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  #1   ^
Old Thu, Aug-09-18, 02:17
Demi's Avatar
Demi Demi is offline
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Default Could a Keto diet increase the risk of diabetes?

Quote:
Sky News
London, UK
9 August, 2018

'Keto diets' could increase diabetes risk

So-called ketogenic diets could have unintended health effects by increasing the risk of Type 2 diabetes.


Ketogenic diets, which involve eating very low levels of carbohydrates and high levels of fat, could cause an increased risk of Type 2 diabetes according to new research.

A study published in the Journal of Physiology raises questions about whether ketogenic diets could be dangerous for those following them.

Type 2 diabetes is an increasingly common challenge in modern societies, and its cause is still not fully understood.

Ketogenic diets are named because they intend to put the body into a metabolic state where it is fuelled by metabolising fat rather than through glycolysis-the process of extracting energy from glucose.

A side-effect of ketogenic diets discovered by the researchers is that it hampers the process for controlling blood sugar levels, and creates insulin resistance.

When the liver is unable to respond to normal levels of insulin to control blood sugar, this could prompt an increased risk of Type 2 diabetes.

Researchers at ETH Zurich and the University Children's Hospital Zurich discovered the side-effects by feeding mice two different kinds of diet.

Christian Wolfrum, one of the corresponding authors on the paper said: "Diabetes is one of the biggest health issues we face.

"Although ketogenic diets are known to be healthy, our findings indicate that there may be an increased risk of insulin resistance with this type of diet that may lead to Type 2 diabetes.

"The next step is to try to identify the mechanism for this effect and to address whether this is a physiological adaptation.

"Our hypothesis is that when fatty acids are metabolised, their products might have important signalling roles to play in the brain."

Tim Spector, professor of genetic epidemiology at Kings College London, told Sky News: "This study is a reminder that any extreme restriction diet can cause unforeseen problems."

Professor Spector noted though that it was based on a study in mice: "Humans are omnivores and benefit from a wide variety of foods, and restricting any one group will usually cause us problems longterm.

"Many people are on carb restricted diets which limits our plant and fibre intakes, with bad effects on our gut health."

"Ketogenic diets are proving to be an amazing treatment for childhood epilepsy for reasons we don't fully understand, and is being tried in other brain disorders, and many people with Type 2 diabetes have come off their medications by cutting out most carbohydrates with the help of their doctor.

https://news.sky.com/story/keto-die...s-risk-11465771


Quote:
The Journal of Physiology
8 August, 2018

Short‐term feeding of a ketogenic diet induces more severe hepatic insulin resistance than a obesogenic high‐fat diet

https://doi.org/10.1113/JP275173

Key points

A ketogenic diet is known to lead to weight loss and is considered metabolically healthy; however there are conflicting reports on its effect on hepatic insulin sensitivity.

KD fed animals appear metabolically healthy in the fasted state after 3 days of dietary challenge, whereas obesogenic high‐fat diet (HFD) fed animals show elevated insulin levels.

A glucose challenge reveals that both KD and HFD fed animals are glucose intolerant.

Glucose intolerance correlates with increased lipid oxidation and lower respiratory exchange ratio (RER); however, all animals respond to glucose injection with an increase in RER.

Hyperinsulinaemic–euglycaemic clamps with double tracer show that the effect of KD is a result of hepatic insulin resistance and increased glucose output but not impaired glucose clearance or tissue glucose uptake in other tissues.

Abstract
Despite being a relevant healthcare issue and heavily investigated, the aetiology of type 2 diabetes (T2D) is still incompletely understood. It is well established that increased endogenous glucose production (EGP) leads to a progressive increase in glucose levels, causing insulin resistance and eventual loss of glucose homeostasis. The consumption of high carbohydrate, high‐fat, western style diet (HFD) is linked to the development of T2D and obesity, whereas the consumption of a low carbohydrate, high‐fat, ketogenic diet (KD) is considered healthy. However, several days of carbohydrate restriction are known to cause selective hepatic insulin resistance. In the present study, we compare the effects of short‐term HFD and KD feeding on glucose homeostasis in mice. We show that, even though KD fed animals appear to be healthy in the fasted state, they exhibit decreased glucose tolerance to a greater extent than HFD fed animals. Furthermore, we show that this effect originates from blunted suppression of hepatic glucose production by insulin, rather than impaired glucose clearance and tissue glucose uptake. These data suggest that the early effects of HFD consumption on EGP may be part of a normal physiological response to increased lipid intake and oxidation, and that systemic insulin resistance results from the addition of dietary glucose to EGP‐derived glucose.

https://physoc.onlinelibrary.wiley....0.1113/JP275173

Last edited by Demi : Thu, Aug-09-18 at 02:27.
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  #2   ^
Old Thu, Aug-09-18, 05:47
teaser's Avatar
teaser teaser is offline
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Default

This "discovery" was first made early in the 20th century. This is basically "starvation" diabetes, but in this case caused by a diet that mimics the fuels sourced from the body during starvation. They may have refined the idea by narrowing down some particulars of what causes the effect.

A low carbohydrate, ketogenic diet seems to be taking its sweet old time making people diabetic, at least on this forum. And everywhere else I'm aware of. In some cases, ten steps backward for every step forward towards diabetes. Here we have a mechanism to explain the rampant increase in diabetes in people eating ketogenic diets that hasn't been observed.
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  #3   ^
Old Thu, Aug-09-18, 06:40
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Ms Arielle Ms Arielle is offline
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Default

WHy could I only read half this article?
What was the movtive behind this article--- to trash ketogenic diets??? Rather than, here is a method that if done right promotes good health.

Is SAD ever examined in this method?
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  #4   ^
Old Thu, Aug-09-18, 07:38
LizardQuee LizardQuee is offline
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Default

Isn't what they are describing "physiological insulin resistance", a normal glucose-sparing phenomenon when carbs are very low?
The same reason why you need to eat more carbs for a bit before a glucose tolerance test, so you dont end up with a false positive?

In my recollection phys insulin resistance is reversible on reingestion of more carbs, unlike true T2.
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  #5   ^
Old Thu, Aug-09-18, 09:23
BillyHW's Avatar
BillyHW BillyHW is offline
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Plan: Keto + IF
Stats: 260/300/165 Male 5' 6"
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Default

Quote:
Originally Posted by LizardQuee
Isn't what they are describing "physiological insulin resistance", a normal glucose-sparing phenomenon when carbs are very low?
The same reason why you need to eat more carbs for a bit before a glucose tolerance test, so you dont end up with a false positive?

In my recollection phys insulin resistance is reversible on reingestion of more carbs, unlike true T2.


So what is the mechanism behind physiological insulin resistance?
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  #6   ^
Old Thu, Aug-09-18, 10:47
teaser's Avatar
teaser teaser is offline
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Posts: 12,838
 
Plan: mostly milkfat
Stats: 190/152.4/154 Male 67inches
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Default

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3312873/
Mechanisms underlying skeletal muscle insulin resistance induced by fatty acids: importance of the mitochondrial function


http://high-fat-nutrition.blogspot....resistance.html

http://high-fat-nutrition.blogspot....al-insulin.html

I find things work differently for me on a more ketogenic diet vs. higher protein. I used to get my highest blood sugar reading of a day, back when I tested it, after doing deadlifts, rather than after a meal (assuming the meal was low carb). On more ketogenic ratios, instead of deadlifts raising my blood glucose by 40 points or so, it was more like 10 or 15. Maybe with the lower glycogen levels, there was less of a glucose response to stress.

It's... involved. Peter at Hyperlipid points out that pathways involved for oxidation of polyunsaturated fat result in higher insulin sensitivity than pathways involved for palmitic acid, the major saturated fat in dairy. The switch from glucose to fat metabolism that we hope for and call "fat adaptation" has tremendous overlap with physiological insulin resistance/glucose "intolerance." It's a glucose-sparing state, keeping glucose rare increases its value, it must be spared for those processes to which it is more essential. This can involve all sorts of things, decreases in glucose kinase to trap glucose in a cell, without this, cells can't use glucose for energy. A decrease in activity or expression of the pyruvate dehydrogenase complex--needed for mitochondria to be fueled through glucose metabolites also decreases glucose metabolism. A reduction in pyruvate feeding in to the citric acid cycle decreases production of malonyl-CoA, malonyl-CoA is a metabolite of the citric acid cycle that depresses fatty acid oxidation and is a signal for increase in fatty acid and triglyceride synthesis.

The mainstream sometimes blames palmitic acid for inducing insulin resistance, Peter praises it, I think there are probably contexts where one or the other is appropriate, I'm hoping the context I'm eating it in is the latter.
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  #7   ^
Old Fri, Aug-10-18, 05:01
teaser's Avatar
teaser teaser is offline
Senior Member
Posts: 12,838
 
Plan: mostly milkfat
Stats: 190/152.4/154 Male 67inches
BF:
Progress: 104%
Location: Ontario
Default

One more thing, after some prodding on facebook, I looked up the diet used.

https://www.envigo.com/resources/data-sheets/96355.pdf

This is the hydrogenated, Crisco version of keto. So even though there are ways in which a well formulated keto diet can increase insulin resistance, this isn't a good test of that.
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  #8   ^
Old Fri, Aug-10-18, 06:24
GRB5111's Avatar
GRB5111 GRB5111 is online now
Posts: 2,315
 
Plan: Ketogenic (LCHFKD)
Stats: 227/186/185 Male 6' 0"
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Location: Herndon, VA
Default

I can go only with my own experience. Having followed a well-formulated ketogenic WOE over the past 4-5 years, my NMR Lipid tests (multiple times) give me an IR (insulin resistance) score that is off the low end of being measurable. I'll take that as my key indicator rather than any poorly designed mouse study. And further, my WOE is hardly an "extreme restriction diet." Now, onto the real news . . .
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  #9   ^
Old Fri, Aug-10-18, 11:18
M Levac M Levac is offline
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Plan: VLC, mostly meat
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Default

The paradigm of insulin resistance exists within the context of eating according to the official dietary guidelines, i.e. eat lots of carbs. A ketogenic diet does not include lots of carbs. Any particulars about that paradigm no longer makes any sense. We couldn't possibly imagine the pertinence of a glucose tolerance test, when we don't eat glucose in the first place.

Since the diet is ketogenic, we should instead find out what that diet does with something like an oral fat tolerance test. I mean, isn't that the purpose of an OGTT with regards to the official dietary guidelines, i.e. how well we tolerate eating that diet?

I have a brilliant analogy here. Let's say I drive a road car, it's designed specifically to be driven on paved roads, that's its intended purpose. Now I want to test it to see how good it is for that purpose. I bring it on the mountain and drive it off-road where there's no paved road or anything like that. I measure stuff, I time stuff, I observe stuff, I write it all down in a result sheet, draw conclusions, then in a brilliant stroke of genuise, I determine the car is poorly designed to be driven on paved roads.

I could spew insults at these experts right now.
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  #10   ^
Old Sun, Aug-12-18, 02:14
BillyHW's Avatar
BillyHW BillyHW is offline
Registered Member
Posts: 378
 
Plan: Keto + IF
Stats: 260/300/165 Male 5' 6"
BF:
Progress: -42%
Location: Alberta, Canada
Default

Quote:
Originally Posted by teaser
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3312873/
Mechanisms underlying skeletal muscle insulin resistance induced by fatty acids: importance of the mitochondrial function


http://high-fat-nutrition.blogspot....resistance.html

http://high-fat-nutrition.blogspot....al-insulin.html

I find things work differently for me on a more ketogenic diet vs. higher protein. I used to get my highest blood sugar reading of a day, back when I tested it, after doing deadlifts, rather than after a meal (assuming the meal was low carb). On more ketogenic ratios, instead of deadlifts raising my blood glucose by 40 points or so, it was more like 10 or 15. Maybe with the lower glycogen levels, there was less of a glucose response to stress.

It's... involved. Peter at Hyperlipid points out that pathways involved for oxidation of polyunsaturated fat result in higher insulin sensitivity than pathways involved for palmitic acid, the major saturated fat in dairy. The switch from glucose to fat metabolism that we hope for and call "fat adaptation" has tremendous overlap with physiological insulin resistance/glucose "intolerance." It's a glucose-sparing state, keeping glucose rare increases its value, it must be spared for those processes to which it is more essential. This can involve all sorts of things, decreases in glucose kinase to trap glucose in a cell, without this, cells can't use glucose for energy. A decrease in activity or expression of the pyruvate dehydrogenase complex--needed for mitochondria to be fueled through glucose metabolites also decreases glucose metabolism. A reduction in pyruvate feeding in to the citric acid cycle decreases production of malonyl-CoA, malonyl-CoA is a metabolite of the citric acid cycle that depresses fatty acid oxidation and is a signal for increase in fatty acid and triglyceride synthesis.

The mainstream sometimes blames palmitic acid for inducing insulin resistance, Peter praises it, I think there are probably contexts where one or the other is appropriate, I'm hoping the context I'm eating it in is the latter.


Thanks. I just posted a video by Dr. Eades that talks about localized physiological insulin resistance here:

http://forum.lowcarber.org/showthre...685#post9292685

He also quotes that blogger Peter!
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