Absolutely. I suspect you’ll see an improvement over time.
Best Diet for Insulin Resistance (+ Extra Tips) • Dr Benjamin Bikman
@PaulL one can get a HOMA-IR test to measure IR on the liver. One can get an NMR which gives LP-IR for fat. I assume your muscle cells have their own IR that is not measured? Any thoughts on which we are talking about when we look at trig/HDL in this context? Thoughts?
I think trig/HDL builds all of that in.
I know there’s an insulin clamp technique… oh heck, looks like I stumbled upon a good reference:
That is a great reference. No idea why I haven’t seen it before.
AST and ALT also give that information. Interestingly, liver fat clears up in a week to ten days, when sugar and alcohol are eliminated from the diet.
I don’t know how you would measure it, except by an oral glucose tolerance test. The late Joseph Kraft identified five insulin-response patterns, only one of which is healthy. The rest indicate insulin-resistance/metabolic dysfunction/pre-diabetes, or what Dr. Kraft called “occult diabetes” and "diabetes in situ."
Thanks @PaulL! Yea, only 7 months carni after a few weeks of keto. I’ll get lab tests done again in a few months to track my progress.
Good idea! Fatty liver disease, which is basically insulin-resistance of the liver, can clear up within a couple of weeks, but reversing insulin resistance can easily take a year. You’re well on the way, though, from the sound of things. Did they test your HbA1C? I’d be interested to know the number, if you don’t mind sharing. (Don’t mind me, I’m just nosy, lol!)
HbA1c: 36 mmol/mol ( < 41 ) in Sept 2022
The test results I can access go back to 2016. It’s been between 34-36 the 6 times it’s been tested.
That’s definitely non-diabetic, and you can probably expect it to go down somewhat over time.
Thanks for the link @ctviggen it is indeed a good one.
@PaulL Here’s why I was pondering. My AST and ALT are great since keto a year ago. But as of last measurement my HOMA-IR has not changed much if at all. Meanwhile, my LP-IR has indeed halved within just the past few months and has me in a good range. Meanwhile, my trigs and hdl have not changed in this same time. So while the ratio has remained the same, my particle count and LP-IR score have changed significantly. I would have guessed that trig/hdl would measure your adipose tissue IR in particular as lower trigs would imply more pickup by adipose tissue and consequently a lower IR score for those tissues. My levels are not matching this hypothesis however (but I think they should). Back to HOMA-IR, I have lost 50 pounds, I am now quite thin and one would think that after a year of carnivore my liver IR would be close to zero. I am guessing fructose fructed up my liver good, more than just what would be evident from visceral fat therein.
To those who understand all the numbers…
My husband recently had some bloodwork done because of a high blood pressure reading. He’s not keto but lower carb than the majority of the world (because I do the cooking ) His serum trigs were 0.76 and serum HDL 2.42. The Dr was ok with this (the receptionist said he might mention cutting down on cholesterol adding foods - though he didn’t) although both numbers outside the range and only mentioned statins once in passing but by working out the ratio it seems fine to me or am I working it out wrong? UK units
I’m not sure I’m following you there. Fasting triglyceride is a measure of how much carbohydrate we are eating, since it is the fat formed from the excess glucose and distributed in chylomicrons. (I’m pretty sure I have that correct.) HDL-C is what has been picked up and is being transported back to the liver to be broken down and recycled. How that works to measure the adipocytes’ insulin resistance is not clear to me.
Liver insulin resistance is related to how much liver fat we have, and that gets cleared rapidly, as soon as our intake of fructose/ethanol/branched-chain amino acids drops low enough. In one study, children’s liver enzymes (AST and ALT) normalised within ten days after their fructose intake was eliminated. Fortunately, visceral fat is the first to be dealt with, apparently; it’s the sub-cutaneous fat we all struggle with.
That HDL number is a bit on the high side, but assuming those are the correct numbers, then his ratio of triglyceride to HDL (0.314) is excellent and indicates minimal cardiovascular risk.
If your husband were to have an NMR analysis done of his LDL, it would definitely show the healthy Pattern A, another sign of minimal cardiovascular risk. So statins are really contra-indicated at this point, so far as I understand it.
Paul - Thanks for the reply. That is definitely how I understood it. But how does the HDL number become too high.
Has it not now been proved that dietary cholesterol has little to do with serum cholesterol? And if this is so, then why are some peoples cholesterol levels higher than others if the body is only making as much as is needed?
That was conclusively shown in the 1950’s, by none other than Ancel Keys himself.
I don’t think this is known, although Dave Feldman has some interesting ideas about it, which you might want to read about at www.cholesterolcode.com.
But I’ve lived through several iterations of the diet-heart hypothesis, and each time the evidence has turned unsatisfactory, the hypothesis has been refined and narrowed. From what I’ve learned on these forums, and elsewhere, it appears that the idea that cholesterol is the cause of cardiovascular disease is not actually supported by the data, which tend to suggest otherwise. At best, we can say that probably high cholesterol and cardiovascular disease share some common cause, so that cholesterol levels can serve as a marker for other problems.
In a number of studies (including one designed by Keys, who had his name removed from the study when it didn’t yield the results he wanted to see), elevated cholesterol has actually been shown to have a protective effect. These are epidemiological studies, of course, so we have to be careful about drawing inferences from them, but the fact that high LDL has been observed to associate with less cardiovascular disease should give us pause for thought.
Cargo left on the ship (as Feldman would say) is a high measure of trigs. This is a sign of a lack of pickup of the trigs for energy use by the cells, which is what happens with diabetics and Insulin Resistance - both with carbs and fats. I eat zero carbs and my trigs have not changed, while my LP-IR score has changed drastically. These statements are at some odds with each other.
My AST and ALT scores changed quickly when I started Keto (as you note they should have). My HOMA-IR score however has not changed despite wonderful AST and ALT markers and very low to no visceral fat within my liver. Again, these statement are not congruous and lead to my queries.
Well, I’m not sure what HOMA-IR has to do with hepatic insulin-resistance, specifically. I was under the impression that it is a more general index. I have no idea how it’s calculated, to be sure. Do you happen to know?
Given that your triglycerides have not gone down on a ketogenic diet, then either they are as low as they need to be already, or you have some problem that you might or might not need to address. What is your ratio of triglycerides over HDL? Apparently, hypertriglyceridaemia, unlike hypercholesterolaemia, can be dangerous. What are your other lipid markers like? And how are your HbA1C and inflammatory markers (WBC, CRP, ferritin, and the like). I am not familiar with LP-IR. What is it, and how is it calculated?
I didn’t realise the cholesterol myth was debunked that far back though I knew about his study with fat. It’s quite shocking that everything takes so long.
In the UK doctors have just been given new guidelines which could lead to an extra 15 million people being offered statins.
I stupidly had a conversation with my friend about what’s tested on the standard lipid panel blood test and the affects from eating dietary saturated fat in respect to heart disease, lipid panel numbers, and about Ancel Keys etc. It was a general conversation, not technical, b/c I’m no scientist and I don’t pretend to understand many of the details. Her response? All fringe fake science b/c it’s not what the bulk of mainstream science/medicine says. /sigh!
Your friend is right. To some extent, this is fringe science, because it contradicts the standard dogma.
But then, the germ theory of disease was once fringe science, and they hounded Semmelweis to his death for daring to suggest that doctors should wash their hands between patients. The Australian researchers who discovered that stomach ulcers were caused by Helicobacter pylori, and not by excess stomach acid, worked for years to make their discovery known, and there is still doubt about their discovery even today.
In cases where the standard dogma is entrenched, the fact that the new hypothesis has excellent data on its side is, alas, irrelevant. When commercial forces have aligned around the standard dogma, change becomes even more difficult.
For example, if you were the CEO of a pharmaceutical company that made a statin, would you want to know about data showing that cholesterol is not the cause of cardiovascular disease? As Upton Sinclair once put it, “It is difficult to get a man to understand something, when his salary depends on his not understanding it.”
in the UK it’s a very basic testing that’s done on a standard lipid panel test. Certainly no doctor would voluntarily suggest looking at particle sizes and types.
I was also very disappointed when my husband went to the doctors with high blood pressure that the first thing they did was give a prescription (which he got but never took). How about discussing why it was high
Apparently there’s a new HDL method since 2018 and LDL is just calculated. I’ve also just noticed on the form that it actually says “consider statin”
Love that Upton Sinclair quote.