Q: What's worse than an education in Human Metabolism from a journalist?

A:  An education in Human Metabolism from a comedian.

Blogger stats are interesting things at times.  It's curious to see where people find this place from.  Following my Insulin Wars series, I was rather shocked to see the Tom Naughton, aka Fat Head, installment shoot up my most read posts list, where it remained for a very long time.  As that series went, that particular post was no big deal.   I had quite a lot of traffic coming from Tom's blog.  What this tells me is that a LOT of people are getting their information from a comedian!  This guy actually has a lecture DVD out now.

This isn't good folks!!




Now, a lay person can certainly teach themselves about metabolism and such.  There are many examples on the internet that I'll leave unnamed.  But whenever I hear folks like Tom talk about LC, I'm reminded of Judith Mazel and her Beverly Hills Diet.   I'd read parts of her book when friends of mine tried this diet.  (I thankfully spared myself at least this kooky scheme).   You see Mazel had you eating certain fruits, fruits like papaya my friend was basically having to choke down by the third day, because of the fat-burning enzymes they contained.  This confuses digestion with metabolism.  For weight loss (but not health) the goal would be to minimize digestion!

So anyway, I came across this interview with Naughton and just had to comment after reading this:

Interviewer:  Beyond “Fat Head,” you have also made one of your lectures available which is titled “Big Fat Fiasco.” Within that lecture you state that people are “as fat as they need to be.” Now, leaving the data and other scientific minutia to the lecture, could you succinctly define what that means? ...

Naughton:  It’s tough to explain it simply, but here goes:  Your body absolutely must keep blood sugar within a very narrow range.  If blood sugar goes too high, it’s toxic.  If it goes too low, you pass out and maybe slip into a coma.  Your body keeps blood sugar level by alternately storing and releasing fatty acids.

When blood sugar goes up, you store fat and burn glucose first to bring it down.  When blood sugar begins to drop, you release fatty acids to serve as a primary fuel and preserve the glucose for your brain. 

Now Naughton is describing the Randle cycle linking glucose-fatty acid metabolism, and what he states of the relative reciprocal levels of FA's and glucose is all factually correct.  But he is implying that the adipocytes, through regulation of the triglyceride/fatty acid cycle (TG/FA) are the prime regulators of blood glucose, and this is innacurate.  There are a number of things demonstrating the Randle cycle is far too simplistic to explain blood glucose control in higher animals.  For starters, while fatty acid levels can vary five fold, blood glucose varies only around 30% in the post-absorptive (basal) state.  Secondly, there are situations that elicit a rise in both glucose and fatty acid levels - for example cortisol raises both glucose and FFA levels.  Therefore it's fair to say there's a hormonal network that under most conditions regulates glucose and fatty acids (according to energy needs and energy sources available, I would add) in a reciprocal manner, but if anything, it's the glucose levels that regulate the fatty acid trafficking.

But it is the liver that bears the primary responsibility for regulating basal circulating glucose levels.  It does this through the interplay between glycogenolysis (breakdown of glycogen) or glycogen synthesis as well as gluconeogenesis.  Postprandially, our bodies regulate blood glucose levels by "disposing" of the exogenous glucose - the glucose is taken up by the cells and oxidized (oxidative glucose disposal = burning glucose) or stored as glycogen (non-oxidative glucose disposal).  In humans de novo lipogenesis is a relatively minor pathway for non-oxidative disposal and insignificant absent significant carb overfeeding.

The other issue with this is that elevated fatty acids - e.g. excessive supply - tends to lead to increased blood glucose levels, not decreased levels - especially in the postprandial state.  They do this by inhibiting clearance from circulation.

If your fat cells release fatty acids too slowly, which is what happens when you become insulin-resistant, they can’t provide you with enough energy to keep your glucose within the safe range.  So your body works to make them bigger, and they keep on getting bigger until they overcome the insulin resistance and are once again capable of releasing fatty acids at the necessary rate.

So yes, some people unfortunately need to become hugely fat to maintain a state of energy balance.  Otherwise, even though they’re fat, they end up starving at the cellular level.  Your body doesn’t care how much food you have in the pantry; if the pantry door is locked, you can still starve.

This is just wrong.  Wrong.  Don't believe me, though.  Read the works of Frayn, Boden and McGarry and others of that ilk that I've blogged on regularly here. 

Pathological insulin resistance is characterized by (1) failure to properly suppress NEFA release from adipose tissue and/or (2) failure of adipocytes to adequately clear and trap dietary fatty acids.  Furthermore, this leads to loss of blood glucose control in the fasting state because the liver becomes insulin resistant so insulin fails to adequately suppress gluconeogenesis.  Adipocytes get less sensitive to insulin as they grow.  They don't grow to restore insulin sensitivity!


Naughton is actually correct that the problem with IR begins in the adipocytes.  Hat tip there .... shhhhh ... don't tell Gary Taubes though.  But not in the manner in which he tells us.  The constellation of symptoms that comprises MetS includes amongst it elevated circulating fatty acid levels accompanying insulin resistance.  You're fat cells are simply not efficient enough at locking that pantry door.   


Let's look at the "reality" so many often suggest I need to meet.  As folks get fatter and fatter, do their blood glucose levels eventually stabilize out?  Nope!  Quite the opposite.  Yes, there are the "metabolically obese thin people" that can be explained by the FA hypothesis (but that's a topic for other blog posts past and surely at some time in the future).  But the link between obesity and metabolic derangement flows from the fat cells.  You get fat then you (some not all) exhibit some degree of IR and impaired glucose tolerance, IGT.  As you get fatter and fatter do these conditions get better and alleviate the problem?  NO.  They get worse.  


So please folks.  If you're going to be your own armchair scientist, seek authoritative sources.  And I recognize that with my anonymity and such there's no reason to consider me to be one.  This is fine by me.  Allow me, instead, if you're reading my blog, to act as a channeler of sorts to real science.  It should not be about the "buy-in" (Mark Sisson) or hopelessly simplifying something "for Dummies".  As complicated as the science is, it serves no purpose to get "educated" in hopelessly inaccurate simplifications made up by those with absolutely no qualifications to do so.