Quasi-rhetorical questions re: carbs, leptin, and other

January 24, 2009

Or: I’m in ur experimunts, cnfoundin ur vriables

Weirdly, I’ve been amenorrheic since August, not long after I took up intermittent fasting. TMI, no doubt, but it’s my blog, and I’ll whine if I want to.

What is weird about this is that my body fat percentage is still pretty normal, even high (somewhere between 17-20%), and these days I spend only about 2-3 hours of the week resistance and interval training (just in case overexercising caused the problem).

My latest hypothesis about the cause (a fasting-precipitated drop in leptin, followed by continuing insufficient leptin) prompted what was probably an ill-advised (although at least premeditated) binge on simple carbs (honey, cereal, bread) about two weeks ago.

It hurt. It hurt with pain, a racing heartbeat, rapid weight gain (mostly fat, some inflammation), and reactive skin. It has taken the past two weeks of careful eating and exercise to feel, physically, more like myself. Yikes.

However, I’m still amenorrheic. Either the hypothesis is a bust or the sugar didn’t boost leptin high enough or long enough. I don’t think I can bear going through that again (heart palpitations? scary, you guys), so I decided to just add more fruit to my meals (mid-day probably best). I’ve also started eating breakfast more often, moving from a 15 hour fast 5x a week to a once weekly 20 hour fast, if that.

Quasi-rhetorical questions include:

Is glycogen actually beneficial for muscle cells? Harmful? Neither? Both in different situations?

Chronically elevated insulin would appear to be harmful. Therefore, insulin resistance would appear to be harmful. But are (very) occasional insulin surges in the absence of fat harmful in the long term (as is marathon running, with all that oxidation and stress)?

It seems like Gary Taubes thinks leptin resistance is a marker of metabolic syndrome, but not a cause. In contrast, there is an actual, physical mechanism by which insulin locks fat into cells. Fair enough. But also: Lyle McDonald seems to indicate that leptin does play a role (hence my admittedly fail-tastic self experimentation) in that it sends a signal to the brain as to the body’s state of energy availability. According to McDonald, Leptin scales with 1. body fat percentage, and 2. carbohydrate metabolism within fat cells. Falling or low leptin or leptin resistance registers as starvation and prompts hormonal adaptations that allow the body to conserve energy. In my understanding (or lack thereof), when there is excess energy (sugar) insulin traps the fat inside fat cells, causing fat gain. When there is an energy deficit, declining levels of leptin prompt hormonal changes that protect against fat loss. Leptin resistance causes (mal)adaptations as well.

If, as McDonald says, “Leptin and insulin also both change with changing food intake; leptin levels can drop significantly within a few days of dieting even with no change in body fat levels. Insulin changes meal to meal,” this might have implications for both carb ingestion and intermittent fasting, and the trick would be to find the optimal time tables for each. So, insulin may be the primary mechanism for obesity, and lepin may be a secondary cause (in that it stops the overweight from losing the fat they’ve gained).

No doubt the real story is infinitely more complex, but it’s intriguing so far.

Where would that leave the oft-referenced Paleo people? A moot issue, possibly, as for them energy supply was what it was – either high or low – and if it was intermittently low enough to cause starvation-level drops in leptin, it was never chronically crazy high enough to induce leptin resistance, at least long-term. And if it was generally high (as hunter gatherers tended to be a well nourished lot), well, even the most indolent of hunter gatherers…er…hunted (intermittently?) and gathered (steadily?), and shared their meals with their tribe (probably damn near always). Pure conjecture, of course…

Another question: When does the taste of sweet (fructose containing sugars) track, in nature, with dietary fat? Never? Rarely? Seasonally? My wish list includes a time machine and a microscope powerful enough to show atoms and molecules in action in a human being. Dream big, I say.