An article published in April 2012 by the Nature Reviews Neuroscience (Ziauddeen et
al., 2012) calls for cautiousness in applying the addiction model to obesity. This
scrupulous review described the highly consequential results from B. Hoebel's lab
concerning binge-like eating behaviors of rats (Avena et al., 2008, 2009; Bocarsly
et al., 2011). Referring to these results, Ziauddeen and colleagues concluded that
the binge behaviors relate to the palatability of the foods independently of their
macronutrient composition. Earlier, also basing on the works of Hoebel and colleagues,
I have been able to draw quite a different conclusion – fat per se, although highly
palatable, is not as addictive as carbohydrates and is not obesogenic (Zilberter,
2011). In yet another paper (Peters, 2012), A. Peters interpreted results of Avena
et al. (2008) as a proof that “sugar addiction” fails causing obesity. Here, I take
a closer look at the Hoebel's model of addiction (Avena et al., 2008, 2009; Berner
et al., 2009; Avena, 2010; Avena and Gold, 2011; Bocarsly et al., 2011) while keeping
in mind the role of macronutrients.
Food Addiction
An opinion exists that rather than an observational link, a causality exists between
food addiction and obesity (Gold, 2004; Liu et al., 2006; Corsica and Pelchat, 2010;
Johnson and Kenny, 2010). Another opinion is that such a causality does not exist
(Peters, 2012) or even that a mere link between them should be considered with caution
(Ziauddeen et al., 2012). The caution notwithstanding, it has been shown (and is discussed
by Ziauddeen et al., 2012) that drug addiction and food addiction have similar effects,
e.g., on the dopaminergic system (Volkow et al., 2008; Gearhardt et al., 2009; Stice
and Dagher, 2010) where they “overlap” (Avena et al., 2012). In human subjects, food
addiction has been associated with similar patterns of neural activation as substance
addiction in anterior cingulated cortex, medial orbitofrontal cortex, and amygdala
(Gearhardt et al., 2011b). “Common hedonic mechanisms may therefore underlie obesity
and drug addiction,” concluded Johnson and Kenny (2010). Addiction liability is being
discussed inline with development of obesity pharmacotherapy (Greene et al., 2011).
Carbohydrate Addiction
Carbohydrate (CHO) bias in brain's control of energy homeostasis (Zilberter, 2011)
reveals itself in several well known ways including the phenomena termed “positive
reward,” “hedonism,” “wanting,” “liking,” etc. (Berridge et al., 2010; Gold, 2011).
The “sweet-addiction” comparable by magnitude with alcohol addiction (Kampov-Polevoy
et al., 2003) and drug addictions (Stoops et al., 2010) is well documented. Gold (2011)
argued that deficit in “reward” is coupled with obesity and this coupling is common
for sugar, cocaine, and heroin addictions.
Gearhardt et al. (2011b), referring to the aforementioned work of Johnson and Kenny,
argued that only “hyper-palatable” foods rich in fat and sugar can cause addiction.
Indeed, the combination of fat and sugar resulted in a “reward dysfunction associated
with drug addiction and compulsive eating, including continued consumption despite
receipt of shocks” (Gearhardt et al., 2011a). A link between food addiction and obesity
has also been explicitly postulated (Avena et al., 2009; Corsica and Pelchat, 2010;
Gold, 2011).
Fat Addiction?
Studies from B. Hoebel lab suggest that access to CHO produces different addiction-like
behaviors compared with access to fat (Avena and Gold, 2011; Bocarsly et al., 2011;
Avena et al., 2012). Nutrient specificity in control of eating behavior was also shown
in this lab (Berner et al., 2009). During the “sweet-chow” feeding protocol, rats
compensated for the increased sucrose or glucose calories by decreasing chow intake.
The authors (Avena et al., 2008) suggested that the increase in sugar intake, while
not resulting in obesity, lead to an upregulation of affinity for opioid receptors,
which in turn leads to the vicious circle of sugar abuse and might contribute to obesity.
In a later study (Avena et al., 2009), when rats were given intermittent daily access
to “sweet-fat” food, they voluntarily restricted their intake of standard chow, similar
to what has been reported with “sweet-chow” food (Avena et al., 2008). However, this
time rats did become overweight unlike in the “sweet-chow” experiment. Authors concluded:
“fat may be the macronutrient that results in excess body weight, and sweet taste
in the absence of fat may be largely responsible for producing addictive-like behaviors.”
Yet pure fat, unlike the CHO-fat combination, lacks obesogenity (Dimitriou et al.,
2000). Fat combined with limited CHO content failed to cause overeating and weight
gain, while excess CHO in high-fat diets caused obesity and metabolic impairment (Lomba
et al., 2009).
Metabolic studies show that CHO restriction in high-fat diets exerts neuroprotective
effects (Figure 1) via induction of heat-shock proteins (Maalouf et al., 2009), growth
factors (Maswood et al., 2004), and mitochondrial uncoupling proteins (Liu et al.,
2006). Naturally, CHO excess has neurodeteriorating effects as discussed in Zilberter
(2011), Hipkiss (2008), or Manzanero et al. (2011).
Figure 1
High-fat/high-CHO versus high-fat/low-CHO diets: Addiction, obesity, neurotoxicity
and neuroprotection are affected diametrically opposite ways. Summarized from Avena
and Gold (2011), Bocarsly et al. (2011), Avena et al. (2012), Berner et al. (2009),
Maalouf et al. (2009), Maswood et al. (2004), Liu et al. (2006), Zilberter (2011),
Hipkiss (2008), Manzanero et al. (2011). Red arrows: increasing a function or a process.
Green arrows: decreasing a function or a process.
Conclusion
Taking into account the well-defined metabolism-related features of a diet can help
avoiding ambiguity in definition of diet types and aid in data interpretations. From
this standpoint, macronutrients play a crucial role in determining diet's behavioral
and metabolic consequences.