High Cholesterol

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For me insulin resistance and insulin sensitivity is a very broad sliding spectrum. It isn't a static/specific condition, but that might be partly because I am Type 1 rather than Type 2. When my levels get above 8 I start to become less responsive to insulin and above 10 even more so, but if I do exercise I become much more sensitive to it.
I know we often refer to being more insulin resistant on a morning on the forum when what we actually mean is that our insulin (whether injected or endogenous) is having to fight against the glucose being released by the liver due to DP or FOTF rather than actual resistance, so I think @Docb is right that we use the term insulin resistance rather too loosely sometimes and it may have more to do with liver output and the pancreas not balancing that than actual insulin resistance. My feeling is that people who are at their personal fat threshold will have insulin resistance as the cells of the body have reached the point that they can't store anymore glucose as fat.... a bit like trying to eat more when you are already full to the gunnels.... I would guess that the statins may somehow affect the liver output of glucose or the pancreas' ability to deal with that glucose, perhaps confusing the signaling between the two organs resulting in imbalance, but that is just a gut feeling with no scientific knowledge.
I know from my own experience that my liver can chuck out a heck of a lot of glucose when it wants to and I have to be on the ball sometimes monitoring it to counteract that with an injection of insulin.
 
@Spathiphyllum - you use the phrase "insulin resistance" as do others on the forum. What do you mean by that term?

Please be assured that I am in no way trying to start an argument or even a debate on the subject. I'm not sure what is meant by it and Its just that i think it important that we have a common understanding of terms being used.
'Insulin resistance', or 'impaired insulin sensitivity' means that, for a given quantity of glucose in your blood, your body needs a higher than normal amount of insulin for your cells to take up that glucose and thus remove it from your blood. To say that someone is insulin resistant is the same as saying that s/he has a low 'glucose disposal rate'.

The gold-standard test involves, basically: You stick two tubes into your subject; let's call him John! One tube infuses insulin at a steady (and high) rate. The other infuses glucose. If you have to infuse a lot of glucose to keep John from becoming hypoglycaemic, he is very insulin-sensitive. If you only have to infuse a little glucose to keep John from becoming hypoglycaemic, he is insulin-resistant. (See for example https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3379600/ , or for that matter Wikipedia.)

Type 2s by definition suffer from insulin resistance. Type 1s may be highly insulin-sensitive, or highly insulin-resistant, or anything inbetween.

Hope that helps!
 
Thank you everyone. So the reason I thought they were high is because I got them back on the NHS site and they looked worse than my husbands and he had got a call from doctor to ask him to go in and talk to someone and had been given some recommendations. However, a week has gone by now and no one has called me. I won’t post results here but happy to do so after I have spoken with the diabetes nurse who said she would call me next week. I don’t really understand the cholesterol numbers so probably sensible that I speak with her first as wouldn’t want to spend the next few days really worrying. Hope that makes sense.
Unfortunately for the first time in a couple of years had to take a day off sick as struck down with a bug. Managed to get covid twice in the past without a single symptom and testing negative at the moment so probably just a bug. On the bright side have lost my appetite which may help with the penultimate weigh in before Xmas at Weight watchers. Really wanted to get to two stone before then.
 
Thank you everyone. So the reason I thought they were high is because I got them back on the NHS site and they looked worse than my husbands and he had got a call from doctor to ask him to go in and talk to someone and had been given some recommendations. However, a week has gone by now and no one has called me. I won’t post results here but happy to do so after I have spoken with the diabetes nurse who said she would call me next week. I don’t really understand the cholesterol numbers so probably sensible that I speak with her first as wouldn’t want to spend the next few days really worrying. Hope that makes sense.
Unfortunately for the first time in a couple of years had to take a day off sick as struck down with a bug. Managed to get covid twice in the past without a single symptom and testing negative at the moment so probably just a bug. On the bright side have lost my appetite which may help with the penultimate weigh in before Xmas at Weight watchers. Really wanted to get to two stone before then.

I had a bad stomach infection when I was dieting.
It certainly made a big difference to my weight loss!!
Hope you feel better soon.
 
I had a bad stomach infection when I was dieting.
It certainly made a big difference to my weight loss!!
Hope you feel better soon.
It’s Christmas lunch at work today which would have been a three course (delicious) meal. I think my feelings towards food are definitely changing because in the past I would have been very upset to miss it but I kind of feel relieved that I won’t have to deal with the temptation and potentially ruin the chances of a loss at WW on Saturday.
 

It's usually as part of a response to hyperinsulinemia which some believe is the root cause of T2.

Surely IR leads to pre-diabetes & hyperinsulinemia, which if left can develop into T2?

The pancreas makes more insulin to overcome the IR and this leads to elevated levels of insulin?

T2 follows on when (Some) of the beta cells stop working and it can't keep BG levels down.
 
Surely IR leads to pre-diabetes & hyperinsulinemia, which if left can develop into T2?

The pancreas makes more insulin to overcome the IR and this leads to elevated levels of insulin?

T2 follows on when (Some) of the beta cells stop working and it can't keep BG levels down.
Not necessarily hyperinsulinemia can lead to insulin resistance.

Depends on your view I'm a Bikman fan he actually studies and teaches it.
If you produce too much insulin due to overconsumption of carbs then your body gets "used to it" and it has less and less effect so you constantly have to produce more. As every organ and vessel gets packed full of glucose then more insulin is required to force it in.
It's a pretty vicious cycle.
If the beta cells "stopped working" then remission wouldn't be possible and we know that it is either through loss of visceral fat through starvation (Newcastle Diet) or reducing the insulin requirement through sensible low carb/keto eating allowing the insulin function to return to normal.
 
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Not necessarily hyperinsulinemia can lead to insulin resistance.

Depends on your view I'm a Bikman fan he's actually studies and teaches it.
If you produce too much insulin due to overconsumption of carbs then your body gets "used to it" and it has less and less effect so you constantly have to produce more. As every organ and vessel gets packed full of glucose then more insulin is required to force it in.
It's a pretty vicious cycle.
If the beta cells "stopped working" then remission wouldn't be possible and we know that it is either through loss of visceral fat through starvation (Newcastle Diet) or reducing the insulin requirement through sensible low carb/keto eating allowing the insulin function to return to normal.

Beta cells do stop working in T2 diabetes.
I’m not sure what your point is? This is well known and has been seen and is one reason why blood sugar rises to dangerous levels.

In some people they can start working again with weight loss. This has been shown with bariatric surgery and the Newcastle diet.

This failure of beta cells has nothing to do with ‘your body getting used to to it’ That’s an almost laughable statement. If you read the paper recently published by Oxford, they have seen a mechanism that stops beta cells from producing insulin,

I suppose you don’t believe it, though, as it’s not posted by some one with a book to sell.

Also, if you have 30g of carbs or 200g, enough insulin is produced to get levels back down to normal in the same time. That is how the system works. And yes, I know that if can take longer of fat and protein is mixed up.

As for this Bikman guy… I read an article where says this, which is clearly stating the well known fact that insulin resistance leads to Hyperinsulinemia. You said it was the other way round.


First, as mentioned, insulin resistance increases the risk of Type 2 diabetes. This is true, but this relationship warrants further clarification. Type 2 diabetes is insulin resistance. That is, type 2 diabetes is insulin resistance that has progressed to the point where the body is unable to keep blood glucose levels below the clinically relevant 126 mg/dL. We’ve known this for almost 100 years; German scientist Wilhelm Falta first proposed the idea in 1931.(2) In other words, any time you hear someone speaking about the evils of diabetes, you can just substitute in “insulin resistance” and it’s immediately more accurate. For example, your neighbor doesn’t have a family history of diabetes; she has a family history of insulin resistance.

Second, insulin resistance is a hyperinsulinemic state. That means a person with insulin resistance has more insulin in the blood than normal. (This particular point will become highly relevant when we discuss the unfortunate effects of being in this state for prolonged periods.)

Harbottle, PhD.
 
Beta cells do stop working in T2 diabetes.
They don't though, think about it.. if they stopped working how do they magically restart again?

They just keep pumping out insulin in larger and larger amounts until we stop overfeeding carbs. Then we can regain insulin sensitivity and our BG goes back to "normal" and we can achieve remission.

From the article you linked to

" insulin resistance is a hyperinsulinemic state"



they have seen a mechanism that stops beta cells from producing insulin,
In T1's?
 
They don't though, think about it.. if they stopped working how do they magically restart again?
This has an outline of the proposed mechanism: https://www.researchgate.net/public...the_mechanisms_of_reversal_of_type_2_diabetes


Clinical and pathophysiological studies have shown type 2 diabetes to be a condition mainly caused by excess, yet reversible, fat accumulation in the liver and pancreas. Within the liver, excess fat worsens hepatic responsiveness to insulin, leading to increased glucose production. Within the pancreas, the β cell seems to enter a survival mode and fails to function because of the fat-induced metabolic stress. Removal of excess fat from these organs via substantial weight loss can normalise hepatic insulin responsiveness and, in the early years post-diagnosis, is associated with β-cell recovery of acute insulin secretion in many individuals, possibly by redifferentiation.
 
This has an outline of the proposed mechanism: https://www.researchgate.net/public...the_mechanisms_of_reversal_of_type_2_diabetes


Clinical and pathophysiological studies have shown type 2 diabetes to be a condition mainly caused by excess, yet reversible, fat accumulation in the liver and pancreas. Within the liver, excess fat worsens hepatic responsiveness to insulin, leading to increased glucose production. Within the pancreas, the β cell seems to enter a survival mode and fails to function because of the fat-induced metabolic stress. Removal of excess fat from these organs via substantial weight loss can normalise hepatic insulin responsiveness and, in the early years post-diagnosis, is associated with β-cell recovery of acute insulin secretion in many individuals, possibly by redifferentiation.
Not really.. again which comes first.. and logic.. fat deposits are controlled by insulin so if your beta cells weren't working (like in T1 ) then you wouldn't be depositing fat.. hyperinsulinemia is a far better explanation.
ND could be considered relatively low carb due to the starvation nature and the early Taylor studies tested for ketones...
No mention made in DIRECT about that because it may have been a tad inconvenient if the remission was because the participants were in ketosis...
 
Not really.. again which comes first.. and logic.. fat deposits are controlled by insulin so if your beta cells weren't working (like in T1 ) then you wouldn't be depositing fat.. hyperinsulinemia is a far better explanation.
ND could be considered relatively low carb due to the starvation nature and the early Taylor studies tested for ketones...
No mention made in DIRECT about that because it may have been a tad inconvenient if the remission was because the participants were in ketosis...

Thank you Eddie for confirming the Newcastle diet is a keto diet, and no one should be worried about carbs while on it, and that it works.
Many will be pleased it has your endorsement of that.
Others low carbers have said it is fine as well for both low carb, and low calorie diets.
And it's also a lot faster on the 8 week timescale it needs for results.
 
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Not ALL the beta cells stop working in T2, just some of them, up to 50% of them in fact.

It seems all the research, clinical trials and known facts from observations are wrong and Eddie is right.
 
Not ALL the beta cells stop working in T2, just some of them, up to 50% of them in fact.

It seems all the research, clinical trials and known facts from observations are wrong and Eddie is right.
And how precisely can you measure how many beta cells are "working"
 
Thank you Eddie for confirming the Newcastle diet is a keto diet, and no one should be worried about carbs while on it, and that it works.
Many will be pleased it has your endorsement of that.
Others low carbers have said it is fine as well for both low carb, and low calorie diets.
And it's also a lot faster on the 8 week timescale it needs for results.
Starvation ketosis is a well known phenomenon.
However as we all are aware (or should be) crash diets rarely lead to long term weight loss and a diet that contains precisely half the calories from the "Minnesota Starvation Experiment" shouldn't really be prescribed by the NHS in my opinion. It's hardly "low calorie" it's pure starvation.
 
Starvation ketosis is a well known phenomenon.
However as we all are aware (or should be) crash diets rarely lead to long term weight loss and a diet that contains precisely half the calories from the "Minnesota Starvation Experiment" shouldn't really be prescribed by the NHS in my opinion. It's hardly "low calorie" it's pure starvation.

Eddie, you've put two and a half stone back on on your diet.
I think that adequately defines the quality of your opinion.
 
But you are assuming that higher levels of cholesterol are "bad".
This is often simply not the case.
Many people with CVD have "normal" levels of cholesterol so....

Well they are bad, as vast majority of cardiologists agree on this, few mavericks suggesting otherwise makes no difference whatsoever.

Wonder if your trying to find means to a end by searching out these mavericks, on one hand your pleased that diabetes is under control but on other hand your secretly disappointed that your chosen diet has led to high cholesterol, can see in some way why you'd do this but you can't outrun the facts my friend.
 
But you are assuming that higher levels of cholesterol are "bad".
This is often simply not the case.
Many people with CVD have "normal" levels of cholesterol so....

You say high levels of cholesterol are so protective, really good to have, and it prevents disease.
Many people with CVD have "high" levels of cholesterol so.....
 
Many people with CVD have "high" levels of cholesterol so.....
Its fairly obviously not "cholesterol" that is causative of CVD.
 
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