Tuesday, March 11, 2014

Food Quality Counts: Processed Foods Are Obesogenic + Induce a Nasty Self-Perpetuating Vicious Cycle of Reduced Reward Responses and Increased Effort Avoidance

Due to the vicious cycle of pizza, coke, ice-cream and an ever-increasing lack of motivation, you have to be great to start.
I know...,  I know. We are, as so often, dealing with a rodent study here, but the results are simply too representative of what I see in less hairy individuals on a daily basis to ignore the data Aaron Blaisdell and his colleagues from the Department of Psychology at the UCLA and the  Molecular Biosciences Degree Program at Kansas University present in a soon-to-be-published paper in Physiology & Behavior (Blaisdell. 2014).

In the corresponding experiment the scientists tried to proof that refined diets (=processed foods) would lead to "greater weight gain and greater disruption of motivation processes" than regular not exactly "unrefined" chow in rodents.
You can learn more about fat loss at the SuppVersity

Maximize glucose control

Sucralose obeso- genic sweetener?

Bigger belly shrinking brain

Weight loss acupuncture

Optimal HIIT WO for fat loss

Veggies are fat loss kings
To this ends, the researchers assigned their "subjects" (they call them subjects ;-), 32 experimentally-naive female Long Evans rats (Rattus norvegicus) on diets containing either ...
  • REF (Research Diets 12450B) = refined chow, or
  • CON (Lab Diets 5001) ) = more or less unrefined chow.
Unfortunately, the diets didn't really 'hit the rodents macros' with 28% protein,  13% fat and only 58% carbohydrates, the CON chow was not just less processed, it did also have a minimally "better" macronutrient profile than the refined diet with 20% protein, 10% fat and 70% carbohydrates.
"The diets, both commercially available rodent chows, differed in the amount of refinement and processing that wen into their production. The Lab Diets 5001 was also selected as the CON diet because it is a common diet in other behavioral experiments, including in our laboratory. Specifically, we should observe less persistence in lever-pressing and earlier breaking points in rats consuming a REF diet."
While this comparison may be practical and realistic - a refined human diet would also be higher in carbs, and lower in protein and fats than a whole foods diet -  the (albeit minor) differences in macronutrient composition are still a minor bummer, because we can't tell for sure, whether it's just the processing that's responsible for the astonishing effects on body weight and behavior the researchers observed in the course of the 6 months study period:

Figure 1: Body weight after the intervention and inter-response time in experiments that were designed to measure the rodents motivation / breaking point (=how long it takes until they gave up and would have drowned, if the scientists hadn't rescued them) with water (exp2) and sucrose (exp3) as a reward (Blaisdell. 2014)
As you can see, the animals on the refined (REF) diet gained significantly more weight than those who received the control (CON) chow. Interestingly, this also lowered the number of lever presses and correspondingly lower breaking points (=giving up, when confronted with an obstacle) than the rodents in the control group.

Blaisdell et al. explain these observations, of which I'd bet that it reminds you of a couple of pizza eating, coke guzzling, "I don't care" individuals who come to you winning about their inability to lose weight and the unfairness of live in regular intervals, as follows:
Table 1: Diet composition (based on manufacturer data)
"Rates of lever pressing are affected by many factors other than motivation, such as satiety, sensory adaptation, habituation, and hyperactivty.

The breaking point on a PR schedule is thought to more directly reflect the motivational component of instrumental lever pressing, independent of these other factors. A breaking point is the time at which a subject gives up on making a reinforced response." (Blaisdell. 2014)
In the discussion of the results, the researchers point out that this the REF rats lowered motivation to perform an instrumental lever press task would evidence a direct impairment of motivation that was "independent of the within-session drop in lever press response rates which was largely due to changes in satiety" and lead to "a persistent impairment in motivation that was not affected by nine days of consuming a CON diet." (Blaisdell. 2014).

The latter, i.e. the persistence of the diet-induced motivational changes is quite intriguing, it does after all explain why your aforementioned pizza munching, coke guzzling acquaintences don't see the expected immediate improvements whenever they try to finally make a change. Luckily, the same goes for the opposite extreme, your all-inclusive holiday binge on one of the cruisers in the Atlantic is - at least this is what the rodent study at hand would suggest - not going to induce any (not even momentary) motivational impairments. Needless to say that these findings ...
"lend support to the hypothesis raised by scientists (Kenny. 2011; Sutin. 2013) and journalists (Taubes. 2007) that obesity may not be the result of impaired motivation (lethargy). Rather, an obesogenic diet, such as that consisting of highly processed, refined foods, may induce obesity and disrupt motivational mechanisms of the central nervous system. This hypothesis awaits further empirical scrutiny and does not necessarily rule out the lack of will power as a contributing factor to obesity." (Blaisdell. 2014)
In other words, while a lack of motivation is the fundamental reason weight loss efforts fail, it is not necessarily a genetically determined lack of will power, but could also be brought about by diet induced changes in the neurotransmitter levels in the brain. The increased effort-avoidance Salomone et al. observed in response a depletion of dopamine in the nucleus accumbens (Salamone. 2009), as it can be brought about by an obesogenic diet (Johnson. 2010), for example, would be perfect candidate to explain the the impaired motivation and perseverance that keeps overweight and obese individuals from making changes of which most of them know that they will be life-saving.
Ephedrine, dopamine and effective weight loss. I know it is politically incorrect to remind you of the great success both obese and lean individuals had with the old ephedrine based fatburners, but when I read about reduced dopamine levels and effort avoidance, I can't help, but think of the results of studies by Angrist (1977) or Wellman (1998). The results of their experiments demonstrate quite that it has never been the meager thermogenic effect (which is blunted in the obese, anyway) that made caffeine + ephedrine an effective and above all scientifically proven (Astrup. 1992) and surprisingly safe (Toubro. 1993) weight loss tool.
I will have to stop here, because any further details about brain-chemistry would take me further away from the central message of this article, which w that both, food quantity and food quality matter! ... and if I may add, I am astonished how the way the pendulum is constantly swaying from one extreme to the other is hampering the weight or rather fat loss success of millions of people worldwide.

Against that background I have to disagree with Blaisdell et al. who demand further "investigation[s] of the effects of highly-processed “junk food diets” in motivation and engagement in effortful tasks in humans." What we need is not a confirmation of the obvious, but tools that would help individuals that are trapped in the vicious cycle of junk food dieting, ever-decreasing food rewards and the avoidance of effortful tasks to make and stick to the lifestyle (not just dietary) changes that are necessary to break free.
References:
  • Angrist, Burton, et al. "Dopaminergic agonist properties of ephedrine-theoretical implications." Psychopharmacology 55.2 (1977): 115-120. 
  • Astrup, Arne, et al. "The effect and safety of an ephedrine/caffeine compound compared to ephedrine, caffeine and placebo in obese subjects on an energy restricted diet. A double blind trial." International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity 16.4 (1992): 269.
  • Johnson, Paul M., and Paul J. Kenny. "Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats." Nature neuroscience 13.5 (2010): 635-641.
  • Kenny, Paul J. "Reward mechanisms in obesity: new insights and future directions." Neuron 69.4 (2011): 664-679.
  • Salamone, John D., et al. "Dopamine, behavioral economics, and effort." Frontiers in behavioral neuroscience 3 (2009).
  • Sutin, Angelina R., et al. "I Know Not To, but I Can’t Help It Weight Gain and Changes in Impulsivity-Related Personality Traits." Psychological science 24.7 (2013): 1323-1328.
  • Taubes, Gary. Good calories, bad calories. Random House LLC, 2007. 
  • Wellman, Paul J., et al. "Effects of (–)-ephedrine on locomotion, feeding, and nucleus accumbens dopamine in rats." Psychopharmacology 135.2 (1998): 133-140.