Early warning
Sugar addiction has been correlated with the increase in per capita consumption of sugar and other high-glycemic-index compounds such as corn syrup and selected starches. The USA per capita soft-drink consumption has increased by 500% over the last 50 years. This is bad news for everyone, except shareholders of this lucrative industry.
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Addictive substances are generally speaking, either illegal, or regulated. We are not allowed to use morphine for run-of-the-mill headaches, we are not allowed to smoke until we are 18 (or 21), and we are not allowed to consume alcohol before roughly the same age yet, we expose our children to what has been labelled “the most dangerous drug of our time” by a Dutch health official in an official health communication. It goes by thy name Sugar. But more generally, glycemic carbohydrates.
The threat of massively increased morbidity due to the ever-increasing health challenges associated with obesity is thoroughly publicized in international media, and I believe warrants an assumption that requires little validation. (Read into that my laziness in providing an exaggerated list of supporting scientific literature on the topic, but I assure you that it does exist)
Sugar has, on numerous occasions, and not just recently, been associated with increased incidences of obesity, diabetes mellitus, cardiovascular disease, stroke and these components have been correlated with one another in various elaborate combinations, very extensively and thoroughly. Little doubt remains that glycemic sugar is one of the major, if not the major, causes of health complications in modern society.
Add to that, the fact that the underlying mechanism of sugar addiction mimics that of opioid addiction. That is right. Being addicted to sugar is like being addicted to heroin light, but the worst thing really, is that most of us remain unaware of this fact, and attribute the problem to ill discipline.
Binge eating and sugar addiction
In a well cited study by Avena, Rada and Hoebel on the topic of sugar addiction, the authors succeeded in producing a relevant animal model of binge eating and sugar dependence.
They would subject rats to food deprivation for 12 hours, followed by 4 hour normal circadian driven activity and then 12 hour access to ordinary rat food and a sugar solution. Both were made available simultaneously.
After one month, it was found that the behavior of these animals mimicked that of drug seeking behavior. These animals would exhibit the following behaviours:
- Increasingly over consuming the sugary solution – Bingeing
- Opiate like withdrawal
- Craving
- Locomotor and consumatory cross sensitization of sugar and drug abuse. (Simulates drug dependence at a neurological level)
After one month, the rats were addicted to sugar, and they were bingeing on every occasion that they gained access to sugar.
The neurological mechanism of sugar addiction
A well known characteristic of drug use is the cause of repeated, intermittent increases in extracellular dopamine in a brain region responsible for behavior reinforcement, called the Nucleus Accumbens (NAc). This characteristic is shared by large, intermittent doses of sugar (and other equally palatable treats), albeit to a lesser magnitude than exhibited by drugs of abuse.
The increased intermittent release of dopamine over time, causes changes in dopamine receptor expression/availability in the NAc, which relates to the development of tolerance similar to drug addiction, and withdrawal in the event of abstinence. Decreased dopamine release in the NAc and increased acetylcholine release from neurons in the NAc in the event of abstinence, is the cause of the majority of withdrawal symptoms, and very closely mimics the mechanism whereby which opiates cause withdrawal symptoms.
The theory proposed from the paper of the authors above states that intermittent, excessive intake of sugar, can have dopaminergic and cholinergic effects that is similar in mechanism, but smaller in magnitude, than opiate addiction. Simply stated, sugar is addictive in the same way heroine is addictive, just not as potent.
The physiological consequence of sugar addiction
Different sugars have different effects on blood glucose levels, blood insulin response, satiety response (feeling of not being hungry), and ultimately, energy and weight homeostasis.
The capacity of carbohydrate to reduce hunger is directly correlated with the rate at which your blood glucose level rises. The higher the glycemic index (GI) of the carbohydrate you are consuming, the higher the satiety peak will be, but the shorter the effect will last, and vice versa for low GI carbohydrates. This is why a sugary treat provides greater satisfaction for hunger and/or cravings than does meat or raw oatmeal. This is the reason why children have to forced to eat their vegetables before they are allowed to have pudding.
The best example of the addictive properties of sugar can be seen when compared to the habits of a smoker. After a meal, a smoker is very rarely too “full” to enjoy a cigarette. It is because the nicotine in that cigarette provides an addictive stimulus that is not replaced by his dinner. In a similar manner, people always seem the have a little extra space for desert after dinner, and it is simply because, more meat, more vegetables will not supply the addictive stimulus that sugar can. You are no longer hungry, yet you crave a very particular high calorie nutrient. Isn’t that strange?
The solution?
Their are many short term solutions to losing weight, but odds are small that you have been one of the lucky minority who have succeeded in losing weight and keeping it off. I say lucky, because those who have succeeded where others have failed, were the ones, who in all likelihood gave up their sugary binge habits for good but failed to realize the significant impact of the absence or restriction of sugar in their diet.
In a key-note address by Professor Timothy Noakes in this very topic, he made mention of a number individuals who have given up carbohydrates in their diet. A resounding agreement by a number of subjects who had written to Prof Noakes, expressing gratitude, exclaimed that they have lost weight, but most importantly, eating significantly smaller volumes of food, but being less hungry. How can that be?
Eating less, but being less hungry, means that you are no longer consuming high calorie nutrients for that craving that you aim to satisfy, but you allow yourself to recalibrate, in order to realize the difference between hunger, and cravings. It is made immensely difficult by the fact that sugar cravings, present the same as hunger, and the indulgence in sugary sins, provides a feeling of satiety in the same way as many other food nutrients do. Or not quite, but hopefully you get the idea.
The cause of the problem is hiding in plain sight, but the significant realization that is yet to dawn upon the larger global health community, is that the problem to the addictive pandemic is hiding in the staple diet of modern society.
One last thought
The significance of the addiction is frequently underplayed to a large extent. The level to which one could rationalize against giving up an addictive substance has power beyond your imagination. If you get a cold feeling when you imagine never ever again consuming chocolate, or sweets of any kind, bread from your favorite bakery, cake, pizza, pasta, fruit juice, McDonald’s, ice cream, sugar in your tea… If you find yourself rationalizing that you will not go through life without enjoying any of a number of those, you have only just begun to experience the power of addiction. You need none of those to enjoy life from nutritional perspective. In fact, the less of those you enjoy, the more life you will end up enjoying.
Selected references:
[1] Nicole M Avena, Pedro Rada, and Bartley G Hoebel. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, exces- sive sugar intake. Neuroscience & Biobehavioral Reviews, 32(1):20–39, 2008. [2] Wendy Foulds Mathes, Kimberly A Brownley, Xiaofei Mo, and Cyn- thia M Bulik. The biology of binge eating. Appetite, 52(3):545–553, 2009. [3] David Benton. The plausibility of sugar addiction and its role in obesity and eating disorders. Clinical Nutrition, 29(3):288–303, 2010. [4] David IG Wilson and Eric M Bowman. Nucleus accumbens neurons in the rat exhibit differential activity to conditioned reinforcers and primary reinforcers within a second-order schedule of saccharin reinforcement. European Journal of Neuroscience, 20(10):2777–2788, 2004. [5] G Terence Wilson. Eating disorders and addiction. Drugs & Society, 15(1-2):87–101, 2000. [6] G Harvey Anderson and Dianne Woodend. Effect of glycemic car- bohydrates on short-term satiety and food intake. Nutrition reviews, 61(s5):S17–S26, 2003. 1 [7] MP St-Onge, F Rubiano, WF DeNino, A Jones Jr, D Greenfield, PW Ferguson, S Akrabawi, and SB Heymsfield. Added thermogenic and satiety effects of a mixed nutrient vs a sugar-only beverage. Inter- national journal of obesity, 28(2):248–253, 2004.
