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Insulin Resistance or Lack of Insulin

Mr_Pot said:
That's the bit I don't understand, what has permanently changed in the body so that it remains insulin resistant. I am not saying it doesn't happen, I just don't know what the mechanism is.
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Maybe resistance isn't a helpful term as it implies it is the cells which are somehow faulty (the gummed up lock and key analogy) whereas it could be looked at as an insulin signalling fault.
The analogy I've heard is that the cells of the liver, muscles and fat become 'deaf' to the request of insulin to enter in with it's delivery of fuel. This develops over a number of years until a point is reached when the pancreatic cells can't shout any louder so the energy (glucose) can't get in and is then found in the blood (type 2 diagnosis).
I think it was believed and still is by some GPs that the beta cells can't keep up production hence the belief that eventually all type 2s need insulin which as many here can attest isn't so and the Direct study also refuted this idea of inevitable progression due to failing beta cells however not everyone got into 'remission'.
In this study those that had been diabetic and therefore insulin resistant for longest were also the slowest to reverse their diabetes/insulin resistant and I am sure in some cases it is not going to be possible to get back to the insulin sensitivity we had in our youth. Possibly because even with a low carb diet we may struggle to regain the muscle mass we had then.
However because the medical profession measures blood glucose rather than insulin levels, the hyperinsuliemia goes undiagnosed unless the patient eventually becomes diabetic. Whether or not you get to be type 2 seems to be based on their individual fat threshold (genes) e.g. Asians struggle to expand their fat cells whereas others can become very fat but their pancreases can produce huge volumes of insulin (loudspeakers) to amplify the force of the insulin so that it does get into the cells or get turned into fat cells.
This is what I've gleaned from reading Jason Fung and latterly Ben Bikman (Why We Get Sick).
 

@JoKalsbeek, I read the forum every day and when I see you posting I know I will learn something and presented normally in an entertaining way.
 
We can all be forgiven for having to ask the question about insulin, as in too much or not enough, as most of the population is still hugely confused about the difference between type 1 and type 2, as the name of the disease is the same, due to the symptom of too high blood glucose being the same, although the condition is very different.

It took me some years to get this myself, which stuns me now, but I have to remind myself that I read a lot of books, and forums in here which were utterly irrelevant to 'my' type 2, due to the blanket term 'diabetes'. I am not alone, as I have come across medical professionals who get this wrong too.

There are two things I would like to go back in time and change - I would like to have called the autoimmune disease and the metabolic disease by different names (the 'type 1' and 'type 2' distinction is not good enough!), and, I would like to get the phrase 'lifestyle choices' and 'lifestyle changes' out of the type 2 vocabularly enitrely! I consider choosing (in pre Covid days in Europe naturally) between a holiday in Athens, or on a Greek island a very pleasant lifestyle choice. I do not consider the hard work of making sure I get enough physical activity and exercise, and keeping my Way Of Eating in tandem with my insulin resistance in the same ilk as a choice of where I take my hols!

Anyway. I make the distinction when talking about type 2 of saying 'insulin-resistance based type 2 diabetes', which is where we produce too much insulin due to too much glucose due to excess carbohydrate in the presence of excess and bad fats, and mentioning that some folks have pancreatic damage and do not produce enough insulin.

When it comes to the numbers - well - as insulin resistance is our bodies preventing too much glucose and insulin getting into our cells is a default physical response for all mammals that have blood glucose regulation - it is by far the most common. I am just drinking my morning coffee and haven't had breakfast yet, so I am not getting the numbers out or providing links - but it is awfully easy to find these online.

My understanding is insulin resistance is our friend! It is keeping us alive (as in our cells functioning). Our enemy is the too high glucose and glucose-forming food we put into our bodies (and put into our bodies historically due to ignorance of what this would do to us). Is my understanding.
 
Jim Lahey said:
If we routinely tested insulin rather than obsessing over glucose until it's too late then we would have our answer. Unfortunately most doctors seem to think that insulin testing is some kind of mumbo jumbo black magic, but there we have it.
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I thought I'd heard somewhere that they don't est for it here in UK because the est is expensive. It is tested more for more routinely in USA AS the patient/insurance company pays
 
MrsA2 said:
I thought I'd heard somewhere that they don't est for it here in UK because the est is expensive. It is tested more for more routinely in USA AS the patient/insurance company pays
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The best proxy here would be triglycerides/hdl ratio which are routinely done here with the lipid panel although you'd need to work out the ratio yourself...
 
Newbie here... first post... diagnosed as Type 2 on July 12th after being hospitalized for hyperglycemia. Was tested for COVID-19 before admittance to ICU as this is standard procedure here during this pandemic and was told the next day that the test was positive. Pulmonolgists told me that the Diabetes was “ triggered” by COVID-19. Had no idea that I had Covid as there were no symptoms such as a fever or a cough; have since been tested for antibodies which are still present. Anybody else been in this situation ....would love to know as there is very little research out there about Covid and diabetes....
 
It could also be said that the description of “not enough insulin” could refer to not enough to maintain normal blood sugars. That doesn’t mean it’s actually low though or explain why it’s not enough. It can be high but with a great delay of insulin resistance hence not enough to do the job

This fits with the historic regime of “let’s whack some exogenous insulin in too to do the job” rather than sort out why the high amounts aren’t enough.
 

Hi @Lady Jayne and welcome

You’d likely get a better response if you posted your question as a new thread. It’s likely to get lost here in the middle of another thread. Let me or one of the other moderators know if you need help with that.
 
I know someone who developed myocarditis after having covid19 with no symptoms.
 
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Thank you. Don't have the energy to read that thread right now, but what you say is what I have always thought to be true. I have no links or clever reasoning, it just makes total logical sense to me.
 
Jim Lahey said:
Basically the body doesn't necessarily remain permanently insulin resistant. Depends largely on whether you are treading water in glucose or have well and truly pulled the plug and drained the pool.
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The problem with that blaming diet and eating patterns for hyperinsulinemia (aka insulin resistance) is that it assumes that eating patterns are the root, and basically the only, cause. This is most definitely not the case for those of us with more complex health issues, including hormonal issues. Indeed, some medications contribute to insulin resistance. So just ‘pulling the diet plug’ is by no means the entire solution for everyone.
 
True, but it can be a useful tool in the battle.
 
I am 12 years into being diagnosed T2.
Unfortunately I wasn't tested for insulin production on diagnosis so I have no evidence to show that I was an over/normal/under producer at that time.

I do know that a year or so back I had a privately funded IR test which showed that my insulin production was on the low side of the normal range, but that my fasting BG was elevated above normal.
[Conclusion, some level of IR.]

I am therefore currently not an insulin over producer.

I also weigh around 170 pounds (12 stone 2 lbs) and am 6 foot tall so I am well towards the centre of the "normal" BMI. I have been as low as 161 lbs but I struggle to keep my weight that low.

I don't have massive upper body musculature but my legs are reasonably muscly from cycling.

All this suggests that the blanket statement "T2 is all about over production of insulin" does not apply in my case.
However I am still diagnosed as T2 and still managing on just Metformin, diet and exercise.

Firstly, IMHO T2 is a catch all label for people still producing their own insulin but with impaired BG control.
[Without a more specific diagnosis.]

Secondly, IMHO people should have a c-peptide test on diagnosis to confirm the level of insulin production.A decade or so back this might not have seemed significant as the treatment pathway was the same whatever, but if we had some reasonable baseline data we might not have to be having this discussion.
 
I draw on the sick fat cell theory, and the insulin resistance coming from too high glucose and too high insulin theory, for how insulin resistance comes about. It is in fact very complex, as any look at what is called the Randle Cycle will show!

And absolutely, our hormone cycles are incredibly complex too - I am one of the many women who became full blown type two diabetic at perimenopause, and absolutely I get that connection. But our hormone cycles have a chief hormone regulator, is my understanding, which is - yep - insulin! Insulin is just not about blood glucose regulation but basically regulates our life cycle too, as in, our life span tranjectory. Awe inspiring stuff.

My understanding is too high insulin production (which I definitely have, and have had for decades) is from too high consumption of high-glucose forming food and drink historically, in the presence of fats, and bad fats in particular. I am talking ribena in my baby bottle historical! . I have a body type where a very wee tip over my personal fat threshold (using Prof Taylor et al's theory here, which I also like a lot in its simplicity and logic) starts the metabolic chaos which can be insulin resitance and then the full-blown type two diabetes.

I don't mean the 'diet plug' to be overly simplistic - it is not. But type two insulin resistance based diabetes is an interrelationship between our body types and metabolism-types (genes!), and our environment, specifically what we put into our bodies, or had put into us (thinking about the ribena,), called the food environment. Again - I say - this is in regards to insulin-resistance based type two. Not some of the other forms of diabetes. (I am very careful to make this clear. If I have not made it clear enough, I hope this does it.)
 
I've always assumed insulin resistance gave a genetic advantage to our ancestors - but easy access to carbs and less physical work has made it a lot less advantageous these days.
 
The NHS definition of type 2 diabetes is still 'where the body does not produce enough insulin, or the body's cells do not react to insulin'. https://www.nhs.uk/conditions/diabetes/

Prolonged high glucose levels can cause beta cell failure:- Glucotoxicity and beta-cell failure in type 2 diabetes mellitus
https://pubmed.ncbi.nlm.nih.gov/125...ct of excessive,referred to as 'glucotoxicity'.

Beta cell function tends to reduce with age:- Age-Related Impairment of Pancreatic Beta-Cell Function: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4153315/

Some researchers have suggested there are 5 types of diabetes, one of which is 'Mild age-related diabetes (MARD)'. The news coverage of the research was analysed here:- https://www.nhs.uk/news/diabetes/are-there-actually-5-types-diabetes/
The link to the original research is at the bottom of the article.


 
@Dark Horse very interesting and I remember reading about this a while ago

The researchers identified 5 main disease clusters.

  1. Severe autoimmune diabetes (SAID): this tended to start at a younger age, in people with a relatively low BMI, poor blood sugar control, insulin deficiency and GADA. About 6% of the people in the ANDIS study had SAID.
  2. Severe insulin-deficient diabetes (SIDD): GADA-negative but otherwise similar to SAID. Identified in 18% of the people in ANDIS.
  3. Severe insulin-resistant diabetes (SIRD): characterised by insulin resistance and high BMI. Identified in 15% of the people in ANDIS.
  4. Mild obesity-related diabetes (MOD): characterised by obesity but not insulin resistance. Identified in 22% of the people in ANDIS.
  5. Mild age-related diabetes (MARD): people were generally older than those in other clusters and had only mild problems with glucose control, similar to MOD. Identified in 39% of the people in ANDIS
I think those that show excellent improvements in hb1ac and great weight loss without drastically cutting carbs would be more likely a 4. There are quite a few of these in these forums. Those of us that find it hard despite weight loss and carb reduction maybe a 3? Or perhaps if older a 5

I’ve speculated in the past about type 2 having at least the 3/4 differences and this seems to support my musings.
 
They appear to have forgotten about those who are extremely insulin resistant and yet built like a bean pole.
 
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