After having given Jack's seemingly inexplicable lipid panel some thought, I think I may have figured out what occurred. Because Jack has very little body fat, he is broadcasting a fairly weak leptin signal to his hypothalamus. Under normal circumstances, this wouldn't be a problem and no red flags would be raised. However, with the introduction of a relatively small amount of fructose, I believe that Jack spiked his VLDL and thus serum triglycerides via de novo lipogenesis in the liver. Because of how little circulating leptin there is, it didn't take much in the way of triglycerides to block leptin's passage across the blood-brain barrier. Suddenly, the hypothalamus thinks that Jack's body fat has somehow plummeted and he's starving to death. The hypothalamus then upregulates de novo lipogenesis and triglycerides rise further. These triglycerides then further cement the simulated starvation as viewed by the hypothalamus. Only with an intervention like the one I described in the aforementioned post can this cycle be interrupted and VLDL/TGs be cleared from circulation.
It would seem that with regard to lowering serum triglycerides, people with more fat mass actually have an advantage due to the greater strength of their leptin signalling. It's a novel theory, anyway.