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Sugar Addiction

Most addictive substances stimulate increased Dopamine release, a 'reward' neurotransmitter. Over time, habituation can occur, and to achieve the same level or sensation of reward, an increasing stimulus is needed. In both animals and humans, the evidence in the literature shows substantial parallels and overlap between drugs of abuse, and sugar intake, from the standpoint of brain neurochemistry as well as behaviour (DiNicolantonio, J.J et al., 2017).


Sugar addiction is a behavioural and physiological response to excessive sugar intake (Avena et al., 2007). Animal data shows dependence to sugar and signs of Dopamine habituation, opioid dependence, when given intermittent access to sugar (Rada et al., 2005). Sugar addiction seems to be characterised by a dependence to the natural endogenous opioids that get released with sugar intake (DiNicolantonio, J.J et al., 2017). These behaviors are then related to neurochemical changes in the brain that also occur with addictive drugs (Avena et al., 2007). Additionally, in at least a subset of vulnerable individuals, high-glycemic-index carbohydrates trigger addiction-like neurochemical and behavioral responses (Lennerz, B., Lennerz, J.K, 2017).


Hyperglycemia, or substantial blood glucose rises, have been observed to increase the contractile response in vascular smooth muscle causing vasoconstriction, a stress response, even after typical carbohydrate-rich meals (Jackson et al., 2016). Additionally, hyperglycemia has been observed to bleed the brain and cause intracerebral hemorrhage, in rats and mice (Nieswandt and Stoll, 2011).

Dietary carbohydrate is mostly digested to sugar


Stored fat, not stored carbohydrate, provides energy at rest, and during most activity

There are only two major energy stores in the body: adipose tissue (fat) and muscle tissue. This is in the form of fatty acids and protein. Carbohydrate stores are limited, and are maintained by gluconeogenesis; the making of new sugar. Muscle tissue serves as a starvation reserve, once adipose tissues have been exhausted. Muscle tissue also undergoes a process of constant recycling and remodeling, highlighting the importance of sufficient daily intake. The main function of adipose tissue is to provide energy to the body, which is sufficient even for sugar-dependent tissues (Cahill, 1970).


With high blood sugar levels, most energy will be derived from glucose, and in the post-prandial or ‘fasted’ state, once blood sugar levels return to normal, most energy is produced from fatty acids (Alabduladhem and Bordoni, 2021).


Fight-or-flight, stress response

Glycogen stores are spared for energy and are not used as the primary source of energy, unless for an acute emergency, such as high-intensity exercise, our in-built fight-or-flight mechanism (Cahill, 1970). When we are 'stressed' our liver naturally increases the blood sugar concentration to prepare for high-intensity exercise. Repeated high-intensity exercise efforts can be maintained for exercise performance with carbohydrate intake, and is nuanced.


So what?

Focusing on nutrient-dense foods sourced from complete proteins, is a simple and effective strategy for a healthy diet. Tolerance to carbohydrate-rich foods, while maintaining a high rate of fat oxidation is individual, and can change over time. Refined carbohydrates can have addictive qualities, cause vascular dysfunction and ingestion can simulate the fight-or-flight response.


Take Home:

Take the test: do you crave sugar and rewards shortly after ingestion of sugar-rich foods? If so, take the 7 day no-sugar challenge.


Nutrient-density promotes health and performance


References:


Ahmed SH, et al. Sugar addiction: pushing the drug-sugar analogy to the limit. Curr Opin Clin Nutr Metab Care. 2013;16(4). doi: 10.1097/MCO.0b013e328361c8b8.


Avena NM, et al. Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008; 32(1). doi: 10.1016/j.neubiorev.2007.04.019.


DiNicolantonio JJ, O'Keefe JH, Wilson WL. Sugar addiction: is it real? A narrative review. Br J Sports Med. 2018;52(14):910-913. doi:10.1136/bjsports-2017-097971


Hasin DS, et al. DSM-5 Criteria for Substance Use Disorders: Recommendations and Rationale. Am J Psychiatry. 2013; 170(8). doi: 10.1176/appi.ajp.2013.12060782.


Kalon E, et al. Psychological and Neurobiological Correlates of Food Addiction. Int Rev Neurobiol. 2016; 129. doi: 10.1016/bs.irn.2016.06.003.


Kolarzyk E, et al. Assessment of daily nutrition ratios of opiate-dependent persons before and after 4 years of methadone maintenance treatment. Przegl Lek. 2005;62(6).

Lennerz B, Lennerz JK. Food Addiction, High-Glycemic-Index Carbohydrates, and Obesity. Clin Chem. 2018;64(1):64-71. doi:10.1373/clinchem.2017.273532


Lundqvist MH, et al. Is the Brain a Key Player in Glucose Regulation and Development of Type 2 Diabetes? Front Physiol. 2019; 10. doi: 10.3389/fphys.2019.00457.


Lu H, et al. Abstinence from Cocaine and Sucrose Self-Administration Reveals Altered Mesocorticolimbic Circuit Connectivity by Resting State MRI. Brain Connect. 2014; 4(7). doi: 10.1089/brain.2014.0264.


Mysels DJ, Sullivan MA. The relationship between opioid and sugar intake: Review of evidence and clinical applications. J Opioid Manag. 2010; 6(6).

Nieswandt, B., Stoll, G. Sugar rush bleeds the brain. Nat Med17, 161–162 (2011). https://doi.org/10.1038/nm0211-161


Saha TD, et al. Analyses Related to the Development of DSM-5 Criteria for Substance Use Related Disorders: Toward Amphetamine, Cocaine and Prescription Drug Use Disorder Continua Using Item Response Theory. Drug Alcohol Depend. 2012; 122(1-2). doi: 10.1016/j.drugalcdep.2011.09.004.


Veldhuizen MG, et al. Integration of sweet taste and metabolism determines carbohydrate reward. Curr Biol. 2017; 27(16). doi: 10.1016/j.cub.2017.07.018.


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