Craig had some great questions that the answers for may benefit readers:
Interesting post. Some thoughts….
I tried intermittent fasting of the 16:8 variety, for about 3 months. I had lots of fat to lose. I did drop maybe 3-4 lbs initially, and then nothing. Perhaps it works for some people as a weight loss strategy, but there are others for whom ad libitum eating outside the fasting period will overwhelm everything else.
Three months is, simply, too short a period of time to see the full effect. Again, I’ve been doing this for years, and while I did lose fat initially (to the tune of ~5 pounds), the great value has been in the ease of weight maintenance, the metabolic profile that it has provided me, and the volume of food I can consume in the eating window.
The fasting literature is interesting in this way: for some fasting doesn’t make them hungry, but eating a little bit does. I also know from experience that the early days/months of fasting did result in psychologically-mediated compensatory overeating. However, when I understood that my muscles weren’t going to fall off, I stopped that behavior.
Of course, you can still shove thousands of calories of junk in an 8 hour window, but that’s not a failing of the structure. That’s your shitty habits. 😉
Regarding Longo’s protocol: I can’t speak to the cellular level metabolic effects, but for someone with a pleasure eating problem, a 5 day stretch of low calorie ketogenic dieting which subsequently permits ad libitum eating for 25 days doesn’t seem likely to produce a net reduction in calories.
Well it has in the studies that Longo has performed. It also has good adherence. That said, these individuals were not already lean (though not morbidly obese either).
Further, and the point of the post, it wasn’t about fat loss per se, but rather about the metabolic profile modifications that are conducive to improved health outcomes with regards to cancer, diabetes, etc. The mention of the two different diet trials was specifically to highlight the blood chem changes from different fasting structures, suggesting that the “magic” is in the fasting+refeeding, whether you do it acutely or chronically (or both).
Regarding cancer: it seems that certain kinds of diets or eating patterns can, in the the short run, slow the growth of a tumor. However, it is an extrapolation to go from that kind of intervention with an already ill person to the conclusion that such strategies will prevent cancer. I saw a recent study which suggested that 2/3rds of all cancers are the result of random mutations. How much will intermittent fasting, or ketogenic fasts, impact that roll of the dice?
Given the above, it’s important to note that I am in no way suggesting that this is a panacea. In my case, I have family history so the cost of going hungry has a much higher potentially upside.
What I’m attempting to modulate is largely IGF-1, as that’s the derangement seen in Laron’s Syndrome. It is suggested that the IGF-1 derangement found in these individuals is the root of their having almost zero rates of cancer or diabetes (read more here). This is why I noted that both 25:5 and “lean gains” style eating result in low IGF-1, with the latter having high protein, high carbs, and muscular individuals in that particular trial. They even gained muscle, so the reduction in IGF-1 was not a negative insofar as muscle tissue was concerned.
If there is any “extra” benefit that can be explained from the “cancer as a metabolic disease” perspective, great.
Finally: You seem to be suggest that reducing body fat below 15% (for a male) will likely mean sacrificing lean muscle mass, which is generally not a good thing. Is that a correct interpretation? I’ve had my suspicions for a while that getting really ripped (as in Clarence Bass lean) might be mostly for aesthetics, with no real upside in terms of health.
Great question for clarification! Reducing below 15% requires a smarter strategy, where things like calories, macronutrients, and refeeds matter a great deal more. That’s not to say that living below a given level for certain individuals is muscle wasting on its face: clearly it wasn’t for Clarence.
Rather, I was noting that using the low protein/low carb fasting mimicking diet as an intervention might not be the best approach if you are already lean (or <15% body fat, male). Put another way, if you can get the decreased IGF-1 outcome (And the metabolic extras) while also ensuring that you don’t waste your hard-earned lean mass (because being weak and frail is no way to go through aging), wouldn’t that be a better option?
Skyler Tanner 
Skyler,
Glad that you found my questions a useful starting point for another interesting blog post.
In your reply you mention Laron’s syndrome as one source of information about the potential value of lower IGF-1. Unfortunately, having no IGF-1 (as in Laron’s syndrome) has big downsides; it is a significance disease that most Doctors would recommend treating with IGF-1 injections. So I’m curious about how much difference there is between “normal” and “low by IF” levels of IGF-1, and how do those numbers compare to zero? Is there a threshold above which you need to stay?
Also, in reading about this a year or two ago, I seem to recall that IGF-1 levels are high in children, and then tend to fall as you age. But I can’t remember how sharply they decline. Again, I’d be curious about how the age related decline compares to the drop produce by IF eating patterns.