Story at a Glance.
But the truth is, none of us really think sugar is as bad as everyone is making it out to be.
After all, let’s face it, it’s just sugar.
For most of us, at worst it’s a wicked indulgence and at best it’s a moment of respite in an otherwise hectic/bored/depressed/crazy day. If you have a sweet tooth, what’s a person to do? A little ice-cream after dinner or one chocolate bar isn’t going to kill you. Is it?
Well, no it’s not.
But neither (if you’re lucky) is jay walking across a six lane highway. But it isn’t recommended.
The truth is, and science is now confirming it, we are only just starting to understand exactly how damaging sugar is. And what’s more, the astounding correlation between sugar and other addictions.
For starters, sugar is more addictive than cocaine.
Now that’s a statement for you.
Rats in a study regularly chose sugar water over cocaine. Even the rats who had developed cocaine addictions prior to being exposed to the sugar water, still chose the sugar water first (1).
But it’s not just cocaine addiction that sugar mimics in the brain.
What science has started to understand is that sugar has a symbiotic link to alcoholism.
It’s exactly the same dopamine receptors in alcoholic brains that light up when we consume sugar. In fact, it’s the same D2 dopamine receptor that identifies alcoholics and addicts that we see in sugar addicts (2).
Alcohol is full of one essential ingredient. Sugar. Drinking alcohol is potentially one of the fastest ways to mainline sugar into your system, straight through your very absorbent stomach lining and into your blood stream. Then it’s on the super highway straight to the pleasure receptors in your brain.
So what’s going on biologically when we consume sugar or alcohol?
We now know that initial exposure to the drug means the brain undergoes very mild, brain chemistry changes. However, repeated exposure to alcohol induces longer lasting changes in neuron function and habit formation. It’s when the brain undergoes neoplastic changes that the drug-taking behaviour is no longer under voluntary control.
These brain chemistry changes start from an increase in the levels of dopamine.
But what exactly is dopamine and what does it do?
Dopamine is a chemical, a neurotransmitter, that is sometimes called the reward chemical because it produces pleasurable feelings. It’s so pleasurable that we will pretty much do anything for a hit dopamine. But the responding crash in our serotonin levels and the damage that, in this case, alcohol does to the dopamine receptors, means we require more sugar or more alcohol to get the same level of dopamine rush. In one study, rats showed a distinct correlation between the dopamine released when consuming sugar to that when consuming alcohol (3).
It is generally thought that alcohol is used socially for its positive affect. But with chronic alcohol exposure, it leads to adaptation in brain function that results in dependence. This is what neuroscience refers to as a transfer from social use to addiction via the process of neuroplasticity in the brain. Neuroplasticity is the brain’s ability to change and reorganise itself by forming new connections between nerve cells. It’s a bit like re-routing the GPS in your car to take a different path. With alcohol and sugar it’s the change in brain chemistry, that is, a change in the neurotramsimtters, such as levels of dopamine and serotonin, that trigger the neuroplasticity of your brain to re-route.
It is the levels of dopamine that we look first when observing the neuroplastic changes in the brain. Dopamine levels increase from cells in the brain in an area called the Ventral Tegmental Area (VTA). This is the same area of the brain that is induced by addictive drugs. The VTA is essentially the main branch of the drug and reward circuitry system. It is important in cognition, motivation, orgasm, drug addiction and intense emotions, like love.
The dopamine spreads out from the VTA to the pre-frontal cortex, which is the main problem solving area and thinking area of the brain, to the nucleus accumbens, the part of the brain focused on reward, pleasure and addiction. We call this the mesolimbic dopamine system, and it’s this system that ultimately changes the neuroplasticity of the brain, and more importantly, the gene expression. It’s the changes in the gene expression that is now considered the reason for the change from social drug use to dependency and ultimately, relapse (4).
What does this mean for recovering alcoholics?
The mesolimbic dopamine system in the brain is what drives the addict to choose alcohol but it’s also what drives us to choose sugar too. Studies show a link between recovering alcoholics and food addiction, or more particularly sugar addiction (5). The study shows that as with drug addiction or alcohol addiction that compulsive eating habits like obesity or bulimia involve the same reward circuitry in the brain. Obese people and drug addicts show altered D2 dopamine receptors in the brain.
Secondly it means recovering alcoholics instead of turning to sugary foods in recovery, a method that used to be employed to help alcoholics avoid the craving for alcohol – you stay as far away from it as possible. The outdated model of giving an alcoholic sugary sweets, merely mimicked the exact neural pathways trying to be avoided. That approach simply swapped one addiction for another. But by removing sugar entirely, alcoholics stand a much better chance of remaining sober.
Whilst many may not suffer the debilitating effects of alcoholism, if you are trying to reduce how much you drink you may want to look at reducing your sugar intake too. If you’re planning on swapping your nightly glass of wine for a bowl of ice-cream, all science has to say is that you’re merely swapping one addiction for another. Might just be better to grab a cup of green tea instead. Not nearly as exciting as trying to cross a six lane highway, but you’ll live longer.
 Intense Sweetness Surpasses Cocaine Reward. Magalie Lenoir,# Fuschia Serre,# Lauriane Cantin, and Serge H. Ahmed* PLoS ONE. 2007; 2(8): e698. Published online 2007 Aug 1. doi: 10.1371/journal.pone.0000698 PMCID: PMC1931610
 Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Paul M Johnson & Paul J Kenny. Nature Neuroscience 13, 635–641 (2010) doi:10.1038/nn.2519. Received 29 December 2009 Accepted 16 February 2010 Published online 28 March 2010 09 July 2010
 Daily bingeing on sugar repeatedly releases dopamine in the accumbens shell. Rada P, Avena NM, Hoebel BG. Neuroscience. 2005;134(3):737-44. PMID: 15987666
 Drug addiction as a pathology of staged neuroplasticity. Kalivas, P.W., and O’Brien, C. Neuro-psychopharmacology 33:166–180, 2008.
 Dopamine signaling in food addiction: role of dopamine D2 receptors. Baik JH. BMB Rep. 2013 Nov;46(11):519-26. Review. PMID: 24238362