Skinny fat guy pre-T2DM Keto Woe, high unsut. fats

(Rossi Luo) #8

I had the same thought like yours when I saw my LDL level after 6 months of keto diet. My thought was to use unsaturated fat to replace saturated fat, for example, eating fatty fish, avocado, olive oil. But after reading lots of different studies on the LDL things, I chose to believe that high LDL levels are not blamed for cardiovascular disease.
Actually, my uncle (60) just had a cardiovascular event month ago, he just fell down and couldn’t talk, and his right or left arm couldn’t move. But his LDL level was in the normal range after being sent to the hospital, but his trig was quite bad.

(Peter - Don't Fear the Fat ) #9

What might be more appropriate for my Keto Diet? For the first time I’m looking at my figures!
(Sorry to hijack thread)
Triglycerides 1.8 pre keto
HDL was 1.23 pre keto

(Bacon is a many-splendoured thing) #10

What is an appropriate measure to indicate cardiovascular risk? The ratio of triglycerides to HDL. For example, your pre-keto ratio is 1.8 ÷ 1.23 = 1.43, which is high. Ideally, you want it under 0.9. Eating a low-carb, high-fat diet rich in saturated and mono-unsaturated fats will help you achieve that goal. A high triglyceride level is a sign of excessive carbohydrate intake, nothing to do with fat.

And for the record, if your ratio of triglycerides to HDL is below 0.9, you don’t have to worry about whatever your LDL decides to do.

(Robin) #11

I’m always glad when @PaulL answers these questions. He knows numbers and the science. I just follow along. la la la…

(Jennifer M Worth) #12

If you weren’t a little hesitant I would be surprised. A surgeon told me to eat keto and I can honestly say I never would’ve considered it otherwise. Hesitation is a form of wisdom imo. Keep researching and you’ll figure it out.

(Peter - Don't Fear the Fat ) #13

I shall follow too … though I’m looking forward to my next blood test

#14

Thanx Paul. But my Apo b is also high. Is that worrisome?

(Bacon is a many-splendoured thing) #15

It depends more on your diet than the fact that you produce more ApoB.

I’m old enough to have seen the concern move from fat to no, it’s saturated fat, to no, it’s your cholesterol level, to no, it’s your LDL cholesterol level, to no, it’s the particle size/count, to no, it’s the oxidised particles or this or that bad particle.

The idea that fat/cholesterol intake/level causes heart disease was pushed in the 1960’s for reasons of economics (the AHA had to justify why they supported Crisco oil) and ego (Ancel Keys), and enough people who believed the idea got into positions of power to make it standard dogma. And they threaten people who challenge the dogma, even though there is actually plenty of evidence to the effect that cholesterol and lipoproteins don’t cause heart disease.

At most, they are affected by the same causal factors and can serve as markers of disease. But manipulating the marker usually leaves the root cause unaddressed. If we are right and hyperinsulinaemia is the root cause, then addressing the insulin level by changing diet will improve both our cardiovascular health and our lipid numbers. Simply manipulating cholesterol levels with drugs does nothing to lower the hyperinsulinaemia that is the real problem.

(Michael) #16

Do you think that higher ApoB is a concern as compared to lower ApoB in the presence of 1) high trig 2) high inflammation 3)hyper insulinemia or 4) endothelial damage and therefore is the reason studies on SAD populations reveal (and revel) higher ApoB is a problem, while the LMHR directly contradicts the higher AppB notion due to the lack of instigating factors? If so, we may be agreement.

I also like to think of ldl as over reacting to endothelial damage when the damage is persistent and the higher concentration of ApoB leads to this over reaction. Without the insults to the lining there is no over reaction, almost like an allergic reaction.

Of course here is the rub, what if you low carb now, but you metabolism is very damaged and insulin resistance causes hyperinsulinemia despite low carb, and you , like me are an ApoB hyper-responder. Unfortunately, I think the study on IR LMHR people will not happen in time for me, still decade away I would think.

(Bacon is a many-splendoured thing) #17

The hyperinsulinaemia is what causes the high triglycerides, inflammation, and arterial damage. It may do something to your ApoB, as well; I don’t know. But lower the insulin by eating a much smaller quantity of carbohydrate, and the triglycerides and inflammation will certainly decrease, and you will be giving your arteries a chance to heal from the damage.

There is no evidence to show that elevated LDL in lean-mass hyper-responders is either beneficial or harmful (though, looking at other studies, it is possible they might benefit from their high LDL). David Ludwig has just published a paper asserting that it is clearly not harmful, but I haven’t looked at it yet. Dave Feldman is recruiting for a study of lean-mass hyper-responders to see what gives with the high LDL level. However, while there are more hyper-responders out there than anyone guessed before Dave started collecting data, it is still true that most people’s LDL goes down, not up, on keto.

In that case, your lowered carb intake, if sufficiently low for your degree of insulin-resistance, will stop triggering hyperinsulinaemia, allow your body to get into ketosis, and permit it to start healing all the damage. Inflammation comes down fairly quickly, as do blood pressure and heart rate, but reversing metabolic dysfunction/insulin-resistance takes a year or two.

It’s the carbohydrate intake that triggers the major portion of our insulin response. Protein in the absence of carbohydrate triggers a matching glucagon response, so that the insulin/glucagon ratio remains low. And fat never triggers more than a negligible insulin response, which is why we want it as our main source of energy.

The point is that elevating serum glucose by eating a great deal of carbohydrate (as the government tells us we should), is what causes insulin resistance. In the absence of that kind of carb intake, insulin has no reason to rise all that much, though it takes a long time before someone might safely be able to eat a bit of extra carbohydrate.

Alfred Pennington wrote up a number of cases of du Pont employees he helped to lost significant amounts of fat on a low-carbohydrate, high-fat diet, and one of those patients was an executive who normalised his weight, but who would start to regain if he ate a single extra apple. I suspect that today, we would consider that guy highly insulin-resistant. It would certainly have been interesting to study him further and see if he later on became able to tolerate a bit more carbohydrate.

(Alec) #18

And the roundabout is yet to stop…

(Bacon is a many-splendoured thing) #19

Especially if there’s a drug they can sell us. As Richard likes to say, “Follow the money.”

(Alec) #20

But it does make the drug companies rather rich… which is the point, right? :joy::joy::joy::man_facepalming:

JINX!

If only there was a way to reduce the hyperinsulinemia…. Oh, wait….

(Bacon is a many-splendoured thing) #21

I don’t know what the situation is in Oz, but here in the U.S., all the pharmaceutical companies either own health insurance companies or are owned by a health insurance company. And the big chain chemists/pharmacies are in there, too, either as owners or subsidiaries. It’s completely incestuous.

(Alec) #22

Ah, I didn’t know that. Well, that explains one of the biggest mysteries around keto and low carb for me… why on earth are the insurance companies not funding research to make people healthier? Surely it is in their interests that we are healthy… but apparently not.

(Bacon is a many-splendoured thing) #23

Nope.

(Peter - Don't Fear the Fat ) #24

Sorry, I’m wandering off again. I’ve seen this point a few times and it’s bothering my understanding of Fat to Protein ratio!
Please point me in the direction of an appropriate thread (or explanation)
My beef steak (only 5g/20g) plus butter and cream etc … I’m still not getting enough fat. :man_shrugging:
My terrible lack of newbie understanding again :scream:

(Michael) #25

Bit of a long read (and I am biased to the author) but here GNG, protein and blood glucose re-visited

(Bacon is a many-splendoured thing) #26

As Benjamin Bikman explains it, the metabolic state of the body is regulated by two key hormones: glucagon and insulin. They work together to determine whether we are in fat-burning or fat-storing mode. So the key to our metabolic state is not actually insulin by itself, but its ratio to glucagon. Glucagon is what stimulates ketogenesis by the liver, insulin inhibits ketogenesis and tells the body to metabolise glucose instead, and to store any excess as fat. Both hormones are made in the pancreas, in the Islets of Langerhans, glucagon in the α-cells, insulin in the β-cells.

Her e is a video by Prof. Bikman, discussing how the two hormones work together:

#27

There is such a drug…anounced UK this week.

15% weight loss.

(Apologies- I didn’t read whole thread.)