Does low carbing improve insulin sensitivity?

bulkbiker

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The BMJ here
Conclusions
Low carbohydrate-high protein diets, used on a regular basis and without consideration of the nature of carbohydrates or the source of proteins, are associated with increased risk of cardiovascular disease.
http://www.bmj.com/content/344/bmj.e4026
Well being neither Swedish nor female I'm not sure I see the link.. both studies show "associations" and nothing stronger.. as I said choose your own path.. There are plenty of Vegetarians and Vegans following a LCHF way of eating who are members here. So I'm not sure exactly what you are claiming is deception?
You say elsewhere that neither you nor anyone in your family has diabetes I recall so what is your agenda?
 
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Oldvatr

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The BMJ here
Conclusions
Low carbohydrate-high protein diets, used on a regular basis and without consideration of the nature of carbohydrates or the source of proteins, are associated with increased risk of cardiovascular disease.
http://www.bmj.com/content/344/bmj.e4026
This study only monitors young women (only). The main rejection criterion on enrolement is that there has been no pre existing CVE, bit no ither screening on pre-existing conditions ws ma

SORRY : this got incorrectly posted here, and has been superceded by my following post.
 
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Oldvatr

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The BMJ here
Conclusions
Low carbohydrate-high protein diets, used on a regular basis and without consideration of the nature of carbohydrates or the source of proteins, are associated with increased risk of cardiovascular disease.
http://www.bmj.com/content/344/bmj.e4026
This study was conducted on women only, who were young and had no previous CVE. There seems to be no other screening of pre existing conditions, such as diabetes.

The study makes the observation that the reason why women only were studied included the gem that 'women are more likely to use a low carb diet'. The study lasted 15.7 years, and i find that assuming that the diet applies over the full period by all participants to be a weak argument.

There seems to be no note taken of fat intake, or whether the fats were sat , unsat, or transfats

In the years of the study, it was most likely that the type of diets being followed would have been commercial meal replacemenrt type using whey or soya proteins as bulker. The adverse effects of both of these is now known to be harmful in prolonged use. This may also be at play in skewing the results.

It is acknowledged in the report that a similar cohort study in USA did not show any such correlaton as being declared in this report, I assume they mean the Harvard Nurses Study, but they do not identify it.

All in all I have low confidence in this study which is an observational type study that makes too many assumptions. The monitored population is NOT representative of the general populace, and does not seem to have any control of the test environment. It also uses the statistical trick of ranking, i.e. applying fiddle factors to boost or suppress portions of the data. Although these fiddle factors are declared in the report, without the raw data being available then these are meaningless, but look impressive to non staticians.
 

slinkimalinki

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My agenda is the truth and the health of people. Why do Diabetes UK want every one to remain diabetic what is their agenda
You do realise that this site is NOT Diabetes UK?

Nothing I have read here leads me to believe that this site wants people to remain diabetic. I think you have things a tad confused.
 

AngelaLynch

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I just had a notification of your comment from a Diabetes UK email and I was led here originally, from a link, by Diabetes UK and even if this forum has nothing to do with Diabetes UK, Diabetes UK is in a large way responsible for the conversation about diabetes.
 

bulkbiker

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My agenda is the truth and the health of people. Why do Diabetes UK want every one to remain diabetic what is their agenda
You're not diabetic (according to what you have written elsewhere).. why do you come here and tell people who have put their diabetes in remission (well controlled.. reversed.. choose the words) that they are doing it all wrong by not doing it your way?
dabetes.co.uk and diabetes.org.uk are two different entities.. I would say that diabetes.org.uk are the one's causing the problem not diabetes.co.uk.
 
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Oldvatr

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You're not diabetic (according to what you have written elsewhere).. why do you come here and tell people who have put their diabetes in remission (well controlled.. reversed.. choose the words) that they are doing it all wrong by not doing it your way?
dabetes.co.uk and diabetes.org.uk are two different entities.. I would say that diabetes.org.uk are the one's causing the problem not diabetes.co.uk.
Sorry BB I would not fully agree with your last sentance about DUK, We would all like to see the Diabetes dragon slain, and whilst I do disagree with much of the advice that DUK supports, I believe we see different paths to get there.

Angela is saying that she sees another path that also differs from both DUK and DCUK, which is that a High Carb High Starch diet is the Holy Grail we seek, and that all of us are misguided in thinking a LC diet is a possible route for us. I also disagree with that surmise, and have to say that I have yet to see evidence that has validity to support that HCHS POV.

Angela has also posted elsewhere on this forum that Milk and Milk products are poisonous for diabetics and that we should avoid them. I also disagree with this POV. I think that the Good Doctors that support WFPB diets are naive and overzealous in banging their drum. I used to work with a colleague who followed their type of diet, and he was the most unfit and unhealthy individual in the factory, He took way too many sickies, and looked to be in terrible shape. He tried to convert me to his diet, but he was not a fine upstanding example, so had no credibility, He retired at the age of approx 28 due to ill health grounds.

It is interesting that there are some journalists who have attended and even been invited to speak at the WFPB annual jamborees, and the surprising comment that they have in common is 'how ill everybody looks'
I add a final link to one such blog but there are many others:
http://www.marksdailyapple.com/vegan-island/
 
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CherryAA

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I just had a notification of your comment from a Diabetes UK email and I was led here originally, from a link, by Diabetes UK and even if this forum has nothing to do with Diabetes UK, Diabetes UK is in a large way responsible for the conversation about diabetes.


what very strange post

so someone who is not diabetic, is coming along to shout at an organisation that is not this one - Maybe brain fog applies to more than just diabetics!
Is this some kind of bot ?
 
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ickihun

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I need insulin to cover my protein too so low carbing isn't a insulin resistant solution just an aid.
I'm hugely insulin resistant due to not being able to walk well and I'm 20st. The insulin changes my fat into better fat cells but still creates them or sustains the level of fat in them. Fat cells make insulin work harder to unlock glucose conversion. Good ones and bad ones.
Bad or the wrong kind of fat cell stops type2 diabetes going into remission. I feel.
The unlocking of cells is what resistance is.
I'm resistant to most medications, a tiny bit. I fall short in pain relief and durietics etc.. they should work better. I blame the fatty liver for that. But when I did strictly 30g carb higher protein and no restriction on fats I had far less enzymes from my liver, effectively no more fatty liver I still had huge insulin resistance. No difference for me. Just less carbs to cover with insulin.
Exercise and weight loss is how you improve insulin resistance. I have to become an athlete to reduce my insulin resitance. I'm no way able to do that right now nor sustain it til I die.
 
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ickihun

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The BMJ here
Conclusions
Low carbohydrate-high protein diets, used on a regular basis and without consideration of the nature of carbohydrates or the source of proteins, are associated with increased risk of cardiovascular disease.
http://www.bmj.com/content/344/bmj.e4026
I believe I've read that too.
I only started with palpations on low carb high protein foods. I wasn't following lchf like some posters. It effectively increased my protein intake due to replacing carbs with protein.
I believe carbs increase your risk of harding of the arteries too soooooo eat nothing and you'll die of starvation rather than cvd.
 
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Oldvatr

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what very strange post

so someone who is not diabetic, is coming along to shout at an organisation that is not this one - Maybe brain fog applies to more than just diabetics!
Is this some kind of bot ?
This is an open forum for discussion. The poster has a point of view that may not be in line with our own, but nonetheless should be considered on its merits.

It is incumbent on us to challenge these ideas, question the scientific backing being claimed, and provide commentary as to whether the claims are valid or not. I did that with LCHF diet before I comitted to it, and I still try to be vigilant to new discoveries.

In this instance I have not found any supporting evidence that I consider to be compelling, but I see a lot of pseudoscience and naturist blog chatter that does not fill me with hope for a cure by this route. I do see things being put forward that would actually present me with personal injury and would be unhealthy for me to even consider,

This poster is not the first to offer a cure through this methodology, and will probably not be the last.
 

ickihun

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One more thought about reducing insulin resistance and resistive training exercise from Wikipedia:
"Muscle fibers grow when exercised and shrink when not in use. This is due to the fact that exercise stimulates the increase in myofibrils which increase the overall size of muscle cells. Well exercised muscles can not only add more size but can also develop more mitochondria, myoglobin, glycogen and a higher density of capillaries. However muscle cells cannot divide to produce new cells, and as a result we have fewer muscle cells as an adult than a newborn."
Within each muscle cell all these great things happen:
More mitochondria are created to convert more glucose to ATP at about 1:19 ratio. This requires oxygen in the cell to convert glucose to ATP.
Myoglobin is like hemoglobin only it stores oxygen in the muscle cell instead of transporting it in the bloodstream.
Glycogen is a HUGE molecule that stores more than 30,000 glucose molecules within the cell. Exercise promotes more of these. The more glycogen molecules within each cell the faster high levels of BG are cleared from the blood stream.
Capillaries feed cells oxygen and remove CO2, a process / by product to convert glucose to ATP.
It all goes back to the basic idea that the most effective way to reduce insulin resistance is through anaerobic exercise. Go through all the muscle groups spaced at 2 - 3 days, tearing down and then building up.
Ugggh! Why isn't there a pill I can take instead????:arghh::bigtears::arghh::(:hungover:
Exercise is the best form of insulin resistant breakdown I've found. Why it is sooooo frustrating when im in agony walking, let alone exercising very regularly like i did before diagnosis.
One of my heart meds causes tiredness/lethergic mood, alongside underactive thyroid problems and the painkillers do too. :(
Some work does need doing on IR. For all our sakes!
If my only problem was diabetes i'd be laughing!!!
 

slinkimalinki

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You're not diabetic (according to what you have written elsewhere).. why do you come here and tell people who have put their diabetes in remission (well controlled.. reversed.. choose the words) that they are doing it all wrong by not doing it your way?
dabetes.co.uk and diabetes.org.uk are two different entities.. I would say that diabetes.org.uk are the one's causing the problem not diabetes.co.uk.
Thanks, that is what I was trying to get her to understand, they are two different beasts.
 

Oldvatr

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Good News or Bad News??? It now looks like exercise may not reduce IR. It may actually reduce the appearance of IR by stimulating glucose transporters GLUT4 as muscle is stressed or stretched. This allows more glucose to enter the cell. In a muscle resting state, insulin typically stimulates the same GLUT4 transporters.
It may be that an LC diet causes the muscle cell to become more dependent on fatty acids for energy versus glucose. It's not much of a leap to suggest an LCHF diet increases IR or at least won't bring it down.
It may be that an intense workout should be combined with carbs and protein.
Wish I had a way to measure IR as easily as BG, then it might be easier to play with some of this stuff.
Comments welcome.
I am not sure what it is about the logic you are using in your thread, but something is setting off my alarm bells. I think it is this assertion <<< It's not much of a leap to suggest an LCHF diet increases IR or at least won't bring it down.It may be that an intense workout should be combined with carbs and protein.>>> that i find I disagree with, but not sure why.

If we go back to basic principles, then I find that defining Insulin as the storage hormone is acceptable. So IR means that the body does not store glucogen or lipids as efficiently as it should. One of the diagnostic pointers to diabetes is high levels of glucose in the blood, with unexplained weight loss. So for a T2D then for example, having high bgl that does not start to reduce by the 2hr PP after a meal would show that either insulin is not being produced or there is resistance.

So if a diet regime leads to improved response times to mealtime bgl levels, then this might indicate lessening of the IR, in terms of carb glucose storage in the muscles. The other form of IR is mainly felt by T1D, and seems to be triggered by eating high levels of fat (pizza effect). Again this IR seems to delay the response to insulin being administered thus prolonging the PP peak. Either way it might be possible to devise a diagnostic method to measure this increase or decrease in PP response to give an indication of IR being made worse or better. However, RH colleagues will have to wait for a different method than this.

It would need a stable medication regime, and probably involve a period of fasting followed by a standardised meal that can be repeated. In fact it is sounding like the GTT test used in diagnosis.

We cannot use meds reduction as an indicator of reducing IR since changes in carb intake will prompt this reaction anyway, without necessarily being linked to changes in IR. Similarly weight gain / loss, although linked to IR, has too many variables to control in order to isolate the insulin response. Like wise the actual meter reading of bgl is a poor method due to too many variables. So unless we can find a way of home testing for insulin levels in the blood then we are stuck. Maybe CGM technology will help here/

Remember that IR in T2D is mainly acting as a bouncer on the gateway to the muscle cells. Exercise needs insulin to be absent in order to effectively deal with bgl levels. So when there is high IR then the excess insulin hangs around for a while until excreted, and this will make exercise after a meal or snack less effective. Some meds like Gliclazide boost levels of insulin in the blood and in this case act as a sledgehammer to force feed the fat cells with the excess bgl, and also opens up the lipid storage pathway to the adipose fatcells hence bypassing the muscle storage that is locked out by IR.

It was generally accepted that T1D did not suffer IR, which has been regarded mainly as a T2D problem, but recent studies have discovered the Pizza Effect which can affect T1D, but it is not so common.
https://www.ncbi.nlm.nih.gov/pubmed/12112937
https://www.ncbi.nlm.nih.gov/pubmed/8462382

There is another thread on this site that is related to this topic.
http://www.diabetes.co.uk/forum/threads/why-isnt-hyperinsulinemia-talked-about-more.120514/
 
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Oldvatr

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Hello @Oldvatr,
Thank you for a great response. Can you help me understand the above quote? From what I've been reading the process of letting glucose into cells due to exercise is independent of the insulin pathway but I don't have anything specific to base it on. I would greatly appreciate it if you can point me to something.
Again, I like your response and would like to discuss it more, there's so much there to talk about.
Thanks...
The process for muscles is governed by what is termed the Krebs cycle or Citric cycle. In each muscle cell there is the equivalent of a multiway switch, controlled by hormones. Insulin is one and this controls the cells storage path. If insulin is present, glucose can move from the bloodstram into the local fat cell in the muscle for future use. If insulin is absent then that stops. If adrenalin is present then the cell burns energy /initially from the local store, but then direct from the bloodstream. There are other switches that control passage of stored glucose back into the blood. And others control burning lipids for energy if there is a lack of glucose (these can kick in when the body thinks it is facing starvation so the muscle cells can burn glucose, glucogen, lipids, and even ketones, bit like a multifuel burner.

Of all these modes, exercise burns most when aerobic exercise is happening, and deriving energy from lipids and ketones is more efficient than glucose burning. Glucose storage provides the cell with immediate access to energy to help with fight or flight situations, but it soon gets used up. When this happens we get puffed out. Then the second wind kicks in and lipid burning starts. So sprinting uses up carb sourced glucose, and long distance running uses lipid fat from the fat cells. Touching your toes does precious little.

Insulin also opens up the storage cells around the liver where the lipid fat gets stored. These stores only start providing energy when the body is stressed either by exercise, extreme temperature, or impending starvation, so it is difficult to burn off this fat by dieting with reduced calorie intake, but a ketogenic diet such as LCHF mimics starvation so leads to fat burning as well as burning up the carb stores. You must have insulin to move carb dourced glicise to or from the blood. You must jave insulin to make the fat cells store lupuds, but only to store, using lipid fat requires low bgl as well as NO Insulin in the blood. Then ketosis can occur. Increase carb intake and ketosis stops, and the gut starts increasing again.
 

Oldvatr

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Hello Again @Oldvatr,
I'm still looking into my original question trying to find a reference to cell utilization of glucose with and without the presence of insulin. I agree with you that glucose uptake and utilization are two different things. Haven't found anything about insulin actually being physically present inside the cell to instruct enzymes to catalyze glucose or attach to an existing glycogen molecule. If I'm understanding you correctly (given that the body burns only ATP not glucose) the presence of insulin prohibits the conversion of glucose into ATP?
Sorry it's hard to process everything your saying at one time so I'll need to digest it a little bit at a time.

Great image of glycogen molecule inside muscle cell; can store about 30,000 glucose molecules in an amazing little sphere. Building muscle size through exercise increases the number of these in each muscle cell. Thanks to Häggström, Mikael (2014). "Medical gallery of Mikael Häggström 2014".

View attachment 22895
I look on insulin as being like the bouncer on the nightclub door. At the cell level most communication is by molecular keys and electrical charge, which is unique to each of us. I do not think insulin actually enters a muscle cell it is just the key specifically for glucose. Yes, I also reckon that the presence of insulin inhibits the conversion to ATP for glucose, but does not impair the lipid conversion to ATP which is how we still function on a keto diet. I think insulin only works to control admission to the cell, but glucose in stored glucogen as depicted in that lovely pic is still converted to ATP as required

Edit to add the scientific bit
https://www.ncbi.nlm.nih.gov/pubmed/21864752
 
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