Dr. Ben Bikman

The liver has to store it.

The pancreas starts to store it.

But as I mentioned earlier, the triglycerides are not the cause of insulin resistance, but now we have the high insulin, which is an acute cause of insulin resistance and a lot of free fatty acids.

And where some of those are going to be palmitate, because palmitate is some of the stored triglycerides, you have palmitate coming out that will directly be activating TLR4, the receptor that's going to then drive ceramides to be synthesized.

And not to mention the inflammatory cytokines that are also being released from the hypertrophic fat cell at the same time, also stimulating ceramide accrual.

Thus, we end up having the perfect metabolic milieu to promote insulin resistance.

And it all started because the fat cells got too big.

Atherosclerosis, yeah.

C-reactive protein is a better predictor of heart disease than LDL cholesterol is.

And the fat cell is the main source of a protein called plasminogen activator inhibitor 1, PAI1, whose main job is to erode clots as they form.

So why is it that bigger fat cells relate so well with stroke and cardiovascular disease?

Because you are producing a protein that's inhibiting the breakdown of clots, making it just more likely that someone's going to have a stroke.

There is, yeah.

I'll just mention one just for the sake of time, which actually is linoleic acid.

So my view on seed oils is that they can contribute to insulin resistance through a secondary process.

route by influencing the dynamics of the fat cell.

Specifically, when linoleic acid is taken into the cell, one of its peroxide metabolites that it can turn into is a molecule called 4-HNE.

And 4-HNE has been shown to inhibit the fat cell's potential for hyperplasia.

thus forcing the fat cell to only go down hypertrophy.

So if there is some nutritional link that can drive fat cell storage into one versus the other, linoleic acid does have that effect.