain by initiating and sustaining a chronic state of hyperinsulinemia. Carbohydrate intake stimulates insulin secretion, raising circulating insulin levels, which in turn favours increased fatty acid uptake, lipid biosynthesis, and inhibition of lipolysis, leading to energy storage. Conversely, it had been suggested that insulin stimulates hyperphagia and fosters carbohydrate cravings, producing increased levels of insulin that promote insulin resistance and exacerbation of the hyperinsulinemic condition. This suggests that a vicious cycle is set in motion that perpetuates hyperinsulinemia and weight gain, and that breaking this cycle can promote weight loss.

    Our data suggest that insulin hypersecretion plays a role in the pathogenesis of obesity. Decreasing this hyperinsulinemic state promoted body weight and fat mass loss with concomitant modulation of appetite and food preference in our cohort. These changes were associated with improvements in insulin sensitivity and clearance, and without glucose intolerance or diabetes. Our results propose that suppression of insulin secretion may represent a viable approach in some obese individuals to break the vicious cycle of hyperinsulinemia, insulin resistance and weight gain and to modulate appetite, food preference, and body weight in a beneficial manner."
     
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    #128 zand, Jan 18, 2021 at 7:02 PM
    Last edited: Jan 18, 2021
  9. Sean_Raymond

    Sean_Raymond HCP · Well-Known Member

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    Hi.

    I know you posted 2 links but I believe they were to the same Study?

    I'm only skimming through this and will reply when I get a chance to look at the studies. But I'd just like to respond to a few things.

    First. Even if the drop in insulin led to reduction in calorie intake that would still mean that the weight was lost because of reduced intake rather than any direct effects of insulin on fat tissue Many believe insulin directly makes you fat so reducing its levels makes you lose weight - calories are not so important. This is a bit of a different hypothesis.

    My main sticking point with insulin being the cause of fat gain is that the cell doesn't take direct orders from Insulin. Insulin sends a signal which the cell isn't obliged to follow - the cell will first look at ratios of specific elements to gauge energy status before deciding if it should follow Insulins request. This is because of allosteric control - essentially regulation by enzymes and biological substances (it is very technical but I can put together an explanation more detailed than the one I previously posted a few days ago). The release of Insulin is not the be all and end all of fat burning because the body hasn't evolved direct fat burning/storing pathways that simply say yes or no. Insulin is a hormone which is subject to regulation and can be overridden.

    It is at this level, beyond hormonal control, that I am revisiting to see if there is someway these regulatory processes can fail because many on her clearly reduced calories and didn't lose weight but reduced carbs whilst eating more calories and still lost weight.

    Regarding Insulin stimulating appetite - I had a discussion on here a while ago regarding this. My argument then was that the evidence strongly leans towards Insulin being a satiety hormone - making a person feel full - so reducing intake. I do not recall seeing any convincing evidence that indicates it promotes appetite. I'll look at those studies you posted and comment on them when I can.

    Thanks
     
  10. Resurgam

    Resurgam Type 2 (in remission!) · Expert

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    I think that the impossible fact of calories not being entirely real is beginning to dawn on you - so many believe it implicitly and I am not the only one to experience the venom of a doctor who has been told that the diet isn't working - I have even had one doctor threatening to have my children taken away and me locked up because I questioned his advice on diet.
     
  11. lucylocket61

    lucylocket61 Type 2 · Expert

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    Maybe the idea that many of us appear to have a faulty insulin response, so the traditionally accepted 'normal' insulin pathway and choices are not happening as they would in someone without that insulin response?

    Our bodies are using the insulin to snatch the carb foods away and lock them into inaccessible stores we cant access.
     
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  12. kokhongw

    kokhongw I reversed my Type 2 · Well-Known Member

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    Have you considered the role that ketones may contribute to this cellular energy regulation process? Especially when cells become insulin/glucose resistant...
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5313038/

    Abstract
     
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    #132 kokhongw, Jan 19, 2021 at 2:45 AM
    Last edited: Jan 19, 2021
  13. zand

    zand Type 2 · Master

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    It's interesting that there was a decrease in leptin too and yet the participants still consumed less.

    Yes I did. After posting the first one I was unable to access the full report using the first link so I posted a second. Must have been a glitch as I can see it again now.
     
  14. Sean_Raymond

    Sean_Raymond HCP · Well-Known Member

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    I am certainly reconsidering/reviewing what I had thought I satisfactorily understood. I have looked at this many times before and always came back to calorie ultimately being the cause of weight gain although what drives excess energy intake is far more complicated. I 've had success reducing calories so it is a workable option but for many it clearly isn't - regardless of having T2DM or not. For many on here it does seem calories is just an impossible explanation based on their own self experiments.

    I am utterly shocked at the Dr saying such a thing - having such a view of how food affects the body cannot be used to judge a persons ability or safety to raise a child. That is disturbing.
     
  15. Sean_Raymond

    Sean_Raymond HCP · Well-Known Member

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    I'll look at the study!

    Ketones need to be created so ketogenesis can be thought of as anabolic although it is also understandably and correctly thought of as catabolic. The possibility exists that ketogenic states do confer a metabolic advantage because of this building of new nutrients - so more energy expended. I am aware the idea is to enhance fat burning in this state however to me it has always seemed that much of that fat burning will not be from fat stores but dietary fat. I have not investigated the mechanism of ketogensis in full detail for weight loss as I have not trialled it any patients other than those with some neurological conditions. I will be looking at Ketogenesis soon.
     
  16. Sean_Raymond

    Sean_Raymond HCP · Well-Known Member

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    This is an interesting study. With a simple design. It isn't an RCT and it is conducted in free living individuals which need to be considered. One of the researcher's is Robert Lustig and I feel his clear position needs to also be considered in interpreting some of the things said here.

    I'll put down some observations

    The intro states that Insulin regulates Acetyl COA Carboxylase - which to a degree is true. ACC is the enzyme which converts Acetyl COA into Malonyl COA which is then converted to a fatty acid. In simple terms Insulin promotes the activity of an enzyme (ACC) which is instrumental in fat synthesis. BUT the enzyme insulin upregulates needs a substrate before fatty acids can be synthesised and that substrate is citrate. Citrate will only be available when the citric acid cycle becomes overwhelmed causing citrate to spill out of the mitochondria and into the cytosol of cells where it then can be used as a substrate (indirectly by insulin) for conversion into fat. BUT that spillage of citrate into the cytosol is NOT under hormonal/insulin control. It is driven by an abundance of energy which overwhelms the citric acid cycle.

    I am working on trying to work out if, in an insulin resistant high blood sugar state, maybe this can cause this citrate spillage independent (to some degree) of positive energy balance. Basically insulin resistance causes a pseudo energy abundant state because of the high glucose/fat levels typical in insulin resistance fooling the body into thinking it has more than it has to promote fat storage (beyond hormonal control).

    It then states that acute glucose stimulated secretion and fasting hyperinsulinaemia predicts weight gain - both claims are massively disputable and debatable.

    May I ask why you say the weight loss WAS because of reduced insulin. The researchers acknowledged there could be other reasons for the reduced calorie intake other than insulin (they say these are less likely with no real evidence) and Ocretide has been shown to potentially reduce fat absorption in the gut. Also. he drug is a Somatostatin analog. Somatostatin has been shown to slow gastric motility and this can very plausibly cause a greater prolonged feeling of fullness after eating. So a compelling reason for why Octreotide may cause weight loss is because of its interaction with appetite regulation - promoting satiety. This fits in perfectly with this study as reduced hunger was reported. This warrants further investigation and I have not looked into this enough to say if it is the insulin or Octreotide acting on appetites regulation or a combo of both.

    Also remember that in obese, insulin resistant individuals it isn't just insulin that is raised by glucagon, indeed we may very likely see hyperglucagonaemia accompany hyperinsulinaemia. Ocretide inhibits glucagon release as well as insulin.There may be implications for this reduction? I have no idea if there is a link - I am just throwing it out there to demonstrate much more is going on here than insulin reduction..

    Regarding leptin reduction, this is not surprising given fat loss will cause Leptin reduction as leptin is released from adipose tissue. They had reduced hunger and less Leptin which may seem contradictory because Leptin promotes satiety but they were given a drug which has been shown to possibly reduce appetite.

    I'm offering thoughts at this point although I am still more on the side of an explanation being it is insulin per se although I am trying to find a plausible mechanism to fit this. However it is correct that whatever is happening to explain the posters on here losing weight by reducing carbs/insulin and not calories IS happening. My initial rationale for this was that calories were reduced due to a massive reduction in calories by way of dietary carbohydrate reduction/removal and not fully compesating for this calorie reduction. Posters on here have shot that down with their testimonies that they eat as much if not more.
     
  17. zand

    zand Type 2 · Master

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    Because that was the only thing they artificially altered. You stated that the weight was lost because calories were reduced, and it seemed like you were saying this was there was a calorie limit placed on the participants.

    I stopped trying to reduce calories to lose weight after a bad bout of flu 14 years ago. My son and I were both very ill with it. We ate nothing, only managing a few sips of water for 5 days, and then had only a few small nibbles for the next 6, a maximum of 200 cals per day for those 6 days. He wasn't overweight at all at the onset yet he lost 11 1/2 pounds over those 11 days. I was morbidly obese and lost just half a pound. It was then that I realised that calorie counting was never going to work for me.

    On another thread a poster said he knew he was becoming insulin resistant because of darker skin in the armpits. I never knew that was a sign of IR until I read that. I was young and slim when the change in colour happened to me. I remained slim for a few years after that. Skin tags didn't appear until much later when I was already obese. Just mentioning it as part of the chicken and egg argument re insulin resistance. What comes first weight gain or insulin resistance? I always thought it was the weight gain until I read that other thread. Maybe that isn't so clear cut either.

    To be honest I don't care enough about why low carbing works and low calorie doesn't work for me anymore to bother reading the complicated stuff you and other posters have written. I understand that you need to know why, but I don't. I am glad that you have been listening to us and no longer think it's just a case of calories in/calories out, that is the main reason I have posted on your threads. I hope you find the answers you are looking for and I hope that you keep an open mind.
     
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  18. Lamont D

    Lamont D Reactive hypoglycemia · Master

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    My last diagnostic test was a 72 hour fasting test.
    This was done in hospital under supervision.
    A blood glucose finger prick test was done every two hours, from the moment I arrived till I left the hospital.
    During the test at the end of the second day, after a shower, my bloods being in normal levels, I woke up from the place I had been for over a decade. This sudden clear mind convinced me that I needed to find out what had happened to me.
    Something had given me those symptoms of brain function issues. Because of the hypos it couldn't be hyperglycaemia, because I was getting normal levels fasting and Hba1c test, so what was causing this?
    I had all my tests on most of my hormonal glands and all came in negative for abnormalities. Except my pancreas, only an overshoot of insulin can be responsible for my hypos, my condition and my brain function.
    Hyperinsulinaemia is a common imbalance, as always depending on how high, even a modicum of too much insulin will do you no good.
    As for my condition, if I don't trigger an overshoot, I don't go hypo, my insulin levels are normal when I don't have carbs constantly.
    So to sum up, carbs cause the overshoot, because of the spike and if no intervention, I will certainly go hypo.
    Anyway reducing my carbs intake and eating healthy for me is my treatment.
    So after I had fasted for over 72 hours, I noticed something else that surprised me, my energy levels. My energy levels were unbelievable, no lethargy, no tiredness and my sleep patterns were really good.
    I walked and walked to help me with my health.
    And to the crux of the matter, because my hyperinsulinaemia was reduced back towards normal with having four days free from spikes and hypos. I also noticed my weight loss increased. And within a couple of months I had lost somewhere around five stone and then I plateaued, and as I carried on with very low carb, I lost a little more, then I just stopped losing weight. One of the reasons why I didn't lose more weight at that time was I was still following the advice of eating every three hours.
    The only thing that had changed was my insulin levels. After the weight loss, my insulin resistance went as well, my body started healing itself.

    Because you are not using as much insulin with low carb, and the benefits of that, maybe the alternative fat burning from carbs to ketones produce a different cellular response to how our energy is derived.
    I have on my journey, discovered fasting, which is really great, for me.
    It also controls my intake of food, and because I don't feel hungry, I eat when I want, if I want, too much in a window of a few hours. And of course I don't hypo.

    I have to live the rest of my life, like this. I can never go back to chip butties, or some of my favourite foods.
    Too much insulin will surely shorten my life.
    Control will increase my life span and keep me healthier for the road ahead.

    Keep safe, keep looking for answers and keep an open mind about how just enough insulin is fine, too little and too much isn't.
    This is why people don't understand why low carb works.
    Treatment should be tailored to your intolerance to certain foods, namely carbs and sugars. The supposed healthy diet is not healthy for lot of people who have an endocrine conditions. Especially T2s, and finally that is why losing weight is important but how you do it is more important.

    Stay safe
     
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  19. finsit

    finsit Type 2 · Well-Known Member

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    I would highly recommend "Why We Get Sick" by Dr. Ben, excellent research resource. My conclusion from my personal experience and reading is that you need to eat low carb, moderate protein and then fill the rest with fats (like Dr. Ben says). On the other side the diabetic solution genius Dr. Bernstein is of the view that you eat fat whatever come with the protein, which is a good way to manage your fat intake. Thirdly, i read that not everyone's response to fats is similar, so you can try a low carb high fat diet and do check your lipids and based on results, tweak your fat intake.

    Here is a detailed paper on combination and affect of different diets on blood glucose levels, its quite lengthy but very informative.

    https://www.tandfonline.com/doi/full/10.1080/10408398.2013.792772

    Because insulin is a fat storage hormone, it makes sense that in the absence of high circulating insulin in the blood, you will not store fats and with high glucagon rather burn it, so it should relate to weight loss. My two cents.
     
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  20. Krystyna23040

    Krystyna23040 Type 2 (in remission!) · Well-Known Member

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    That is really interesting. I have, since the beginning of April, started eating whatever fat comes with my protein. So Ribeye steak, shoulder of lamb and pork, cheese, eggs, chicken and oily fish but drastically cutting down on the double cream to only 20ml a day.

    Have kept to my normal 20g and under carbs a day, but have upped the protein using whey and casein protein.

    Since I started low carb I have suspected that having rather high amounts of double cream is a problem for me. Over various lockdowns my cream consumption increased and as I have now discovered - so has my waist circumference and that was even though I never went above 20g carbs.
     
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