Lchf induced insulin resistance

Spiker

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I'm not so sure Spiker, there's been a couple of members on this forum who have experienced it first hand.
I know there are first hand experiences out there and I don't dispute those. But calling these experiences "insulin resistance" is going out on a limb without supporting evidence. Eg @smidge posted an alternative explanation (above) for the same experiences.

Historically "insulin resistance" has been a scientific-sounding term for a group of phenomena (that might have totally different causes), that we don't understand at all at a biochemistry level. Only recently has Prof Taylor's work shed some light on the mechanism of one type of "insulin resistance", and of course he is not mainstream.

"insulin resistance" doesn't describe any set of observable symptoms. Instead it's just an unjustified hypothesis about what might or might not be causing those symptoms. If we described those experiences as "carb intolerance" that would be more accurate, since we know that more carbs are going in and that's causing a problem. We don't really know what role insulin has in those experiences, let alone a hypothetical "insulin resistance".
 
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Applenerd81

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I know there are first hand experiences out there and I don't dispute those. But calling these experiences "insulin resistance" is going out on a limb without supporting evidence. Eg @smidge posted an alternative explanation (above) for the same experiences.

Historically "insulin resistance" has been a scientific-sounding term for a group of phenomena (that might have totally different causes), that we don't understand at all at a biochemistry level. Only recently has Prof Taylor's work shed some light on the mechanism of one type of "insulin resistance", and of course he is not mainstream.

"insulin resistance" doesn't describe any set of observable symptoms. Instead it's just an unjustified hypothesis about what might or might not be causing those symptoms. If we described those experiences as "carb intolerance" that would be more accurate, since we know that more carbs are going in and that's causing a problem. We don't really know what role insulin has in those experiences, let alone a hypothetical "insulin resistance".

Insulin resistance is in effect what happens when regular insulin dose/release does not have the expected impact/effect on blood glucose - it's no more complex then that and the reason why type 2s on insulin often need large doses.

When I first discussed going on LCHF with my dietician, she wasn't convinced going low carb high fat was a good idea and did warn me that I could become insulin resistant... Obviously I didn't believe this until experiencing it myself, fingers crossed it's just temporary and a matter of adapting to carb/insulin metabolism.
 

Applenerd81

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Lucy according to google the definition of insulin resistance is very clear. All the other effects you mention are side effects/symptoms of insulin resistance (and associated hyperinsulinaemia) as per that shown in type 2.

It is becoming more and more widely acknowledged that obesity and the other symptoms you've mention (demonstrated in long term poor controlled type 2s) are caused by insulin resistance, not the other way round.

What I am describing as a type 1 is (temporary) resistance to the effects of exogenous insulin which the only word I have is "insulin resistance", the only cause of which in my case appears to be LCHF (high sat fat to be accurate) induced.

I need a lot more insulin to lower my blood glucose than before - what else is this called? I can comfortably digest glucose, my rising blood sugar clearly shows this.

I am happy to be corrected :)
 
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LucySW

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You're quite right that the consensus is growing that IR is the cause of obesity rather than the other way round, but some Google sources are much better than others. Read Peter Attia on IR.

IR isn't exclusive to Type 2s, btw. Many Type 1s suffer from it too, tho it didn't cause their disorder. That's why keeping weight down helps lower TDD.
 

JTL

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When I first went LCHF I went cold turkey .... none whatsoever of the spuds bread type culprits .... as near zero carbs as I could get but with lots of fish green tea no milk no nothing that was on the obvious list in my mind for about three months.
Then started having a little rice or spuds bread pasta biscuits every day.
Very small portions.
I'm still on small portions but a bit larger now.
I will never go back to what most people would consider normal.
My carb intake today will be decided on meter readings.
4.9 was it this morning so yes ... I could have a bowl of porridge ... with a heaped tablespoon of coconut oil in it .... made from water no milk.
I'll test before main meal this evening and if readings are 5.5 ish or below I'll consider a spud going on the plate .... small helping of pasta or rice.
I can't have pizza no matter what I do unless I have cauli based and that's too much messing about.
But Pizza white bread that kind of stuff and the starting point on my meter is meaningless cos I know I'll rocket into double figures.
 
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Spiker

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Great article. It sounds like we should be ensuring we take lots of marine based omega 3 when doing HFLC.
 

Ali H

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Jackthelad have you seen the fat head pizza recipe online? Dead easy to do.

Ali
 
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Applenerd81

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I like your approach Jack, will adopt when I reach my target weight, 75kg, 7 down, 7 difficult more to go!
 
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JTL

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Jackthelad have you seen the fat head pizza recipe online? Dead easy to do.

Ali
Don't think I have .... link?
 

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The term insulin resistance was first coined by Harold Himsworth when he differentiated between T1 and T2 .http://ije.oxfordjournals.org/content/42/6/1599.full He used it to refer to the amount of insulin required to reduce glucose levels. We now think of it as a continuous variable ie more insulin sensitive more insulin resistant.
, I would say that @LucySW is defining the metabolic syndrome or as Gerald Reaven who first defined it called it 'syndrome X'
http://www.cacpr.ca/information_for_public/archived_issues/2000s/0009Reaven.pdf

Here's my attempt at an explanation as to what I think insulin resistance is.
The cell requires glucose for energy but glucose cannot pass through the cell membrane without a gateway being opened for it. Most skeletal and muscle cells contain receptors which, when stimulated , activate this gateway .These receptors are stimulated by insulin. Insulin resistance occurs when these receptors show a reduced response to insulin requiring more insulin to enable glucose to enter the cell. (exercise can also stimulate the opening of the gate which is why it increases insulin sensitivity by decreasing the amount of insulin required .
Here's one article http://www.todaysdietitian.com/newarchives/070113p42.shtml
If you want to know more about the biochemistry the book quoted from by Wood is a useful read (it's a good basic text, I managed to get a 2nd hand copy) I don't think that the author would totally agree with the article's conclusion about diet and insulin sensitivity (here he also adds exercise )
" Sumo wrestlers are certainly obese, yet as long as they exercise they remain insulin sensitive. Surprisingly, in addition to exercise, eating a diet relatively high in unsaturated fatty acids but low in total calories may actually help lower blood levels of fatty acids...... Yes, a relatively” high-fat diet of “healthy” fats, but low in total calories, may be more healthful than a low-fat high-carbohydrate diet consisting of starch and sugar."

The Dietitian article also mentions genetic variation which is probably extremely important in the way some people are more susceptible to insulin resistance than others and that this may mean people vary in their responses to diet.
.
Certainly there are people (including me) that have found that they require more insulin to cover meals that are proportionately higher in fat and protein. Some have reported finding that metformin helps.
Researchers at Joslin have also suggested that increased insulin resistance is the mechanism behind the Pizza effect ie a later rise is not simply the delayed absorption of the carbohydrate as is often suggested
http://www.joslin.org/dietary-fat-can-affect-insulin-requirements-in-type-1-diabetes.html
http://www.ncbi.nlm.nih.gov/pubmed/23193216
 
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smidge

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I think there is a tendency in all things we don't understand to explain them in as simple a term as we can - but we fall into the trap of equating correlation with cause.

I have no doubt my injected insulin:carb ratio rises when on a low-carb diet - so by that measure I have a correlation between LCHF and requiring more insulin per gram of carb - but that doesn't mean LCHF has caused me to become more insullin resistant, more carb sensitive or anything else (that might be the case, but I have no evidence) - there are other things going on - like conversion of protein, lower basal dose and the fact that carb:insulin ratio is simply an inappropriate measure of my insulin needs when low-carbing - so what I have is an unexplained phenomenum showing a correlation between two things - I do not have a cause.

Regardless of my diet, regular exercise correlates to lower background insulin requirements - it does not seem to impact my spikes or bolus requirement - so, again, I have a correlation between exercise and lower basal requirements - I do not have evidence that this causes me to be more insulin-sensitive.

Smidge
 
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Applenerd81

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But Peter Attia explains it better.

Lucy, I am not aware of Peter, but having googled him, his definition of insulin resistance is the same:

"Insulin resistance – As the term implies, insulin resistance (IR), involves the tissues of the body (especially muscle cells and fat cells) becoming resistant to the effect of insulin, thereby requiring greater and greater amounts of insulin to achieve the same outcome" taken from eatingacademy.com glossary
 

donnellysdogs

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My basals went up to 18 a day when increasing saturated fat. Now that saturated fat is minimal but the poly/moly/etc from avocados, olives etc has been increased instead my basals have dropped to 15 and still reducing.
Another reason for the basal drop though is warmer weather again. Within 3 weeks I'll be back down to 13 daily units.
My bokus ratio's have dropped to give less insulin too. I was up to 1.3 per 8g in evenings and this is back to 1 to 10g.

Whether its all dairy fat or warmer weather I don't know but my carb content daily remains at 50g pretty much everyday. Certainly not over.

However I do not believe its all because of the extra dairy. For me personally I know I have far less insulin in summer for both bolus and basal.

I think with type 1's sometimes people don't actually watch to see how much their basal/bolus may be swinging outside of the ratio's that suit them. Ie 50/50 or 60/40 say. I know of a few type 1's that don't monitor how their basal/bolus ratio

Open minded on this but am never worried about the qty of insulin I take.

To me the formula they use to calculate insulin needs being based upon the weight of the person would be more interesting.
 
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Spiker

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@phoenix as ever thanks for the great links. The definition of insulin resistance at the cellular level is how I understand it too. But my reservation is in labelling any change in insulin:carb requirements ratio as being causally this type of cellular level insulin resistance. We don't know, and as @smidge points out, there are lots of confounding factors.

I do accept that the higher fat or proportionally higher fat in LCHF causes an increase in insulin:carb requirements. I just don't like calling it insulin resistance because for me (and maybe it's just me) that's making a causal claim that it's a cellular level uptake sensitivity change. When actually it could be many other possible mechanisms, and we don't know. But maybe my personal definition of "insulin resistance" is just too narrow.
 
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noblehead

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What I am describing as a type 1 is (temporary) resistance to the effects of exogenous insulin which the only word I have is "insulin resistance", the only cause of which in my case appears to be LCHF (high sat fat to be accurate) induced.

I need a lot more insulin to lower my blood glucose than before - what else is this called? I can comfortably digest glucose, my rising blood sugar clearly shows this.

I remember a couple of years ago there was a type 1 member who was experiencing similar problems to youself following a LCHF diet, he found that cutting back on saturated fat made all the difference, I've just found the thread now so take a look as it might be helpful to you if you want to continue with your LCHF diet:

http://www.diabetes.co.uk/forum/threads/saturated-fats.48599/#p438010
 
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donnellysdogs

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tim2000s

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To me the formula they use to calculate insulin needs being based upon the weight of the person would be more interesting.
That might throw a right spanner in the works. I think the forumla is a lot more complex and depends on weight, body fat %age, diet and activity.

If I look at me now, I'm taking 20-22u of basal dependent on exercise and around 15u of bolus (variable by exercise and food again, mealtime ratio is 1u:12g/ 1u:25g protein) at the moment. I weigh 94kg, have a body fat percentage of 10.5%, can be found in the gym working muscle groups to fatigue 3 days a week and eat 30-50g of carbs daily.

When I was at 100kg (7.5 months ago), cycling to work 4 days a week, eating a non-low carb diet with a body fat percentage of 25%, I was taking 45u of basal a day, and using around 30u of bolus a day (although the insulin carb ratio hasn't changed a lot - 1:10 then).

I suspect that the "model" you are looking for is therefore fairly complex.
 
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