The following blog first came up during an off-site lecture on a nutrition course. It raised an interesting concept for me. One that appeared to have supplanted itself into the psyche of the public domain. That of sugar addiction. So it piqued my interest in sourcing how and where this concept had come about. What follows is my best conclusions after addressing the empirical and public domain evidence regarding this concept.
There is a general consensus within the public domain that since the advocacy of low-fat guidelines in the late 70’s, there has been a very large increase in obesity levels in western populations (Lustig et al. 2010). Some research proposed that acceptance of these low-fat guidelines resulted in over-consumption of sugar as a counter-response to this message and as such, this response is causative in the obesity epidemic (Bray et al. 2004; Lustig et al. 2010). In other words, its the fault of the guidelines and the message stemming from it.
This research gained traction within mainstream media organisations even in the face of clear epidemiological evidence that demonstrated populations were consuming an extra 497 calories DAILY across food types in comparison to 1970’s levels (Rippe et al. 2016). The over-consumption of addition cheap grains, fats and oils appear to be accountable for this extra caloric intake (and not sugar per se). This is ironic considering the government guidelines promoting low fat, actually led to added fat consumption levels (USDA. 2013).
Addiction Guidelines.
An ongoing area of ambiguity that requires attention is a robust and clear set of guidelines that classify and define what exactly sugar addiction is in humans (Moran et al. 2016). If you have no reliable definition it is particularly difficult to formulate a strategy to counter this supposed negative health effect.
The two primary set of guidelines are the Diagnostic and Statistical Manual of Mental Disorders-5 (D.S.M-5) (American Psychiatric Association. 2014) and more recently the Yale Food Addiction Scale (Y.F.A.S) (Gearhardt et al. 2016). Digging deeper, there appear to be well-established inconsistencies that exist between the D.S.M-5 scale and Y.F.A.S. Regarding the D.S.M-5, the criteria that may point to sugar addictions existence include:
Diagnostic and Statistical Manual of Mental Disorders-5.
A) “Tolerance effect”, a diminishing response to the potency of a substance.
This raises the question, “what exactly constitutes a “diminished effect from increasing sugar intake?”
B) “Cravings”.
Everyone gets craving, but does it necessarily lead to addiction?
C) “Excessive time spent using, obtaining, or recovering from use”.
Put another way, do individuals spend too much time eating, buying and physically recovering from sugar intake?
D) “Taken in larger amounts than intended”.
What figure is put on “larger”? Defining “larger” amount is important within the context of the above 497 extra daily calorie consumption. Where is the cut-off point? Does this include TV, Social media, exercise, spending time with your family, working? If a person leads a healthy life, has good health measures and is active, but slightly over consumes sugary foods (with a concomitant reduction in fat intake), are they addicted?
These D.S.M-5 guidelines account for confirming true addiction status. True addiction wrecks lives. So it is imperative to provide clarity on these definitions as they may be considered convoluted, seeking to “softball” the existence of an unproven concept of sugar addiction (Westwater et al. 2016). Furthermore, weakening addiction guideline and amplifying its unproven existence may unnecessarily cause added fiscal pressures on public health budgets with inappropriate policy implementation (Moran et al. 2016).
Yale Food Addiction Scale.
With regards to the Y.F.A.S guidelines, the criteria that may point to sugar addictions existence include recently lowered threshold for food addiction classification. This scale includes criteria such as:
A) Persistent eating despite negative consequence.
Define both persistent and negative consequence?
B) “Unsuccessful attempts to cut down”.
Sounds like every dieter in the history of the world.
C) Impairment of functioning because of overeating.
Everyone qualifies for this after Sunday roast dinner.
Again, these imprecise definitions may be perfectly valid, but there is a degree of looseness about them (Ziauddeen et al. 2013). There is a question mark as to the efficacy of the D.S.M-5 & Y.F.A.S to clinically validate sugar addiction (Hone-Blanchet et al. 2014) and as such these scales could unduly label some individuals who do not over-consume as addicts (Westwater et al. 2016).
Mice & Media Response.
Colantuoni et al. 2002 have shown that mice “binge” on sugar when fed at intermittent intervals. This high-profile trial and its follow-ups by Avena et al. 2008, used the same basic technique with mice. Researchers effectively were deprived (or starved) the mice of access to food for over twelve hours. The researchers then scheduled this feeding time at an unusual time, possibly during the mice’s sleep cycle (presumably to increase the appetite and the probability to consuming the sugary food). This suggested the mice would be bloody starving by the time they were offered a choice of either their chow or a 25% sugar solution at their next mealtime.
Over a four week period the mice showed signs of “addictive-like” behavior (Avena et al. 2008), presumably because they picked the sugary food more often the the chow. Importantly this “addictive” behavior occurred with limited access to food. It could not be duplicated in trials with open access to sugary food (Lenoir et al. 2007). Go figure Pavlov’s dog. After being starved, the mice might be forgiven for thinking, “I better eat as much as possible now, because I don’t know when I’ll eat again”.
From this data, sensationalized headlines declared the existence of sugar addiction with media headlines like, “Is sugar toxic” (Taubes. 2013) and “Death by Sugar” (Lanau. 2014). Articles were written for prestigious organisations like, the New York Times. Furthermore, even peer reviewed medical journals such as the British Medical Journal are implicated in posting inflammatory articles with headlines such as “Sugar is the new tobacco” (Ravichandran. 2013). So word spread about sugar addiction being a reality in public health.
Functional MRI & Media Response.
Further to the mice findings, functional Magnetic Resonance Imaging (fMRI) studies touted sugar as having a likening effect on reward pathways in human brain akin to cocaine (Tang et al. 2012). Some prominent medical professions discussed these findings during documentaries. The mechanism touted was by elevated signalling at an aspect in the brain called the “dopamine receptor”. This causes significantly increased excitement in reward and hedonistic pleasure pathways in a region of the brain called the Meso-limbic system (Tellez et al. 2016).
From this data, disingenuous headlines such as, “Sugar is addictive and the most dangerous drug of the times” hastily equated fMRI evidence from sugar consumption as having as powerful cocaine like addictive-reward response (Waterfield et al. 2013). However, deeper research into the literature indicates that these dopamine pathways can be excited by many different responses.
A) Listening to your favorite music excites these pathways (Blood et al. 2001).
B) Laughing excites these pathways (Mobbs et al. 2003).
C) Winning money in a bet excites these pathways (Breiter et al. 2001).
D) Finding an attractive mate excites these pathways (Noriuchi et al. 2008).
E) A mothers loving smile to a child excites these these pathways (Fisher et al. 2006).
So reliable evidence suggests targeting sugar as addictive is a very short-sighted approach (Lenoir et al. 2007). There is evidence that certain food types consumed by individuals with a high B.M.I are inextricably linked to both high sugar and fat intake. The aforementioned dopamine effect suggests sugar may propagate a “wanting” signal and fat may signal the opioid pathways causing a “liking” sensation. In essence, sugar and fat consumption are synergistic in their effect on taste and reward. They create a ‘double whammy’ effect on consumption (Davis et al. 2009).
Conclusion.
In summary, further clarification is needed to accurately define criteria which confirm the existence of “Sugar Addiction” in humans. Some evidence suggests that sugar may be causative in addiction-like behavior in the mouse model. Moreover, there is examples of consequential publication in the mainstream media of sugar addiction via the hedonistic effect from fMRI studies. These claims do not stand up to rigor of sugar addiction. Presently there is insufficient and a severe lack of strong evidence to confirm the existence of sugar addiction in humans even though this concept has supplanted into the public domain via mainstream media claims.
References.
Avena et al. 2008, After daily bingeing on a sucrose solution, food deprivation induces anxiety and accumbens dopamine/ acetylcholine imbalance. Physiol Behav. 94:309–315.
Blood et al. 2001, Intensely pleasurable responses to music correlate with activity in brain regions implicated in reward and emotion. Proc Nat Acad. Sci USA ;98:11818–23.
Bray et al. 2004, Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutr 79:537–543.
Breiter et al. 2001, Functional imaging of neural responses to expectancy and experience of monetary gains and losses. Neuron;30:619–39.
Colantuoni et al. 2002, Evidence that intermittent, excessive sugar intake causes endogenous opioid dependence. Obes. Res. 10, 478–488.
Davis et al. 2009, Dopamine for “Wanting” and Opioid’s for “Liking”: A Comparison of Obese Adults With and Without Binge Eating, Obesity 17, 1220–1225.
Diagnostic and Statistical Manual of Mental Disorders (D.S.M), 2014 American Psychiatric Association.
Fisher et al. 2006, Romantic love: a mammalian brain system formate choice. Phil Trans Royal Soc London B Biol Sci 2006;361:2173–86.
Gearhardt et al. 2016, Development of the Yale food addiction scale version 2.0. Psychol Addict Behav 30:113–121.
Hebebrand et al. 2014, “Eating addiction”, rather that “food Addiction”, better encapsulates addictive-like eating behavior. Neuroscience and Bio-behavioral Reviews 47; 295–306.
Hone-Blanchet et al. 2014, Overlap of food addiction and substance use disorders definitions: Analysis of animal and human studies, Neuro-pharmacology 85; 81–90.
Lanau. 2014, Death by Sugar How the sweet killer is fueling the biggest health crisis of our time.
Long et al. 2015, A systematic review of the application and correlates of Y.F.A.S-diagnosed “food addiction” in humans: are eating-related “addictions” a cause for concern or empty concepts? Obesity Facts 8:386–401.
Lustig et al. 2010, Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc 110:1307–1321.
Moran et al. 2016, Believing that certain foods are addictive is associated with support for obesity-related public policies, Preventive Medicine 90; 39–46.
Noriuchi et al. 2008, The functional neuro-anatomy of maternal love:mother’s response to infant’s attachment behaviors.Biol Psychiat;63:415–23.
Ravichandran. 2013, Is Sugar the New Tobacco? The B.M.J Blog.
Rippe et al. 2015, Sugars and health controversies. What does the science say? Adv Nutr 6(Suppl): 493S–503S.
Tang et al, 2012, Food and drug cues activate similar brain regions: a meta analysis of functional MRI. Physiological Behav; 106 317–324.
Taubes. 2011, Is sugar toxic? New York Times magazine.
Tellez et al. 2016, Separate circuitry encode the hedonic and nutritional values of sugar. Nat Neuro-sci 19:465–740.
US Department of Agriculture, Economics Research Service. 2013, Calories: average daily per capita calories from the US food supply, adjusted for spoilage and other waste. Loss-adjusted food availability data.
Waterfield et al. 2013, Sugar is addictive and the most dangerous drug of the times. Telegraph 2013.
Westwater et al. 2016, Sugar Addiction: The State of the Science. European Journal of Nutrition.
Ziauddeen et al. 2013, Is food addiction a valid and useful concept? Obes Rev 14:19–28.