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Sunday, May 28, 2017

A Collection of "Accidental Experimental Evidences" Against Sugar/Fructose Addiction

This post will be added to from time to time, to collect in one place evidence against the concept of sugar/fructose addiction.   When added to it will be bumped, and the "skip to using browser search" table of contents below will be updated.  

I am unable in Blogger to link to sections within a blog post.  In lieu of this, you can use your browser search on the phrases below to skip to the following sections:

  • Accidental Experimental Evidences
  • Mice Fed 18% Fructose
  • Mice Fed 60% Sugar or Starch
  • Unmotivated Fat Rats

Accidental Experimental Evidences

Just some definitions and clarifications of what this post will contain.

A scientific experiment is distinguished by applying some "treatment" and observing/quantifying/analyzing the effects. 
This post will not include evidence from observational studies. 
The results of a scientific study reported in peer review journal or scientific conference.
This post will not include any n=1 anecdotes and such, no matter how well some individual claims to document their self-experimentation.
Accidental Experimental Evidences:
When researchers design experiments, they generally outline a purpose for conducting them.  The researchers have a hypothesis, design a rigorous protocol (hopefully) to control for various potential confounding variables, etc., and usually identify outcomes measured.    So if researchers propose A causes B, a very simple experiment may involve varying dose of A, measuring B, with the expected outcome (if it supports the hypothesis) being a positive dose-response relationship between the two.  
To prevent goal-post-moving, clinical trial registrations generally identify primary and secondary outcomes, often with a clinically significant change identified ahead of time.  But the outcomes of a study are what they are, regardless of what priority the researchers put on them, or what cause-effect they were investigating.
Thus, ACCIDENTAL  experimental evidences are scientific experimental evidence that supports a scientific hypothesis other than what the investigators were looking into.  

I consider Accidental Experimental Evidences to be very powerful.

Why?  Because ...
  • Science often progresses by accidents and unexpected outcomes
  • Outcomes are what they are and free from the personal biases of the researchers.  If the researchers weren't looking for something, they are less likely to distort/interpret outcomes to fit these biases, perhaps obscuring or distracting others from concluding on their own ... therefore
  • The outcomes speak for themselves
The nutrition and obesity and related literature actually abounds with such accidental evidences against the concept of sugar addiction (or specifically addiction to the fructose moiety).

Mice Fed 18% Fructose

Fructose decreases physical activity and increases body fat without affecting hippocampal neurogenesis and learning relative to an isocaloric glucose diet

In this study, purified diets as shown in the graphic were compared, the difference was 18% by weight fructose vs. 18% by weight of glucose.  This is one of those studies that must be interpreted with caution, because isolated fructose does not appear to exist much in nature.  Most fruits contain a combination of sucrose, glucose and fructose.  It's unsure whether the glucose from cornstarch or maltodextrin can metabolically "counter" the fructose.

In any case, the fructose-fed mice did gain more body weight as shown below left.  However this was not due to increased intake, as shown below right.  The weight gain could be attributed to reduced energy expenditure.    It is the lack of change in intake, however, that is the accidental evidence countering fructose-as-addictive.  If it were, the intake should have increased.  

Mice Fed 60% Sugar or Starch

In this study, two strains of mice were fed one of four diets designated by Fat-Sucrose -- low or high in fat, low or high in sucrose.   One strain of mice was obesity susceptible, the other resistant.  I've included the diet compositions and full body weight results in smaller graphics below.    The full plot is also inset in the plot of just the low fat diets below.

Both strains of mice gained more weight on high fat diets due in large part to increased caloric intake.  However the low fat diets did result in the obesity susceptible mice gaining more weight.  However, opposite to what a sugar-addictive model would predict, mice fed a 60% sugar diet ate less and gained less weight vs. 60% starch.   The differential in intake and weight gain was amplified in the obesity susceptible strain, again counter to what sugar-as-addictive would predict.  Obesity susceptible mice consumed less of a 60% sucrose vs. a 60% starch diet and gained less weight.  

Unmotivated Fat Rats

In this study, rats were fed a low fat (10%) "junk food diet" -- 35% sugar -- for six months.  They gained considerably more weight than rats fed a normal chow.   To measure "motivation", the rats were subjected to a lever pressing test to dispense sugar water (reward).  A sugar-as-addictive model would predict that rats fed a high sugar diet would press the levers to dispense sugar water more frequently.   The opposite was the case, these rats were "less motivated" as indicated by fewer lever presses.   

The experiment was repeated with water-restricted rats and plain water as reward, and the same outcome was observed.  So the obese rats were less motivated in general.  A sugar-as-addictive model would predict a difference in motivation for sugar water vs. plain water.  No such difference was observed.

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