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Ivor Cummins in keto debate

I watched a Facebook live event tonight and the guest was Ivor Cummings, so very interesting. Obviously came here and did a search for his name on the forum. I just knew you guys would have information on him. Lots of reading and video watching in store for me.
 
I had a short but interesting recent exchange with Ivor Cummings. In response to his interview with Dr Paul Mason I pointed out a concern regarding the Dr where he literally lied about a study.

The study was regarding the removal of a mass insulin producing insulinoma after which a subsequently dramatic amount of weight loss was recorded. The Dr said the individual lost 18kg whilst making absolutely no changes to either her diet or physical activity. It was due to the reduction in insulin levels.

The study made it clear the subject reduced her daily calorie intake by over 2,400kcals per day.

When I pointed this out to Ivor he responded by saying the drop in insulin caused her appetite to "collapse" therefore eating less and so Dr Paul Watson was right.

When I told Ivor that his response directly contradicted what the Dr had said so it was impossible he could agree with him Ivor went silent.

What I personally think was revealed was a very narrow way of thinking with Ivor so wedded to the idea that insulin is the sine qua non of obesity/type 2 diabetes etc that he either cannot be honest about or blinded to facts which are not in line with his thinking.

So please do your own research and do not blindly accept what these people (or I) say as your health deserves that and there is so much mis-information out there as well as much we still do not know.
 

Not sure what to say, @Sean_Raymond, but only that maybe we should consider the fact that that we are all human ... and that as humans we all sometimes make mistakes (even when reporting the results of studies). People interested in science easily read hundreds if not thousands of studies each year -- and one would really need a photographic memory to recall every single detail without fail.

Does this invalidate what has been said? Not in my opinion -- because the effects of insulinoma on hunger and weight have been reported elsewhere. It's easy to find research online when looking for this, so this relationship seems to be pretty well established. Moreover, many T2s and even some T1s on here report that injecting high levels of insulin makes it harder to control weight. Also, the rapid weight loss associated the onset of T1 when insufficient insulin is produced seems to support the fact that there is a relationship more generally between insulin levels and weight gain/loss (even though there are other factors which may impact weight as well).

So, do I personally buy into the research on low carb or keto for T2s? For me, the answer is a clear yes. While it might not be perfect, as a whole I find it very convincing. In terms of scientific rigor, it definitely beats most other research on WOEs for T2s out there. I should also mention the fact that it works for me: Five years of normal non-diabetic blood sugars after a very, very high HbA1c at diagnosis, four of these without medication.

While I agree with you that we all should critically examine the information we find on the internet, I am personally grateful that presentations and other videos by Ivor Cummins, Paul Mason and others like Tim Noakes, Stephen Phinney, Jeff Volek, Sarah Hallberg, Jason Fung, Gary Fettke, and Jenny Ruhl are available. For me, they have been a game changer.

As to to Ivor Cummins' response, I do empathize with him. I am in teaching -- and while I believe it is absolutely fine to correct something a colleague has said, I would also never personally disparage him or her in front of a student.
 
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Hi.
Thank you for the reply.

The error Paul Mason made wasn't a mistake - it was part of a presentation he prepared and he used the study as a key example to demonstrate insulin is making people fat. He deliberately misrepresented the study - I'm happy to post links of the study and his video if I'm allowed.

I've seen a number of other claims he has made which amounts to mere hypothesis - ones not supported by what studies show. For exsmple he claims that lipomas are proof insulin makes you fat. The development of these fatty deposits occur in under 5% of T2DM and 25% of T1DM. The injection of insulin doesn't represent physiological release of insulin and these deposits are as much a result of an immune response to injury as it is insulin. Dr Paul Watson is adamant it's just the lipolytic property of insulin.

Insulin is generally more likely to signal satiety than hunger and the researchers never said what Ivor claimed happened to the subject to explain the weight loss.

Ivor simply reacted as part of a tribe with a pack like mentality when he should have considered what he was writing as he contradicted himself. After all - I'm interested in making people healthy so I am in the same team as him.

To be clear. I'm not opposed to low carb diets at all - i find them metabolically very interesting - but I an opposed to extrapolation or misrepresentation's of data passes of as evidence to support a particular narrative. Much of what is claimed about insulin and low carb just isn't supported by physiology or studies

I'm writing from my phone so apologies for typos etc.
 

Am I missing something here? If the patient had an insulinoma producing (excessive) insulin and it was removed and she subsequently lost weight then that WOULD be the primary cause and she would indeed not have changed her diet. So both Dr Paul Watson & Cummins were correct. A deliberate change of diet for weight loss is a VERY different thing from incidental weight loss caused by a surgical intervention. If someone has gastric band surgery and can no longer eat as much, the corresponding weight loss is not due to a change in diet but to the surgery. This is the same situation. The CAUSE is the removal of the insulinoma, not a "change in diet".
 
Sean_Raymond said:
The study made it clear the subject reduced her daily calorie intake by over 2,400kcals per day.
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Because or in spite of the removal of the insulinoma?
You see maybe she was less hungry... obvious when you add logic in to the outrage.
 
In reso

Yes you are missing something. And so you need to read again. Stop confusing what I said with preconceived bias as that is why I posted this.

I'll repeat it again. Paul Watson said when the insulinoma was removed the patient lost weight. Paul said the patient did NOT change her diet. The study showed she ate 2400 kcal less. Do you understand the difference between not changing your diet and changing it by 2400 kcals a day?

Paul said weight loss was purely down to reduced insulin levels but the study shows it was mostly because she ate less. Which a 2400 kcal reduction would do.

Ivor Cummings said the reason she lost weight was insulin collapsed her appetite proving Paul correct. It is obvious Ivor didn't pay attention to what Paul was arguing because if he did he'd see he disagreed with him as Paul says her appetite was unchanged.

The point made was that Paul lied and Ivor supported it even though it completely contradicted what he himself was saying.

Why is this being ignored? This IS important.

I'm happy to discuss why she may have gained weight and why she lost weight. But the importance of how these people either lie or ignore in order to continue the same point IS the point of why I posted. Everyone seems interested in ignoring this.

I am seeing this forum has the ivor ethos of not reading but reacting here.
 

Thanks for getting back to me, @Sean_Raymond. Great to see that you are generally supportive of low carb.

Based on what you describe, it does indeed seem that Paul Mason may not always use the necessary care when constructing arguments and discussing studies. However, I am not sure this would be true for everyone supporting the low-carb WOE for T2s. Have you had a chance to listen to Stephen Phinney, Jeff Volek, David Ludwig and Ben Bikman?

As to Ivor Cummins' reaction to the mistakes that Paul Mason apparently made in the presentation (don't mistake me, I am not necessarily doubting what you say, just haven't had a chance to do watch the video and do the research myself), I still wonder why you didn't take this up with Paul Mason rather than Ivor Cummins.

I also agree with you that low carbers sometimes seem to be a a bit clanish and very supportive of each other (possibly even to a fault). Maybe this is due to the fact that on the one hand many of us have witnessed amazing results after changing the way we eat while on the other hand we had to make our way without support, often (but fortunately much less frequently nowadays) against advice of HCPs, and were told that the improvements we've seen in health were just anecdotes. Professionals supporting low carb/ketogenic diets such as Tim Noakes and Gary Fettke were even threatened with losing their licences.

Don't forget that those of us supporting a low carb/ketogenic WOE are still a very small minority. Thus, maybe the "clanishness" of low carbers might be reflective of this rather than something inherently wrong with people subscriping to this WOE.

Just my thoughts on this, though.
 
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The patient mentioned in the study had profound and chronic hypoglycaemia. It was reported that her intake had increased in order to maintain her blood sugars which were consistently under 3. Essentially the weight gain occurred in response to increased intake not due to an increased drive to eat from the insulin itself but in response to her continually low blood sugars. The authors do mention very briefly that weight gain was also due to the anabolic effects of insulin in addition to this obvious energy surplus however I do not think, given the amount of calories consumed, the blame can be put at the foot of insulin as Dr Paul Watson does.

The removal of the insulinoma saw a dramatic decrease in energy intake due to the normalised blood sugars reducing her need/drive to eat to raise them. Her appetite isn't discussed just that she frequently ate to try to avoid hypos (she would lose consiousness).

Neither Dr Paul Watson (who blatantly lies about the study) nor Ivor Cummings gave accurate explanations for why the lady lost weight with both citing insulin as the direct cause (in one way or another) when it was not due to either the fat building properties or appetite stimulating effect of insulin.

Insulin doesn't stimulate the appetite in the manner Ivor claims (it does have 'a' role in appetite regulation) nor does it make a person fat in the way Dr Watson says it does.
 
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Despite so many years of claims about the benefits of keto for athletes, the keto lobby is still unable to name even a single older athlete who is anywhere near matching my PBs in the 55-59 year age group.
 
Sean_Raymond said:
. Essentially the weight gain occurred in response to increased intake not due to an increased drive to eat from the insulin itself but in response to her continually low blood sugars.
Click to expand...

Which were caused by excess insulin from the isulinoma?
Thus you could easily say her appetite was triggered by the insulinoma and removal of that reduced the urge to eat?

Sean_Raymond said:
The removal of the insulinoma saw a dramatic decrease in energy intake due to the normalised blood sugars reducing her need/drive to eat to raise them.
Click to expand...

Or the removal caused a dramatic reduction in appetite which then led to lesser intake?
 
nickm said:
Despite so many years of claims about the benefits of keto for athletes, the keto lobby is still unable to name even a single older athlete who is anywhere near matching my PBs in the 55-59 year age group.
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Possibly because people are more concerned with putting a "chronic, progressive " disease into remission as opposed to athletic performance?
 

I have had reactive hypoglycaemia for years (due to over production of insulin in response to carbs) and I know from long and bitter personal experience exactly how much my appetite, blood glucose (and weight) is affected by large amounts of insulin. Hunger and appetite are driven by low blood glucose. Low blood glucose is driven by excess insulin.

In my opinion, anyone who suggests that the two things are not intimately and causally linked, does not grasp what is going on. Unfortunately, most people (and I include many health care professionals that I have met) have no idea what their patients are going through, since they have not had the actual experience of incessant, ravenous, gnawing, carb craving hunger driving them to eat.
 

Hi. This is the argument that Ivor was making however manipulating insulin levels hasn't been shown to massively increase or decrease appetite. On the contrary, studies show insulin to have a suppressing effect on intake or in other words promotes satiety

This change in hunger wasn't an effect that was reported by the subject. They say they were eating to avoid hypos and raise her blood sugars. I would imagine this was done both conciously and unconciously. Hypos are believed to be potent stimulators of hunger (not always shown in studies) so I would imagine there were dramatic shifts in her appetite.

My take home from the study and from personal practice is that it was not insulin orchestrating the drive to eat but likely low blood sugars which were affected by the large amounts of insulin. Once her blood sugar stabilised so did her oral intake.
 

Large amounts insulin driving down blood sugars may indeed impact hunger but it's not the insulin per se which is making the person hungry. When blood sugar drops below the ideal range to something being or approaching a hypo may then stimulate the desire to eat.

The key here is appetite being directlt driven by the low blood sugar levels and not the insulin levels. In someone becoming insulin insensitive we would expect higher circulating insulin and higher blood sugar. In this case we would not expect blood sugar to drive hunger nor would the insulin either. Of course people like Ivor will say such a person is likely gaining weight as they are eating more and this us due to the higher insulin. But this wouldn't likely be correct. The higher insulin levels would be the result of increased adiposity which is interfering with insulin signalling/response causing the body to release greater amounts to elicit an effect. Acute changes in insulin levels not causing a hypo doesn't appear to increase the need to eat.

Obviously I cannot speak or comment on your personal experience but I actually agree with what you are saying but interpreting it slightly differently if that makes sense.
 
Sean_Raymond said:
Obviously I cannot speak or comment on your personal experience but I actually agree with what you are saying but interpreting it slightly differently if that makes sense.
Click to expand...

Thank you.
That means you are also agreeing with the others who posted above - because they have been saying the same thing as me.
Actually, I feel that you are making a distinction where no distinction should exist.

It is like me saying I have arthritis and my knee hurts when I walk.
While you are saying No, your knee hurts because you walked on an arthritic knee.
I see absolutely no reason to make the distinction, and in fact making the distinction actually confuses the issue and causes division where none is necessary.
 
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Brunneria said:
It would be interesting to read those studies. Can you provide some references please?
Thanks in advance.
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Hi

You said that hunger was caused by low blood sugar - this is correct. A frank hypo would drive hunger however whilst it was insulin that will have driven down that blood sugar it just isn't correct to then suggest there is something pathological about Insulin (unless we have pathological conditions causing supraphysiological release of insulin). As I pointed out, someone becoming insulin resistant would typically have higher BM's and higher circulating insulin with no impact on intake.

Ivor Cummings says reducing insulin levels reduces hunger never making the distinction between this being the case only if that insulin was cause a hypo. 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? Ivor blames insulin full stop and this just doesn't hold up. Abnormal release of insulin does not mean insulin is abnormal or deleterious.
 

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.
 
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