Paleolithic Ketogenic Diet

#231

I think that is an important point. Keto does not cure cancer. If you want the duck hunters to appear on mass to hunt the quacks, just go and say that outside this forum. The PKD diet when strictly controlled down to the seasonings has been shown to stop the progression of cancer as long as the patient maintains the diet. The cool bit about that is that it does offer an opportunity to combine that progression halt with a surgical option.

In an interview (with Dr. Saladino) Dr. Clemens did concede that some people try combining PKD with other modalities such as ketone supplementation, hyperbaric oxygen therapy, chemotherapy and radiotherapy. She termed it ‘defensive medicine’. And pretty much said it did not work.

I’m just reiterating your points @Ilana_Rose that with serious cancer and with early diagnosis Type 1 diabetes Zsofia Clemens makes it clear that the patient pretty much only has one chance and can’t come back to PKD expecting miracles if they go and try other things (which is human nature).

(mole person) #233

As far as I can tell, there’s absolutely no evidence that ketone suplimentation is an effective treatment. In another thread recently we were discussing the science supporting the idea that ketones supplementation could help with cancer repression and after reading the paper I concluded there was zero evidence for this, it was just bad science.

#234

Yes, probably, ketone supplements alone are not. I’m not too knowledgeable on the subject.

I am conflating the work of Dom D’Agostino with Prof Seyfried and using the ketone supplements to potentiate the hyperbaric oxygen therapy. The high blood ketones negate the risk of seizures while inside the treatment unit.

The other idea I’m trying to recall is that using ketones to fuel healthy normal tissue while trying to get the blood glucose down as far as possible to deprive some specific glucose dependent cancer types (not all are).

(mole person) #235

To be honest Paleo-Medicina has my normally strong quack detection system in a bit of a muddle. The evidence is murky, and they are clearly approaching this as clinicians and so can only really be guessing at causes and such. But, I think they are honest agents and their approach is being supported by a fair number of sick people who going carnivore,and approaching PM’s diet, experience remission of serious illness.

Also, quacks normally offer easy answers. This is about as far from that as is imaginable. Basically, for some people like the cancer and T1 diabetics, it’s “do this insanely difficult and restrictive diet and never, ever stop or cheat and you will have remission.”

(mole person) #236

Yes, Dr. Seyfreid wrote a paper on this. But I read it and was horrified at the conclusions he came to from the incredibly weak data. Basically, I’ll never trust a thing that I hear from him after that experience.

I’ll dig up that thread for you that contains the link to the paper and a bit of my analysis of it.

(mole person) #237

I haven’t found the one that I’m thinking about yet. But here is my analysis of a paper of Dom D’Agostino which I also found very lacking in actual evidence supporting what he claims as the conclusions.

Edit: Here it is:

I got my articles confused. The paper that made me distrust Seyfried was the one about the value of the GKI measure.

And here is my analysis:

https://www.ketogenicforums.com/t/don-quixote-tilts-at-metabolic-windmills/79146/397?u=ilana_rose

#238

Conclusions
The GKIC is a simple tool that can help monitor the efficacy of metabolic therapy in preclinical animal models and in clinical trials for malignant brain cancer and possibly other cancers that express aerobic fermentation.

GKIC = Glucose Ketone Index Calculator

  • Simple tool - Y
  • Help monitor metabolic therapy - Y
  • In models and trial - Y they did that
  • For malignant brain cancers - Y in mice, 2 children and a woman
  • The word ‘possibly’ signifies a possibility and maybe shouldn’t appear in a scientific paper conclusion but does indicate future areas of research.

Seems OK to me. I’ll remain interested to see what they find. It’s been 4 years since that paper. I wonder how the case series has developed?

…

Found this 2018 feasibility study for application of a modified ketogenic diet (MKD) for treatment of some brain cancers on the National Health Service (UK). Spoiler: application of the ketogenic diet in the socialised medicine system is feasible. 6 adult human case studies involved.

https://www.tandfonline.com/doi/full/10.1080/01635581.2018.1460677

(mole person) #239

How have they demonstrated this? Where is the implied benifit over glucose and ketones taken seperately, which is the entire point?

Without the ability of statistical analysis this shows nothing. What do you actually see it demonstrating?

You can model all sorts of things, it doesn’t make it real. You need data. They have no usable human data. What they show is two cases with a GKI associated, no possibility of analysis. The third had urine ketones taken so I don’t even begin to understand how they are getting a GKI from that since it’s not representative of actual blood levels at all.

Basically, in this paper they fail to show any human value to GKI.

#240

It is that important step between mouse models to application of a hypothesis in human case studies.

I don’t understand the exact point being made. The benefit is the use of a ratio that delineates a proposed therapeutic level. It’s a starting point. Ratios are methods of combining data measurements in clinically meaningful ways. Like Triglycerides to HDL being an indicator of metabolic syndrome. The benefit is in the effect of one factor counterbalancing the other.

To know what data to collect an experimenter needs a hypothesis. I agree it does not generate usable human data and statistical analysis as it is not numerically strong. But it is at that zone where hypothesis has been generated from the mouse studies and early observations and some data collection in human case studies. It is early work and maybe should not be condemned so readily and recognised as such (as early mathematical tool development work).

The people with cancer (including those on the forums) are seeking hope in their cancer treatment and that’s where the wicket gets sticky because it does transfer to real people and life and death situations.
But that is a complicated social situation from not fully understanding the scientific method. It’s not a reflection of the progression of the science. It may even progress the science to the data analysis level.

Yes. Because the paper is about the creation and the development of a mathematical tool not it’s widespread application. They are just showing how the proposed tool may work, for its future application.

The ‘Glucose Ketone Index’ (GKI) was created to track the zone of metabolic management for brain tumor management.

People who are applying the tool are getting ahead of the science but may be providing the data and anecdotes that helps prove the usefulness of the tool.

(mole person) #241

It’s been nearly a month since I read the paper. I was pretty appalled when I did so but need to reread it to recall exactly what was so bad. My memory suggests that it was the disconnect between hypothesis and conclusion. I will reread the paper later today and try to elucidate more clearly why I found it an example of the worst sort of science.

(mole person) #242

Ok, so here is why I thought it so bad. They state in the introduction that they wanted to develop this tool for the following reason:

That the ratio of blood ketones to blood glucose will be a more stable biomarker then glucose and ketones separately. So you’d expect in their analysis that they’d actually show this increased value. But they never do. And they have the mouse data, so there is no reason for them not to calculate it. My feeling is that ketone level alone does the trick and makes their GKI irrelevant.

But this is what angered me.

“We present evidence showing that the GKI can predict success for brain cancer management in humans and mice using metabolic therapies that lower blood glucose and elevate blood ketone levels.”

*My emphasis.

They did nothing of the sort and it’s damn irresponsible of them to say that they have.

#243

@FrankoBear I really liked the BioHackers Lab interview with Zsofia too. I’ve not listened to the other one yet. Hope to do that this weekend, thanks.

#244

It’s great to discuss and get thinking.

I wonder about the benefit of blood insulin levels compared to ketones, and whether that ratio may be an improvement? But that is hampered by non-insulin dependent cell membrane glucose transporters.

The thought came because we often use blood glucose in our ketogenic diet as a proxy marker for insulin secretion (and also for guessing at ketosis, if ketones aren’t measured).

The PKD monitoring is a scenario where the Glucose:Ketone Index may have its best application? (Outside of the sensitive cancer conversation).

(Justin Jordan) #245

My inner cynic notes that this actually offers them an out - if someone has their cancer progress or type 1 diabetes continue, they can just say they’re not following the protocol. Which may be true, because, well, it’s difficult. So there’s lot of room for deflection there.

But extraordinary claims require extraordinary evidence. Or, really, any evidence. Not just claims.

#246

So I looked at the results again.

Both individuals were placed on a ketogenic diet for eight weeks. During the 8-week treatment period, GKI dropped from about 27.5 to about 0.7 – 1.1 in the patients. The patient with the anaplastic astrocytoma, who did not have a response to prior chemotherapy, had a 21.7% reduction in fluorodeoxyglucose uptake at the tumor site (no chemotherapy during diet). The patient with the cerebellar astrocytoma received standard chemotherapy concomitant with the ketogenic diet. Fluorodeoxyglucose uptake at the tumor site in this patient was reduced by 21.8%. Quality of life was markedly improved in both children after initiation of the KD [27].

They show a drop in the GKI in both patients using a ketogenic diet. Both patients have brain tumours. They demonstrate a measurable reduction difference in glucose (labelled) uptake at the tumour site. They state with references a clinical observation, “Quality of life was markedly improved in both children after initiation of the KD“ (KD = ketogenic diet). Within its context and limits this seems successful. They applied the GKI tool in the monitoring.

I didn’t dive into the mouse data as the human case studies have more relevance, I think.

Are those limited results evidence enough for the claim?

I wrote all this then understanding dawned on me. I am slow on the uptake. Thanks for putting up with me ponderously working through it.

I understand we are applying at the root of the discussion a different metric for evidence and that this observational evidence (n=1 x 2) is not the same, nor as good quality, as statistically significant evidence. But is it adequate?

(mole person) #247

Yes, my thoughts have travelled this route as well. They claim that they have tests for compliance and can tell when someone is not following the diet properly but I’m not clear on what these tests are or how certain it is that a failure on the test necessarily reflects inadequate adherence.

On the other hand their diet is essentially a medical prescription. You can’t expect a treatment to work with half compliance.

They are not without evidence. They are clinicians and hence not doing science but treating patients. But they regularly publish case reports and have had some incredible successes that are shocking enough to make ones interest perk up at this treatment.

(mole person) #248

Of course they do. Both patients had reduced glucose and increased ketones. It’s the same with all the mouse data. But we already knew that decreased glucose and increased ketones correlate with improved cancer outcomes. And as long as glucose is down and ketones are up GKI goes down by definition. So they aren’t showing anything interesting at all unless they demonstrate that GKI is a better predictor of reducing tumor load. This is what they claim in the introduction. But they never even attempt to demonstrate it, and then they claim that there is evidence that GKI can predict cancer load in humans.

Do you see what I’m saying? They’ve shown precisely nothing new.

#249

Thank you Flub. I am still PKD. Nausea is done. I am very sensitive to black tea so have cut down to 2 c per day. Today is the first day of eating 400 g total meat and fat. I did not have my liver today.

I think I am going to be hungry, but time will tell.

I had 170 g ground beef (80/20) with 30 g tallow, and then 125 g chicken with 60 g pork fat. I am handling the rendered fat better.

My :poop: is a bit better (every couple of days), and I am hoping that my IBS symptoms will go away.

#250

Thank you ReneeRC! I try to have 40-50 g liver every day. I eat it frozen, raw in small chunks.

Flub, I LOVE brain. I can eat it every day, and in Australia I can buy 400 g for $4.00. So I eat half of that in one meal which means a meal of brain and fat is $2.

#251