G-S,
Here’s a quote about leptin from Elzi Volk; she has worked with both Lyle MacDonald and Mauro DiPasquale:
"This hormone is the long-term circuit braker for energy balance; other hormones and neuroendocrine factors serve as short-term regulators, while some serve as both. Baseline leptin levels depend primarily on fat cell mass, since it is synthesized and secreted by the fat cells. People who are obese have relatively high plasma concentrations of leptin. However, that doesn’t mean that all this leptin is active where it needs to be the most: the hypothalamus (HT) in the brain. Leptin also has direct effects on the cells surrounding the fat cells (called autocrine/paracrine functions) too, and may be important in other body systems, such as the immune and reproduction systems. Consequently, very low leptin levels may interrupt normal functioning of these and other systems.
There are two barriers through which leptin must be actively transported to reach the HT. Those transport systems limit how much leptin from the blood reaches the HT and ultimately influences leptin’s central activity. When blood levels of leptin are high, such as in obesity, these transport systems are saturated, and less leptin reaches the brain. This is one reason for what’s called central leptin resistance. Adequate supplementation with antioxidants, such as zinc and vitamin E, may enhance transport across the blood-brain barrier. As well, obese people may benefit from increasing their intake of omega-3 essential fatty acids. Increased dosages have been demonstrated to reduce leptin levels and increase loss of body fat mass in both rodent and human subjects.
In lean individuals, the issue is not leptin resistance, but low plasma concentrations of leptin. So lean folks have to induce their body fat into synthesizing and secreting enough leptin to reach the HT. Otherwise, neuropeptide Y (NPY) and other factors will upregulate and increase the appetite. In addition, dysfunctions appear in other metabolic shifts and body systems. The metabolism slows, immune functions are suppressed, and the reproduction axes are interrupted.
While leptin levels are highly associated with body fat mass, the more important determinant is energy balance. Long-term usage of a diet that is calorically deficient will cause leptin levels to decrease. One way, and ultimately the easiest way, to prevent this is to incorporate refeed days. Depending on what the current body fat mass is, a person can integrate a day or two of higher than maintenance calories with ample carbohydrates. Insulin has a transient up-regulation effect on leptin levels. A day or two of refeeding will increase leptin levels and “reset” the metabolism. As well, assuring adequate zinc and vitamin E have been shown to increase leptin levels in humans.
The question has been asked: at what level of body fat does this switch take place? There is no single answer to that. Each individual probably has their own ‘switch’ level, depending on many factors such as age, gender, etc. A range may exist with a threshold for the average healthy population subsets, but this has not been investigated thoroughly. Plasma leptin concentrations have been presented, but not specific body fat levels. Perhaps the best method to determine when it is time to integrate reefed days is when the individual becomes chronically and extremely hungry. However, avoiding this point is optimal."
As such, G-S, I’d say that your “switch level” is 8% not only because 8% is pretty lean, but also because 8% is a major change from where you were three weeks ago. By no means am I an authority on leptin, but I’d say that it’s the culprit. Does this make sense?