Study implicates fat in weight gain
 

https://medicalxpress.com/news/2018...eight-gain.html


1. We aren't mice.
2. Flies in face of human reaction to various diets.
3. My thought: Carbs trigger my eating much more than fat does. I eat fat; I stop eating. I eat processed carbs, I continue eating.

Another possible factor is the "sweet spot." Sugar doesn't just get better and better the more you add to a baked good. I'd eat more, if I ate that sort of thing, of a lightly sweetened banana bread than I would something more sickly-sweet. The increase in sugar in the Western diet isn't just about confections, you have to be careful buying things like mustard and mayo these days.

They haven't really captured everything about mice let alone humans, because there are various studies in mice--with very low omega 6 content in the diet, for instance--where fat is not particularly fattening.

There are studies showing that softer chow can be more fattening than harder chow, when eating hurts their mouth maybe mice eat less. Just softening chow with water works. Or adding water to a powdered chow can make it more pleasant. Fat can work as well as water in these cases.

And yes, I'd butter that banana bread, and no, I wouldn't expect that to turn it into health food, I'd even expect the butter to be part of the problem in that context.

Yes, this is expected. Not only are we not mice (very insightful here, I know), but the fact that when fat is combined with a SAD way of eating, it then contributes to health differently than when healthy fats are eaten with a healthy low carb approach. By low carb, I'm talking about 20g of carbs or less and no processed carbage at all. Can this differentiation be made in the mouse studies? (Rhetorical question.)

Did they do one of the mice diets at a level of carbs equivalent to that low? Don't know since it's just a summary without seeing the original journal report, but I kinda doubt it. As many here know, larger amounts of carbohydrate even if still "low carb" in common definitions should still cause enough insulin release to sweep all accompanying dietary fat off into fat storage, so yes I would expect that fat to be more fattening, not burned for energy. And even if they did test at truly low carbohydrate levels, I have no idea what effect compared to humans it would have on mice since their natural optimal diet is different from ours.

Study itself is behind a paywall so impossible to gauge how well/poorly designed it was... nor find out who provided the funding!

But, John Speakman, the head of the lab from whence the study originated, has his own Wikipedia page. I think he is most famous for his "drifty gene" theory of obesity, as opposed to the better known "thrifty gene" theory of obesity.

The thrifty gene theory posits that our genetics predispose us to eat as much as possible when food is available in order to survive times of famine and, now that food is pretty much always available, and we no longer face periods of famine, we are getting fatter.

Speakman's drifty gene theory posits that humans have a broad range of genes for weight, some predisposing to skinniness and some to fatness. When we had to be able to run to escape from predators or get eaten, people with fat genes got caught and eaten more often so their fat-predisposing genes got passed on less frequently to offspring. Now that we're not subject to getting eaten by wild animals, the fat-predisposing genes are getting passed on more and more often so, as a population, we're "drifting" towards being fatter.

My take? We pretty much ceased being subject to getting eaten by predators eons ago but, rather than a slow steady increase in population weight (as one would expect) over the past thousands of years, we have witness and veritable explosion in obesity over the past half century. Drifty-gene can't explain sudden sharp uptick right AT the point in time when processed foods became very widely available AND we were told to stop eating fats and increase our carb consumption.

I think Speakman is simply trying to make himself (and his lab) "relevant" again.

Im surprized none of us here are not petitioned for participating in a study----lots of die hard lcers for life worth studying.

Human models do exist. ANd mice are not a great model as they are seed eaters and one researcher pointed out that to get mice into ketosis, the carb level must drop severely.

The kind of info that is a waste of my time..... and just proves how behind the times too many people still are.

This is the issue and it doesn't make sense that genetic makeup alone can be the sole contributing factor, as it takes many, many generations for genes to mutate. However, recent epigenetic studies indicate that genes can be altered (expressed or not) at the cellular level due to environmental changes influencing that expression. Environment in this case includes dietary consumption. When our diets became distorted at the recommendation of the "experts" starting in the late 70s, we witnessed the power of epigenetics and the influence on physical and metabolic health due to the toxic environment of so many people following a SAD approach. Genes cannot mutate fast enough to be the cause of this, but epigenetics influencing the expression (or not) of genes at the cellular level can and the influences are carried on to offspring in future generations. I'm ascribing the "drifty gene" hypothesis to epigenetics. It's of value to term it this way, as we can all learn to reverse this dynamic by changing our dietary environment. And no, we learn nothing from mouse studies, particularly those studies where the controls and eating environment are of questionable rigor and specificity.

This study contradicts the laws of thermodynamics.