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  #1   ^
Old Thu, Jan-04-18, 09:01
khrussva's Avatar
khrussva khrussva is offline
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Plan: My own - < 30 net carbs
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Default Genetic Evidence That Carbohydrate-Stimulated Insulin Secretion Leads to Obesity

I saw a link to this study on Dietdoctor.com.

Dr. Andreas Eenfeldt had this to say in his post about the study...


Quote:
Is eating big portions of food and laying on the couch for too long the culprit in the obesity epidemic? Eating too much, and moving to little? That’s the message we’ve been fed for decades, during the obesity epidemic, so saying that it has not worked out great is quite an understatement.

Now a new genetic study conducted by Harvard-based Dr. David Ludwig and colleagues provides new support for an alternative explanation, with the fat-storing hormone insulin as the main controlling factor in obesity.

In the study they found that genes leading to higher insulin secretion are very strongly linked to higher body weight. This provides relatively strong support for the theory that the higher insulin (primarily released when eating carbs) actually causes obesity. This as we know that the genes come first, before any lifestyle factors during life.


Here is the link to the actual study...

http://clinchem.aaccjnls.org/content/64/1/192

Dr. David Ludwig did a write-up on this study here...

https://medium.com/~davidludwigmd/g...ty-327d84be6d2b

And Professor Noakes wrote an editorial on the study here...

http://clinchem.aaccjnls.org/content/64/1/7

Last edited by khrussva : Thu, Jan-04-18 at 20:21.
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  #2   ^
Old Thu, Jan-04-18, 10:15
teaser's Avatar
teaser teaser is offline
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Plan: ketosis/IF
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There's a study, "Functional hypoglycemia in early latent diabetes," it used to be free, now it's not. Seems to be happening a lot lately, maybe that's actually a good sign, there's renewed interest in this sort of thing.

Anyways, a couple of hundred obese subjects, given a five hour glucose tolerance test. A fair number showed normal glucose tolerance at the second hour, but most of these showed "early latent diabetes," which is what the researchers chose to call a delayed reactive hypoglycemia, the lowest numbers, below basal, showed up around the four hour mark. Evidence of excessive insulin, a different sort of glucose intolerance than the extended elevation in blood glucose used to diagnose diabetes or prediabetes.

One of the more common undesired side effects of gastric bypass is hypoglycemia, which fits well with the desired side effect of diabetes reversal. Maybe that could be seen as latent hypoglycemia, just as further weight gain might bring somebody from latent diabetes to frank type II diabetes, weight loss could uncover a propensity for hypoglycemia that type II/insulin resistance would actually protect from.

https://www.ncbi.nlm.nih.gov/pubmed/23169787

Quote:
Long-term, intermittent, insulin-induced hypoglycemia produces marked obesity without hyperphagia or insulin resistance: a model for weight gain with intensive insulin therapy.


Quote:
Abstract
A major side effect of insulin treatment of diabetes is weight gain, which limits patient compliance and may pose additional health risks. Although the mechanisms responsible for this weight gain are poorly understood, it has been suggested that there may be a link to the incidence of recurrent episodes of hypoglycemia. Here we present a rodent model of marked weight gain associated with weekly insulin-induced hypoglycemic episodes in the absence of diabetes. Insulin treatment caused a significant increase in both body weight and fat mass, accompanied by reduced motor activity, lowered thermogenesis in response to a cold challenge, and reduced brown fat uncoupling protein mRNA. However, there was no effect of insulin treatment on total food intake nor on hypothalamic neuropeptide Y or proopiomelanocortin mRNA expression, and insulin-treated animals did not become insulin-resistant. Our results suggest that repeated iatrogenic hypoglycemia leads to weight gain, and that such weight gain is associated with a multifaceted deficit in metabolic regulation rather than to a chronic increase in caloric intake.


Fun mouse study. You can't throw a rock without hitting a mouse study where increased food intake isn't necessary for them to get fatter.
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  #3   ^
Old Thu, Jan-04-18, 10:49
khrussva's Avatar
khrussva khrussva is offline
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Plan: My own - < 30 net carbs
Stats: 440/207/210 Male 5' 11"
BF:Energy Unleashed
Progress: 101%
Location: Central Virginia - USA
Default

My light bulb moment in all of this was when I learned that insulin was a fat storage hormone (thank you Gary Taubes). From there I was able to connect the dots with my own experiences and I finally understood why low carb works for me. It keeps my insulin down so that my own fat stores are available for use. I later learned via blood glucose testing that I was very reactive hypoglycemic. But it didn't take 4 hours for me. My BG spike and crash happened within the first hour of eating junky, processed carbs. That is why I had intense cravings for sugar and felt wiped out shortly after eating a high carb meal.

I believe insulin has been my problem since the beginning. In the 'what came first, the chicken or the egg?' discussion, I'd have to say that my first problem was high levels of insulin and that led to obesity and insulin resistance. Even in the better food environment that we had in the 1960's I was predisposed to gain weight. I was a pudgy toddler and overweight or obese throughout most of my youth. The food pyramid and the "Fat makes you fat" mania that came along in the 1980's only made things worse for me. If I have a genetic defect, though, I'd say that is the fact that I don't have strong satiety signals compared to the average person - especially when I eat carbs. I've always been prone to overeat. Feeling full was stuffing my belly with food. I did not (and still don't) have a clear cut "off switch" telling me that I've eaten enough. I'm pretty sure that my body had no trouble producing plenty of insulin to cover all that bread and potatoes that I was eating back then. My family did not adopt the strict mealtime-only eating practices of my grandparents. We snacked on carbs. That kept my insulin high for longer periods of the day. Over time I became more obese. I became more insulin resistant. I tolerated carbs less and wanted them more. My reactive hypoglycemia worsened as my metabolic syndrome symptoms got worse. Eating junky carbs I was almost always hungry and sapped for energy. It was a snowball effect. As time went on I became more addicted to carbs. My preferred foods became those that would quickly get my blood sugar back up. It became harder to stick to a diet. Carb addiction combined with resisting the near constant drive to eat them lead to binging in moments of weakness. I continued to gain weight and become even more metabolically ill. Sticking to low carb reversed this cycle. The snowball started rolling the other direction.

I never could figure out why I could carry 200+ pounds of stored energy (fat) and be so hungry all the time. Learning insulin's behavior in my body helped me figure out why I am the way that I am. It also helped me figure out why low carb is the right way for me to eat. When I eat in a way that keeps my insulin levels down I can burn my own fat for energy. When I was eating pizza, bread, pasta, chips, cakes, cookies, and candy my own fat was locked down tight. My appetite and energy levels lived or died by what I put in my mouth. Episodes of low blood sugar shortly after eating insured that I put food in my mouth often or suffer the consequences... a fight to resist the urge to eat.

I like how I eat now. Satiety from eating a quality low carb meal still takes time to kick in. I can overeat low carb food. But at least I do feel satiety between meals like I never did before. Satiety is a wonderful thing. This WOE works a whole lot better for me that the standard American diet. My body runs better on fat than it does on carbs.

Last edited by khrussva : Thu, Jan-04-18 at 15:01.
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  #4   ^
Old Thu, Jan-04-18, 12:43
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nawchem nawchem is offline
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I'm the same way khrussva. I used to eat fast food every dinner. I would order 2 meals (get 2 drinks because I was embarressed) because within 2-3 hours I would be starving again. Once I threw up when I did that because I my stomach was so full, yet I was hungry at the same time.

Since I've eaten LC for so long I have weaker hypoglycemia.

Its strange most of the foods you listed have gluten and that seems to raise my blood sugar more, the fall is steeper then.
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  #5   ^
Old Thu, Jan-04-18, 14:59
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deirdra deirdra is offline
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My experience has been similar. I was normal weight until ~13 and a switch to a school with carb-based lunches, chubby in HS and "fat" in university and yo-yo dieting on HCLF diets in attempts to lose 40 lbs. In retrospect, now knowing my lean body mass, I was only ~20 lbs overweight, so it is no wonder it was nearly impossible to get down to and maintain 14% body fat. Due to my high-wheat diet I always looked puffy & bloated. When low-cal didn't work, I went vegetarian & vegan - more carbs and the zags in my zig-zag weight chart kept edging higher. The "expert" advice to eat many small carby meals made it even worse - more carbs, more insulin, more often is the perfect way to develop T2 diabetes, and knowing what my friends ate too, that is how they all got there.

Last edited by deirdra : Fri, Jan-05-18 at 11:23.
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  #6   ^
Old Thu, Jan-04-18, 19:22
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RawNut RawNut is offline
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Plan: Very Low Carb Paleo
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  #7   ^
Old Thu, Jan-04-18, 20:23
khrussva's Avatar
khrussva khrussva is offline
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Plan: My own - < 30 net carbs
Stats: 440/207/210 Male 5' 11"
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Location: Central Virginia - USA
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Quote:
Originally Posted by RawNut
This may or may not be the one: ...

Yep - that's the link that I meant to post. Thanks Deirdra & RawNut for catching the duplicate link above. I corrected it to what you provided.

Last edited by khrussva : Thu, Jan-04-18 at 21:38.
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  #8   ^
Old Thu, Jan-04-18, 20:49
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thud123 thud123 is offline
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I really like the way Ludwig wraps it up in that link:

Quote:
Pending further research, all sides of this debate would do well to avoid proclamations of having either proven or disproven the CIM. Ultimately, we will likely find that the truth is more complicated than expected, with important variations (based in part on biological differences) that determine an individual’s optimal diet for obesity treatment, chronic disease prevention and longevity.


Thanks for pointing these articles out Ken et. al
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  #9   ^
Old Fri, Jan-05-18, 11:25
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deirdra deirdra is offline
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Plan: HF/vLC/GF,CF,SF
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Quote:
Originally Posted by khrussva
Yep - that's the link that I meant to post. Thanks Deirdra & RawNut for catching the duplicate link above. I corrected it to what you provided.
Thanks, all three articles are great!
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  #10   ^
Old Fri, Jan-05-18, 11:46
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GRB5111 GRB5111 is offline
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Reading this information now. Excellent thread with good contributors. Thanks.
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  #11   ^
Old Sat, Jan-06-18, 10:09
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GRB5111 GRB5111 is offline
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Plan: Ketogenic (LCHFKD)
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Ludwig is correct in pointing out that the truth is far more complicated. Over the past few years when asked why I was eating the way I do, my response was that I was trying to better manage my insulin, and to improve my health.

Interesting how smart people who did not garner a lot of recognition when they were publishing findings in the past have contributed information that supports the findings in this Mendelian Randomization study: Dr. Joseph Kraft who correctly analyzed the OGTT and found flaws in how the tests were traditionally interpreted, and those who did early research in the 60s and 70s (Dr. Bruce Lipton and other pioneers) which led to the field of Epigenetics. Epigenetics correctly viewed how genes can be expressed (turned on) or not (turned off) by environmental influences which includes diet. The human genome does not mutate that rapidly, but gene tendencies and how they are expressed are largely influenced by environment at the cellular level.

Quote:
From CONCLUSIONS:
A recent Mendelian randomization analysis (26) cast doubt on the carbohydrate–insulin model, finding no evidence for a causal relationship between fasting insulin and body mass index (BMI)7. However, in the carbohydrate–insulin model, it is insulin secretion in response to carbohydrate, not fasting insulin, that influences weight gain, in part because the latter is strongly confounded by insulin resistance (5). Indeed, insulin resistance in adipose tissue protects against weight gain, as demonstrated by the fat-specific insulin receptor knockout mouse model (27). Therefore, we selected genetic variants identified by large genome-wide association studies associated with glucose-stimulated insulin secretion, not fasting insulin, to more appropriately test the carbohydrate–insulin model.

GENETICALLY DETERMINED BMI NOT ASSOCIATED WITH HIGHER INSULIN-30

Finally, we used bidirectional Mendelian randomization to further examine the directionality of the relationship between insulin-30 and BMI (Fig. 1B). Instead of using the combined insulin-30 associated variants as an instrument, we performed Mendelian randomization in the reverse direction, using 97 loci known to be associated with BMI in GIANT (33) as an instrument set (Fig. 2B). We tested this set for association with early insulin secretion in the MAGIC data. We found no evidence of a reverse causal effect for BMI on insulin-30 (β = 0.115, P = 0.43, heterogeneity P = 0.13).

While further studies are required, this information confirms a few thoughts about obesity and health related to diet:
1) The contention that there is no one diet that is healthy for all is true when accounting for one's genetic predisposition and many other factors that must be considered,
2) For people like me who likely have a higher insulin release in response to certain foods (carbohydrates), this enables us to continue to effectively manage our health by following a low carb approach. I know I'm a hyperinsulin responder to processed and unprocessed carbohydrates,
3) Until further studies are done to explore implications of diet in the context of genetics and MR, following an N=1 approach to better learn what works is the best approach to optimize one's WOE for health and longevity.

I'm comfortable with this and am eager to learn from further studies.
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  #12   ^
Old Sat, Jan-06-18, 11:31
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WereBear WereBear is online now
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I also qualify as a "hyperinsulin responder to processed and unprocessed carbohydrates" and suspect most of us here, as well.

It also explains our issues with cravings, the hunger from perpetual low blood sugar, and the disordered behaviors which result.

Since we hyper-respond via insulin, is it possible we also hyper-respond to the effect of sugar on our brains? Those people who eat one cookie and stop... are they just not getting the "jolt" hyper-responders do?
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  #13   ^
Old Sat, Jan-06-18, 12:35
teaser's Avatar
teaser teaser is offline
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Plan: ketosis/IF
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A big problem here is that there's the hyper response of insulin secretion, and then the hyper response to insulin. In the A to Z study, carbohydrate restriction seemed to be more effective for people who were insulin resistant. So is carbohydrate restriction not the way to go if you're insulin sensitive? I don't know if that's true, for somebody whose fat tissue is very insulin sensitive, the absolute level of insulin needed to promote fat loss might be considerably lower. So things get muddy, insulin has an undeniable effect in individuals, it's just that the required dose for a given effect has massive variability from individual to individual.

My own experience--I diet down to 155, 35 pounds lower than my top recorded weight. I've never had insulin resistance measured, but unless I do a serious carbohydrate binge, I've never caught myself with very high glucose numbers after a meal. Between this and much lower blood pressure than I had at 190 on a high carb diet, I'm probably more insulin sensitive--but foods that I wouldn't binge on at 190 pounds, that eating to appetite caused the opposite, spontaneous weight loss from that weight, became binge foods at the lower body weight. At that point, compliance to a more liberal Atkins approach became difficult--but pushing things further, more ketogenic, made compliance easier. In that A to Z study, higher compliance to Atkins among people who were insulin resistant was a major factor.
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  #14   ^
Old Mon, Jan-08-18, 19:32
khrussva's Avatar
khrussva khrussva is offline
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Plan: My own - < 30 net carbs
Stats: 440/207/210 Male 5' 11"
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Frankly, I don't know why the insulin topic is so controversial. There seems to be little argument that insulin is a fat storage hormone, yet some people really want to put it all on personal responsibility and self control.

There is a "success story" countdown on Dietdoctor.com. The post yesterday (HERE ) was about how tweaking the diet broke a stall and lead to weight loss. I found the comments more interesting than the story. Lots of folks posted about watching how much they eat - eating less - being a critical part of LCHF success. I don't disagree with that, at least for some people (me included). But one commenter posted this...

Quote:
Hans

January 16 2017 2

This (like the Kevin Hall study) is another example that shows its not about "insulin insulin insulin".

Keto or LCHF helps to eat less but in the end you also have to actually eat less.
I love this story because with keto I lost a lot of weight and got to normal weight, but when I'm not careful and eat e.g. out of stress and not out of hunger I just as easily regain weight, even with strict carb restriction

I agree with the last line in the comment. I can easily gain eating low carb as well. But why should this invalidate insulin as a significant factor. When I eat even a few too many carbs I am driven to eat more. I lose all control. I suspect insulin is the culprit. When I am careful about the carbs, then eating within reason becomes possible. It is not automatic. So to some extent, personal responsibility is in play. Now that I know how I have to eat to have a reasonable sense of control it is on me to make sure that it happens. Understanding what insulin does in my body and how I seem to have a hyper response to carbs arms me with the knowledge that I need to stay in control of my eating.

It may not be all about insulin, insulin, insulin for everybody. Some people get hyper when they eat sugar. Carbs make me want to take a nap. Perhaps some people get fat simply because they like their carbs too much and they make no attempt at moderation. I've been trying to moderate my whole life. It doesn't work when I'm eating too many carbs. Something else besides personal responsibility was always egging me on to keep eating. For me I think it was insulin.
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  #15   ^
Old Mon, Jan-08-18, 20:15
M Levac M Levac is offline
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Plan: VLC, mostly meat
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Quote:
Originally Posted by teaser
A big problem here is that there's the hyper response of insulin secretion, and then the hyper response to insulin. In the A to Z study, carbohydrate restriction seemed to be more effective for people who were insulin resistant. So is carbohydrate restriction not the way to go if you're insulin sensitive? I don't know if that's true, for somebody whose fat tissue is very insulin sensitive, the absolute level of insulin needed to promote fat loss might be considerably lower. So things get muddy, insulin has an undeniable effect in individuals, it's just that the required dose for a given effect has massive variability from individual to individual.

Insulin-degrading enzyme in the liver, that's the key. For same pancreas insulin output, variation in IDE will result in variation in blood insulin level. So let's find out why there's more or less IDE in the liver, fix it. First it's diet, right? But once we've done that, if there's still a problem, we can't blame any of it on diet anymore - it's fixed.

Even Feinman's work on keto and cancer shows there's something else going on besides how much carbs we eat. For same diet, some just didn't respond at all, while others responded fine. But here, it's even more clear there's something else - we're dealing with cancer.

In the A-TO-Z experiment, it's likely that's pretty much what's going on. Varying degrees of something elses. The more other things, the more potent other things, the greater the effect on compliance. It's the same diet, it's just a different internal millieu. Not DNA either, that argument is refuted, i.e. how could an entire population's DNA mutate within their lifetime? No, it's epigenetics - environment - but we just fixed the main culprit - diet - so there's obviously something else going on.

Another thing is stress, we all talk about stress this and stress that and how important it is to stay calm and whatever. Take a step back, think about this. If the principle whereby there could be something else besides diet that affects insulin is true, then isn't it also equally possible this same principle applies to other hormones as well - stress hormones and some other agent besides a "stressful situation"? Imagine this. We're stressed cuz some dummy broke something, our response is way over the top, we break out, get really nervous, can't concentrate, get depressed, indigestion, get weak, you name it, it's all happening. Now, it's just a broken cup. But even if it was a serious thing, look at the response, it's way disproportionate. No way this is normal. This ain't DNA either. There's obviously something else going on, something that keeps us primed and ready to jump at the tiniest event. Doesn't it sound pretty much exactly like our different individual response to carbs and insulin?
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