Am J Clin Nutr. 1980 Jan;33(1):81-5.
A mathematical relationship between the fatty acid composition of the diet and that of the adipose tissue in man.
Beynen AC, Hermus RJ, Hautvast JG.
Abstract
Based on literature data, the hypothesis is advanced that in human subjects a direct mathematical relationship exists between the average fatty acid composition of the habitual diet and that of the lipid stores of subcutaneous adipose tissue. Since the half-life of adipose tissue fatty acids in man is in the order of 600 days, the fatty acid pattern of depot fat provides a qualitative measure of the fat intake over a period of 2 to 3 years. It is concluded that in long-term experimental and epidemiological nutritional surveys the adipose tissue fatty acid pattern of the subjects is a useful index of the average composition of their habitual dietary fat.
The way I see it: During lipolysis free-fatty-acids (FFAs) are being released as energy. Once energy demands are met, any excess FFA is repackaged inside VLDL and sent back to storage inside the adipocyte. Eating carbohydrates and stimulating insulin lowers lipolysis and FFAs and stimulates lipoprotein-lipase, which removes the fatty-acids from VLDL back into the adipocyte for safe-keeping.
If you are insulin-resistant, you either lack insulin production or your insulin is insufficient enough to stimulate lipoprotein-lipase and are unable to store fat inside the adipocyte, thus you accumulate it outside of the adipocytes, which is unhealthy, it that case your adipose-tissue turnover rate is accelerated, like what is seen in diabetes.
Also since fatty-acids are mobilized and released from the adipocytes by their degree of unsaturation, too much lipolysis would release a huge outpour of free-AA into the circulation, which would be harmful.
Even if someone agreed with your mechanisms, how does that provide advice to the more than 80 million Americans who are prediabetic and insulin resistant? Your advice to load up on carbs would be great for most 25 year olds and a death sentence for those 80 million people.
An insulin resistant person who loads up on carbs ends up with dangerous glucose levels, tissue damage from glycation, and very importantly they get very very fat. Insulin levels always being high signal the body to always remain in fat storage mode. That only makes the insulin resistance worse. For those 80 million people, your advice to load up on carbs is just bad advice.
You are practicing one-size-fits-all nutrition advice, and this is an area where one size does not fit all. There are many possible causes for insulin resistance. In my case, I became mercury toxic. It turns out that the insulin receptor is a di-thiol and mercury binds to it, disabling it! And it turns out that the insulin molecule that fits into that receptor is a single-thiol, so it can also be disabled by high blood mercury levels. Advising the person with that sort of insulin defect to "load up on carbs" would not be good.
Rather than trying to come up with universal theories that simply do not work with large numbers of people, the better advice would be to test, test, test and learn how your body reacts to specific types of food. This is an area where you can solve real problems empirically and with some simple application of the scientific method much better than you can by reading a textbook on fatty acid metabolism.