Back in May of 2007, I began a serious – and successful – weight loss effort. I was ~220 lbs (5’8″), and was, well, fat. I read all about glucose, insulin, glycemic index, and other topics, and after implementing what I learned, I lost ~60 lbs in 6 months.
I’m now at – 6 years later – about the same level of body fat as I was when I finished that weight loss effort: ~10% body fat. Which is pretty good. But for most of those 6 years, I have made serious efforts at becoming even leaner. My goal has been to maintain 6-8% body fat, and it seems no matter what I try – intermittent fasting, calorie restriction, more exercise, fasting cardio, HIIT, carb cycling, low carb, treadmill desk, fasting sprinting – I can’t seem to achieve that 6-8% body fat range. My fasting insulin has dropped by ~1/2 from immediately after my weight loss, which is great for long term health. My fasting glucose is usually 70-80, which is great. But I can’t seem to figure out how to get my body fat down.
A close friend of mine – also with an intense interest in reducing body fat – recently found a very interesting article about leptin. Now, I know the title of this post mentions glycogen – I’ll get there…
Here’s the link to this leptin article: http://www.ncbi.nlm.nih.gov/pubmed/23010500
For those of you knowledgeable about leptin, note the title: skeletal muscle releases leptin in vivo. Maybe this isn’t news to you (after some digging, I found there were earlier papers which suggested the same), but in the leptin research space, this is significant news. It has been thought for some time that leptin was mainly (if not exclusively) secreted from fat cells – adipocytes. That’s why leptin has been called an “adipokine”. It has been observed to regulate the body’s metabolic rate, so much so that injections of it have been tested and used as a treatment for obesity (Wikipedia article on leptin).
But in the paper I linked above, they measured (assuming one can trust these numbers, given laboratory limitations) muscle tissue to secrete 62.5% of the leptin as fat tissue did, per 100 g of tissue. From the abstract:
During saline infusion the adipose tissue release averaged 0.8 ± 0.3 ng min(-1) 100g tissue(-1) whereas skeletal muscle release was 0.5 ± 0.1 ng min(-1) 100g tissue(-1). In young healthy humans, skeletal muscle contribution to whole body leptin production could be substantial given the greater mass of muscle compared to fat.
Now: I find the implications of this very interesting. Consider the following observations:
- Leptin is generally observed to correlate with body fatness, e.g. http://www.ncbi.nlm.nih.gov/pubmed/9497796:
In this study we investigated the relationship between serum leptin levels and body fat distribution in a random sample of women of widely ranging age and body mass index…..Leptin levels…..were not significantly correlated with age, but were significantly positively correlated (P < 0.001) with most anthropometric measures except waist-to-hip circumference ratio. The strongest correlations were with total grams of body fat and percentage body fat (r = 0.68 and 0.76 respectively, P < 0.001).
- In some contrast to the above point, leptin is known to drop quite quickly after short term calorie restriction and/or fasting, much more than any short-term fat loss would account for. For example, an excerpt from http://www.ncbi.nlm.nih.gov/pubmed/11502809:
The purpose of this study was to evaluate the effect of short-term fasting on bound and free plasma leptin concentrations and leptin binding capacity…..in lean and obese women. Six lean…..and 6 abdominally obese…..women were studied after 14 h and 22 h of fasting…..These data demonstrate that both free and bound fractions of leptin in plasma decrease quickly in response to energy restriction, but the decline is blunted in abdominally obese compared with lean women.
- Carbohydrate feeding has been consistently observed to increase circulating leptin levels, e.g. http://www.ncbi.nlm.nih.gov/pubmed/10567012:
To assess the impact of the macronutrient content of a meal on the postprandial leptin response and its relationship with postprandial satiety, 22 young healthy subjects (11 men and 11 women) were given, in a randomized order, an isoenergetic meal [carbohydrate (81%) or fat (79%)] or remained fasting. Blood sampling and hunger and satiety scores were collected hourly during 9 h after the meal. Spontaneous intake was measured at a buffet meal at 9 h postprandially. In both genders, leptin response was higher after the carbohydrate meal than after the fat meal and while fasting. (Emphasis added)
This brings me to my recent epiphany, inspired by a question:
“What, along with leptin, decreases with fasting, and contributes to leptin secretion?”
The answer? Carbohydrate (in the form of glycogen)!
I have more to describe on this epiphany. In Part 2, I’ll describe glycogen metabolism, and how I plan to implement my knowledge of it to optimize for further fat loss. This discussion will also relate to intermittent fasting, carb cycling, and fasted cardio.
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