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You can measure your own Insulin Resistance !

Ah! Chylomicrons.
https://en.wikipedia.org/wiki/Chylomicron
The force is strong in this one.
Even has a diagram of a partially completed Death Star.

"Chylomicrons (from the Greek chylo, meaning milky fluid, and micron, meaning small particle) are lipoprotein particles that consist of triglycerides (85–92%), phospholipids (6–12%), cholesterol (1–3%), and proteins (1–2%).[1] They transport dietary lipids from the intestines to other locations in the body. Chylomicrons are one of the five major groups of lipoproteins: chylomicrons (a.k.a. ULDL ultra low-density lipoprotein relative to surrounding water), very low-density lipoprotein, intermediate-density lipoprotein, low-density lipoprotein, high-density lipoprotein, that enable fats and cholesterol to move within the water-based solution of the bloodstream."

ULDL, eh?

So if you are full to the eyeballs on dietary lipids (as you may well be on a high fat diet) then you would expect to see Triglycerides surging through your bloodstream.

I assume that you would have to fast for a significant amount of time to be absolutely sure that you aren't absorbing any more fat from your gut.

Interesting reading http://healthyeating.sfgate.com/gastrointestinal-transit-3068.html. This suggests 5 hours to empty the stomach, 3 hours for 50% passage through the small intestine. No figure for the other 50%.
Once through to the large intestine then water absorption seems the main remaining activity.
So say 12 hours for all of a meal to pass through, and go for 16 hours for luck?

So in the first place you need to have a proper fasting blood test to rule out most of what you have recently eaten from the gut.

I've started down the route of working out how long it takes the Chylomicrons to transit the hepatic portal vein and be absorbed by the liver but the big word count is tending to maximum.

I am also considering as a side issue that most of the science is not related to people or animals who are in nutritional ketosis. I am guessing that laboratory animals fed on a high fat diet are not generally also fed on a low carbohydrate diet which limits the relevance to those on long term LCHF.

I will wait to see my next blood test, but I am sceptical that triglycerides are solely or even mainly the result of carbohydrates being metabolised to fats since they can still be there in significant quantities if you are in dietary ketosis on LCHF.

Edit: can't get rid of the IMG tag for some reason.
 
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LittleGreyCat said:
So if you are full to the eyeballs on dietary lipids (as you may well be on a high fat diet) then you would expect to see Triglycerides surging through your bloodstream.
Click to expand...
And yet for me (and most people) a LCHF diet results in much lower fasting tryglicerides compared to a high carb diet. This is well known.
 
I have seen recent studies that suggest that atheroscelerosis is not deposited cholesterol as convention thinking suggests. but is actually as a result of the deposit of the trig detrirus that traps passing cholesterol which acts to cover up the inflamed area (similar to the Bonjella ad) in other words, it is trigs that start the blockage, and the cholesterol scar tissue follows much like a blood clot for a surface wound covers the wound. So trigs value indicates risk of thrombosis especially as the HDL does not recognise it as being something to dispose of. )

As you say, your technique will assist in giving you an idea of a change in either fgl or trig value but I am not sure it is connected to IR. Latest thoughts on IR in T2D is that it is the trigs filling up the liver and pancreas fat cells, not the trigs running free in the blood. In fact, fasting or keto diet if working properly should increase blood trig levels while the liver is dumping the trigs into the blood. I would point out that this could be why your earlier trig readings were higher than recent ones on LCHF - liver dump when fasting for the test?
 
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NoCrbs4Me said:
And yet for me (and most people) a LCHF diet results in much lower fasting tryglicerides compared to a high carb diet. This is well known.
Click to expand...

Well, yes, it is well known that this happens for most people. I would be interested to see a percentage figure, though.
It is also well known that most T2s are overweight or obese on diagnosis but there are a significant minority of normal weight T2s.
So it would be interesting to know an explanation which covered the say 20% as well as the 80%.

There are a percentage of people who have elevated cholesterol on LCHF. I do not know that this indicates high insulin resistance.
 
NoCrbs4Me said:
And yet for me (and most people) a LCHF diet results in much lower fasting tryglicerides compared to a high carb diet. This is well known.
Click to expand...

So can anyone explain to me why my Trigs have always been low - as far back as my records show and long before I went low carb?

These are mine from 2009
High carb diet and overweight.
2009 = 0.6
2010 = 0.6
2011 = 0.7
2012 = 0.9
2013 no idea but ate all the wrong foods (mostly sugar based) due to cancer treatment the whole year.
January 2014 on diagnosis = 1.25 and still on cancer treatment
low carb started
2014 = 0.72 finished cancer treatment
2014 = 0.6
2014 = 0.6 no longer overweight
2015 = 0.6
very low carb started
2015 = 0.5
2016 = 0.6
2016 = 0.6
2017 = 0.6

Other than the blip at diagnosis following 12 months of drinking sugary stuff like Lucozade and putting table sugar on fruit and cereals, plus white chocolate and other nasties.

The most noticeable thing about my cholesterol is my HDL. It has increased test after test since diagnosis on low carb, and now 2.5. (was 1.4 in 2009 and 1.6 on diagnosis)
 
Chylomicrons are the bulk carriers in the freight business, these convert into VLDL which are the freight lorries on the motorways delivering to warehouses. Although they will contain trigs, these trigs are not measured by lipid panel tests. The VLDL splits into LDL which are the white van men of the lipid world doing local delivery. Once empty the LDL goes to the liver to get more trigs. etc Leftover or excess trigs are normally collected by the HDL and taken to the liver for re-cycling into LDL.

But on occasions there are accidents, and LDL become small LDL which isn't actually that useful to us and should be scrapped. But it takes a while to get rid of sLDL, and thus it becones a nuisance, causing inflammation while it rusts. It gets oxydized and beyond repair and this is the detritus I referred to, Because fat is not water soluble, it is not often seen outside its lipid bubble, so free trigs in their own in the bloodstream are failing ones,and not good news. It is these that the lipid panel picks out as trigs, not the ones safe inside an LDL package. So eating more fat will create more LDL and also higher HDL but should not appear as loose trigs.

PS ULDL is another name for chylomicron.

Here is an interesting writeup on sLDL
https://www.verywell.com/what-is-small-dense-ldl-698072
 
To counter that can I offer the following rant?
https://drmalcolmkendrick.org/2017/09/05/what-causes-heart-disease-part-xxxvi-part-thirty-six/
Specifically disagrees with:
"
Once LDL becomes oxidized, it goes directly within the inner lining (endothelium) of any artery in the body, including the carotid artery, coronary artery or the arteries that supply your legs and arms with blood.


Once there, it encourages the accumulation of inflammatory cells, such as macrophages, and platelets at the site of the vessel and promotes their adhesion to the damaged area. More macrophages, cholesterol and other lipids begin to accumulate at the site, forming a plaque that begins to grow thicker.


Over time, this can slow -- or completely restrict -- the amount of blood flow that travels to one or more areas of the body. This can result in a variety of health conditions, including coronary heart disease, peripheral vascular disease or dementia.
"
 
I'm a bit confused by your formula. When you say 'log normal' do you mean logarithm to the base e which is also called natural log and abbreviated to ln (as opposed to the normal logarithms we use which are logarithm to the base 10 and abbreviated to log)? Also you have written an asterisk, * , before the 2 which means 'multiply by 2' but you seem to have divided by 2. Did you mean to type a / (meaning divide) instead of a * which means multiply?
 
.

Dear Cherry,

About your “Insulin Resistance (IR) Tests” by its Link Title and Your Title “You can measure your own
Insulin Resistance !” as you introduce and apply here in the Diabetic Forum by the Link : http://www.diagnosisdiet.com/wp-content/uploads/2017/06/insulin-resistance-tests-rev-3-15-17.pdf

A kind of declared as Test, which physically and therefore medically regrettably cannot exist and
does not exist as “Insulin Resistance Test” according of any Profs. in Endocrinology - Diabetology
or by NIH.Gov the world reference in medicine !

At least of what I’m posting here can all been reconfirmed by any Profs. in Endocrinology - Diabetology
or by the NIH.Gov as the applied world reference in medicine or any R&D Scientists in Diabetology ! ! !

That Much About As You Mentioned By Your Manners : . . . or indeed looking at your other post - even some of the basics. That could not be further from the truth for some of us.

Personally I would feel a shame if posting something not existing as you do with this, but that
is my way and others naturally free to handle such kind of matters completely differently.

Happy Weekend To You

PS : It has been you provoked this Post as necessary for the objectivity.

-
 
I see he disagrees with the notion that LDL can enter the arterial walls, which is plausible since LDL is s large molecule. At the end he says it must be due to endothelial damage, but there is no link to a follow on discussing this, so I am in the dark as to what he reckons causes the plaques. The recent discovery of sLDL which is oxidised or damaged LDL is something he has not taken on board yet. It is much smaller than LDL per se, and is ahown in 2011 as being significant risk factor for artheriosclerosis.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3038964/

See also
https://www.hindawi.com/journals/omcl/2017/1273042/
 
You might like to read this paper https://academic.oup.com/jcem/artic...Product-of-Triglycerides-and-Glucose-a-Simple

It seems to be referring to the same formula discussed in this thread but calls it the triglyceride glucose index. The paper says, "Our results show that TyG index closely mirrors the glucose clamp technique in the assessment of insulin sensitivity, suggesting that it could be useful to recognize insulin resistance among subjects with various degrees of glucose tolerance and body weight."

You are therefore right that this is not a test of insulin resistance. However, this and other papers seem to suggest it could be used to identify people who have insulin resistance and are therefore at risk of diabetes. Whether it is useful in people with established diabetes is another matter.
 

Yes, I am not 100% convinced by all his logic chains.

However he does make a strong case for "if LDL is leaking through artery walls a sh*t load of other stuff should be doing that as well".
 
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As I got the right results I can say yes to log to the base e and yes to divide rather than multiply by 2.
LN ( log natural) is the function in Excel.
 
I kind of understand the theory but not sure I see the point once the threshold into diabetes has been crossed. Results of other tests ( BS, Hba1c etc etc) will give a good indication of improving / deteriorating levels of IR. Seems more likely to be of any clinical use prior to diagnosis
 
Just commenting on the formula rather than the theory behind it. It seems the same method in the reference by @Dark Horse appears to give results half those we get above, values around 4 rather than 8. What am I missing?
 
Mr_Pot said:
Just commenting on the formula rather than the theory behind it. It seems the same method in the reference by @Dark Horse appears to give results half those we get above, values around 4 rather than 8. What am I missing?
Click to expand...
I've read a bit more about this and found that different researchers have been writing the formula in different ways and hence getting different results:-
1) ln [glucose (mg/dl) X triglycerides (mg/dl)/2] - in this case glucose is multiplied by triglycerides then divided by 2 and then finally the natural log of that number is found - a high value is above 8
2) ln [glucose (mg/dl) X triglycerides (mg/dl)]/2 - in this case glucose is multiplied by triglycerides then the natural log of that number is found then the number is divided by 2 - a high value is above 4

https://jcbr.goums.ac.ir/article-1-22-en.pdf
 
Very useful. And a tighter range. So my 8.3 is now means I am insulin resistant still - or put another way, if over 8 pre T2D causes insulin resistance then it would suggest I am still causing insulin resistance now. So work to do.
 
It's not just me then - thanks.
 
From the various references people have provided it seems TyG index is a thing rather than the idea of one doctor as I assumed from the original post. I think @CherryAA has been criticised unfairly, apologies if that includes me.
 
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