Ivor Cummins in keto debate

Brunneria

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You could have high insulin levels but not have a hypo and in such a case we wouldn't see this drive to eat - why not if it is insulin?

Please provide references to support this statement.

It would be particularly useful (in light of the high insulin resistance present amongst members of this forum), if you could produce references that establish high insulin and high insulin resistance do not produce a drive to eat.
 

Brunneria

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Regarding your arthritic knee analogy. The cause of the pain is the disease - insulin release is not a disease and only can be considered in this context if there is a pathological condition either driving abnormal release of it or an abnormal response to it. The arthritic knee hurts when you walk but insulin doesn't automatically cause hunger unless it causes a hypo which happens within the context of certain/another condition. I fail to see how you would not see this distinction as important even if treatment may be the same even if you don't.

Actually, again drawing on personal experience is very useful in this, because I can tell you that unless I walk, or move, in a manner that results in pain, I am pain free - therefore your statement that the cause of the pain is the disease is inaccurate.
The pain arises from moving in a way which aggravates existing damage, or generates more damage, not from the arthritis itself.

Anyway, this is a circular argument which, while very entertaining, is unlikely to result in either of us changing our opinions, and while pedantry runs strongly in my family, it is a rabbit hole I try not to indulge in too often.

I very much look forward to your references to support the claims you have made in previous posts.
 
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Sean_Raymond

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Actually, again drawing on personal experience is very useful in this, because I can tell you that unless I walk, or move, in a manner that results in pain, I am pain free - therefore your statement that the cause of the pain is the disease is inaccurate.
The pain arises from moving in a way which aggravates existing damage, or generates more damage, not from the arthritis itself.

Anyway, this is a circular argument which, while very entertaining, is unlikely to result in either of us changing our opinions, and while pedantry runs strongly in my family, it is a rabbit hole I try not to indulge in too often.

I very much look forward to your references to support the claims you have made in previous posts.

The reason a high insulin state would not be expected to produce a drive to eat is because, as suggested by the body of evidence, Insulin exerts anorexigenic effects rather than orexigenic ones. Indeed, an interesting recent study showed that when reducing blood sugars beyond the starting BM (after administration of glucose) from insulin release no impact on hunger was seen. The study indicates that reducing blood sugars in a way that mimicked the so called post meal blood sugar spike and crash did not stimulate appetite. 1 study but an interesting one seeming to confirm that in the absence of a frank hypo spikes/drops in blood sugar do not stimulate a desire to eat. https://www.sciencedirect.com/science/article/abs/pii/S0195666316302604

Conclusive evidence does not exist that insulin increases food intake rather it indicates that it is the opposite way around with a manipulation of insulin levels not producing a drive to eat. Adding in a state of insulin resistance would not change this – whether a study directly looking at the effect of a hyperinsuliaemic insulin resistant state on appetite exists I’m not sure of but if it does not this doesn’t disprove anything I have said.

Hmmnnnnn…you have a disease which has caused inflammation in your joints – this inflammation hasn’t gone away because you do not move to minimise pain. Not moving may mask the condition but this merely helps you cope with it rather than fix it. I don’t think this example accurately represents what we are discussing anyway.

We agree that a hypo stimulates hunger – we seem to disagree about where the fault of insulin lies in this. We also agree it is pointless to discuss this further J. I find it always interesting to have such discussions so cheers.
 

Sean_Raymond

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Well surely it is in excess when caused by an insulinoma..
You can hardly claim that is the "normal" way of things?

I never said excessive insulin was a normal state. It would be a pathological condition causing the excessive insulin release – the insulin itself is not the medical condition. In a case of hyperinsulaemia (if not congenital) this would be a secondary condition resulting from a primary cause

Insulin release (or changes in blood glucose that are within range) doesn’t appear to increase food intake so I do not to see how we can blame insulin even if excessive insulin release (due to an underlying condition) would have a role in that hypo.

For example, in the case of the person with the insulinoma it was the tumour causing excessive insulin release which was causing hypos which caused the increased intake of food which resulted in the weight gain. Ivor Cummings thinks it was just the insulin which increased food intake (one would assume he would say this independent of a hunger stimulating hypo). Paul Watson thinks it was purely the anabolic properties of insulin which made the lady fatter (in this case Dr Watson oddly says she didn’t change her intake when she absolutely did). They are both simply incorrect.
 

Brunneria

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The study indicates that reducing blood sugars in a way that mimicked the so called post meal blood sugar spike and crash did not stimulate appetite. 1 study but an interesting one seeming to confirm that in the absence of a frank hypo spikes/drops in blood sugar do not stimulate a desire to eat. https://www.sciencedirect.com/science/article/abs/pii/S0195666316302604

.

Thank you for the reference, unfortunately, it has no relevance to this discussion.
The title of the study clearly states that the participants were healthy men. Therefore, comparisons cannot be drawn between either the individual who had an insulinoma, or with people who have excess insulin production, and/or insulin resistance - which you yourself (in your next post) describe as 'a pathological condition'.

One thing I most definitely agree with you about, is that you and I should stop discussing my arthritic knee.
Your comments on the subject are very far from the mark, and show some major misunderstandings about arthritis, its progression, and how to 'fix' it.
 

nickm

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Possibly because people are more concerned with putting a "chronic, progressive " disease into remission as opposed to athletic performance?

So all those claims made by keto proponents about it helping sporting performance are justified in your opinion? And made because people are not concerned about sport? Have you seen how many members the many FB groups for T1 athletes have?
 

nickm

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In your not so humble opinion I guess.. his name is Dr Paul Mason by the way.

So what field of health care are you in exactly?

I have offered to speak on the limits of low carb many times, but only people who lack my qualifications in science and medicine get invited. Such is the contempt of the keto industry for data they didn’t generate themselves.
 

Winnie53

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I'm hearing insulin and glucose discussed. What about leptin? How do high and low levels of insulin affect leptin, and appetite?
 

Goonergal

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All, this thread is about Ivor Cummins and Keto. If you wish to discuss sporting performance and low carb/keto or other aspects related to diet and appetite, please do so on another thread. Thanks.
 

Sean_Raymond

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Thank you for the reference, unfortunately, it has no relevance to this discussion.
The title of the study clearly states that the participants were healthy men. Therefore, comparisons cannot be drawn between either the individual who had an insulinoma, or with people who have excess insulin production, and/or insulin resistance - which you yourself (in your next post) describe as 'a pathological condition'.

One thing I most definitely agree with you about, is that you and I should stop discussing my arthritic knee.
Your comments on the subject are very far from the mark, and show some major misunderstandings about arthritis, its progression, and how to 'fix' it.

It is relevant because we are discussing the impact of insulin/blood sugars on appetite and it helps establish the principle that short of hypoglycaemia a large fluctuation in blood sugars in response to the release of insulin does not stimulate appetite. Even if the subjects were insulin resistant why would these results not apply? The changes in glycaemia/effect of insulin would still not be expected to make a person hungry. Indeed, the subject in the insulinoma study says she ate in response to or to avoid a hypo - caused by the abnormal insulin release. This is different to saying they ate because their insulin levels was high.

High insulin levels (like high blood glucose) is a signal of satiety and i've not seen any significant body of research showing hyperinsulinaemia initiates hyperphagia (in health or not). If you think it does I'm genuinely interested in seeing the evidence.

Nothing said was incorrect regarding Arthritis and nothing was said about its cause, how it progresses or is fixed. You brought up an irrelevant analogy about an 'acute' situation where movement caused pain. This is what I responded to,
 

Sean_Raymond

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In your not so humble opinion I guess.. his name is Dr Paul Mason by the way.

So what field of health care are you in exactly?

I am concerned about the ethics of someone saying he is a Dr who would purposefully mislead people (or that Ivor agreed with this whilst at the same time making a point which completely opposed the argument Paul made).

I wouldn't say it is my opinion at all. Independent of calories insulin will not make you fat and nor will it make you eat more as claimed - study after study supports this.
 

bulkbiker

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Independent of calories insulin will not make you fat

Odd that the lack of it makes you skinny very fast though...also independent of calories.

And you still haven't revealed what kind of "HCP" you are have you..?
 

Brunneria

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It is relevant...

I disagree.

Comparing one small (15 person) study where a group of healthy young men ate a small breakfast (284 calories), followed by 50g of intravenous glucose, then experienced non-diabetic blood glucose levels between 9 (highest) and 3 (lowest), compared with a control (no glucose) whose bgs were between 5 and 3.9mmol.

Most noteably, this study lasted a mere 2 hours on 2 separate days.

It is grasping at straws to suggest this is in any way comparable to someone with an insulinoma, or members of this forum with T2 diabetes, with insulin resistance and glucose dysregulation often lasting decades.

In fact, your study itself concludes with a speculation (Certainly draws no firm conclusions) and confirms that it only looked at ‘signals in the short-term regulation of hunger and satiety’ (my bold).

@Goonergal
I realise that this is a continuation of the thread derailment but I had to refute Sean’s unfounded claim.
If you wish to delete this derailing post, please do so.
 
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nickm

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I'm hearing insulin and glucose discussed. What about leptin? How do high and low levels of insulin affect leptin, and appetite?

Yes, many other hormones are relevant to the discussion. Using the story of one patient with an insulinoma to cast doubt on some ways of managing diabetes without considering those hormones and other differences is not something I would do. Weight loss after surgical tumour removal is not uncommon. That applies to many tumours, not just insulinomas.
 

Goonergal

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I think everyone has had their say on the off-topic subjects raised on this thread. From this point on, any further posts not relating to the OP - Ivor Cummins and Keto will be deleted. Please start a new thread if you wish to continue any other discussions.
 
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nickm

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To quote from the link in the OP, this is the “ultimate debate” in “the LDL cholesterol debate” Huh? The lack of utility of LDL alone as a parameter of cholesterol for IHD prediction was first reported in the 50s, as good as proved in the 70s, and accepted by most doctors I know not long after that. The video is from Israel, a country reported to have poor diabetes outcomes. Was that to avoid stronger opposition elsewhere? Many people with diabetes are worried about whether they should take statins. I do not see this video helping with that question. Giving statins to everyone with LDLs above a certain level has not been an official recommendation in my part of the world for a long time. The video is far from the “ultimate debate”. Poorly constructed or straw man arguments concerning cholesterol may do no more than empower the pro-statin lobby.