If high-sugar diets in childhood have long-lasting effects
Reminds me of another idea. If only we can stick with this diet for a month, it's gonna have long-lasting effects, then we can just go back to our regular diet. That's the wrong idea, isn't it.
The correct idea is flow rate. The flow rate of fat into fat tissue vs the flow rate of fat out of fat tissue. Sincce it's a flow rate, it's an on-going thing, not merely some fire-and-forget one-time permanent action with long-lasting effect. The flow rate must be acted on continuously, just like when we're trying to fill a leaky bucket.
On the other hand, since we're talking childhood, it's entirely possible to act during that period and expect long-lasting effects, as we can observe from certain deficiencies that affect growth in various ways (growth hormone deficiency for example), and then observe the effect in adulthood as shorter height, smaller organs, and smaller skeletal structure overall. Is this what's going on here?
"Other independent studies in medicine and nutrition have suggested that sugar consumption during pregnancy can cause an increase in fat cells in children," she added.
"Up to this point, no studies had explicitly explored the temporal delay between increased sugar consumption and rising obesity rates,"
That's not entirely true. We are aware of a phenomenon called insulin-induced lipohypertrophy (or lipodystrophy), where the number of fat cells increases due to long-term hyperinsulinemia. We are also aware that this particular growth results in a different type of fat tissue in some way that responds specifically to a recently developed drug (still in testing phase yet) called Adipotide, which acts on certain cells to cause apoptosis, which then causes fat cells to asphyxiate due to lack of blood and oxygen, thereby reducing overall fat tissue mass locally.
Additionally, we are aware of generational epigenetics, where first, something acts on the parent to cause some disorder, the parent then reproduces offspring and "transmits" (in quotes because it's not exactly like an infection or something, though we can't rule out infections per se) the disorder to the offspring, and where second, this offspring is also then exposed to the same primary cause which produced the disorder in the parent, thereby exacerbating the disorder further in the offspring.
The point is it's been studied, but not necessarily this new idea of temporal delay. The causality here is on-going, not delayed. This means the amplitude of the effect is proportional to the length of action, the longer the action the bigger the effect. It is also proportional to the strength of the action, the higher the insulin the bigger the effect. This is exacerbated further when we're dealing with generational epigenetics.
Finally, the idea here is about table sugar, not all sugars. So when we're looking at a substance that's part of a class of substances whose actions are similar or identical, we must also consider the whole class of substances, not merely one of. I suppose we could find this trick with other substances as well, such as derivatives (I'm thinking ergot derivatives, with pergolide and cabergoline) where we blame one (pergolide) for the benefit of another (cabergoline), typically in the context of drug patents which expire (the patent on pergolide has long expired, while the patent on cabergoline is still in effect, correct me if I'm wrong).
The point is that when we look at associations, we'll find there isn't one when looking merely at one of rather than the whole class of substances.