IS SUGAR ADDICTIVE?
It's important to know about the addictive nature of sugar so that you can protect yourself from the compulsive lure it can so often present.
We use the phrase "sugar addiction" in everyday conversation because our experience is eerily reminiscent of what we think of as drug addiction. You start eating, believing you're only going to eat a certain amount but once you start you can't stop.
You try to get a handle on it. You try to cut down but you repeatedly fail. There's a compulsive quality to it that can start to take on a life of its own. Despite a strong motivation to stop you're unable to get consumption under control.
But here’s a question--do scientists actually believe sugar is an addictive substance? Some do and some don’t. Let’s concentrate on where they agree. Scientists generally view addiction as “a repetitive behavior that some people find difficult to quit."
How Sugar Is Like A Drug
The operative word in that definition is “some.” Not everyone who uses a substance gets addicted. In fact, most don’t. Example: For all the horrifying consequences brought on by the current opioid crisis, only 10% of users actually get addicted to opioids. The riskiest substance for addiction is tobacco (32%). Hence, the consensus among researchers is that addiction is a spectrum where some of us are mildly affected and others fully ensnared.
So far, sugar fits into that line of reasoning. Some people can have one or two Oreos and stop eating. Some won’t stop until they’ve finished the bag. Most people are somewhere in between.
Here’s another way sugar behaves like a drug. fMRI studies show that sugar lights up the same key parts of the brain lit up by drugs like cocaine.
And here’s another: Speed of action. Speed is a defining neurological basis of addiction. The faster a substance get into the bloodstream and then the brain, the stronger its powers of seduction. Nicotine, the chemical compound responsible for tobacco’s astronomical addiction rate, can reach your brain in ten seconds.
Sugar? Half a second.
That wasn’t a typo. Half a second. 600 milliseconds to be precise. This means sugar can reach the brain faster than drugs like cocaine and heroin by orders of magnitude.
Why Sugar Isn’t Like A Drug
There are reasons why many scientists think sugar does NOT qualify as an addictive substance. This includes the definition of “a loss of control” and what qualifies as the harm a behavior causes. But we're not going to get into that here because I don't want this to become a semantic debate.
My point in bringing all of this up is that while many scientists do not agree sugar should be officially labeled as an addictive substance, there is agreement that its properties encourage disordered eating (overeating, binging).
This means we have to be careful around sugary foods. We shouldn’t approach them the way we do other foods that don’t contribute to disordered eating, like fruits and vegetables. We need guard rails to protect ourselves from the substance’s ability to drive us off a cliff. We’re going to talk about those guard rails later.
BE AWARE
The objective right now is awareness: Sugar ignites our instinct to overeat in a way that no other food does. As you'll see elsewhere in the site, the food industry makes things worse by exploiting our vulnerability to sugar.
On average, Americans consume more than 3 times the recommended amount of sugar [1]. This is really bad news because added sugar intake increases the risk of obesity [1], high blood pressure [2], and heart disease mortality [3]. But sugar is not easy to reduce when you start consuming too much of it. Science shows that it is highly addictive, and shares the same neurobiological mechanisms by which drugs result in addiction [4].
Let's take a closer look at what the research says.
Signs of Addiction
Studies conducted on rats show that they display typical signs of addiction when they consume sugar intermittently. These signs include bingeing, craving, withdrawal symptoms, cross-sensitization, and gateway effect [5].
Binging
Bingeing refers to an excessive consumption that escalates. In a study, a group of rats received chow and a sugar solution for 12 hours everyday, and they were food-deprived for the rest of the day. The researchers noticed that the rats binged the first hour of every feeding period, and in 10 days, their sugar intake doubled [6].
Craving
Rats have also been shown to crave sugar when they abstain from it. In another study, rats were divided into 2 groups : the first group was given a sugar solution for 12 hours everyday, and the other was only given 30 minutes of access to the sugar solution. After 4 weeks, both groups stopped receiving the sugar and went on a 2 week deprivation period.
After that, sugar was reintroduced to the rats to see how much they will consume. Surprisingly, the first group cosumed 23% more than baseline. While the second group consumed less sugar than baseline.
This shows that during the abstinence period of 2 weeks, the rats that consumed a large amount of sugar initially were still craving it. The second group apparently didn’t, because they weren’t consuming enough sugar to induce craving [7].
Withdrawals
When rats consume excessive amounts of sugar and suddenly stop receiving it, they show the same signs of opioid withdrawal. Rats in a study were deprived of food for 12 hours, and given a glucose solution and chow for the next 12 hours daily.
Researchers made them withdraw from glucose by depriving them of food or by giving them naloxone, a medication used to precipitate withdrawal from opioids. They noticed that the rats started to behave differently after withdrawal.
They chattered their teeth, shaked their heads, had forepaw tremor and displayed more anxiety than baseline. These are the typical signs of opioid withdrawal. Additionally, their brains underwent changes that are similar to a morphine-dependent rat that was deprived of morphine [8].
Cross-Sensitization
Another property of addiction is cross-sensitization. It means that the intake of one drug makes a subject more sensitive to the effect of another drug. This has also been observed in rats that consume sugar. A study was conducted on rats, where they were given either sugar, chow or both. They were injected with cocaine to see how they would respond.
The sugar group responded more strongly to the cocaine than other groups. Even after 14 days, they were still affected by cocaine. That’s how sensitive they became to it after consuming too much sugar [9].
The gateway effect is a little similar to cross-sensitization, except that it refers to the increase in consumption of the other drug rather than sensitivity. A study conducted on rats investigated the gateway effect between sugar and alcohol. They fed a group of rats in an experiment either sugar and chow or chow alone. After that, they were all given alcohol.
The researchers found that the intermittent sugar group consumed the most alcohol of all the groups. In another experiment of the same study, they found that when given intermittent alcohol daily, the rats consumed more sugar than rats that weren’t exposed to alcohol. So the sugar acts as a gateway to alcohol consumption, and alcohol as a gateway to sugar consumption. Proving that they are both addictive subtances [10].
Human Studies
Sugar addiction has also been demonstrated in humans. A study was done to determine if sugar-sweetened beverages (SSB) can cause craving and withdrawal symptoms in adolescents after cessation. Participants consumed SSB regularly, and then they were asked to stop and only drink water and plain milk. They found that they craved SSB more, and had less motivation and overall well-being than baseline. These results were attributed to the addiction to sugar in the drinks, as the participants reported a decrease of approximately 3 ounces in daily sugar intake after SSB cessation [11].
In fact, sugar is even shown to be more addictive than cocaine.
In a study, rats were divided into 3 groups : a group exposed to cocaine, a group exposed to sugar, and a group exposed to both. They were provided with 2 levers that they can pull to get either cocaine or sugar. The cocaine group chose the cocaine lever more often, the sugar group chose the sugar lever more often, but the group that was initially exposed to both, chose sugar more often [12]. Which proves that sugar is more addictive for the rats than cocaine is. Studies have found the same results in human participants. The effect of sugar on the human brain is stronger than that of cocaine [13].
These studies should make us rethink our relationship with sugar. We might be unknowingly exposing ourselves to an extremely addictive substance that poses significant health risks including obesity, diabetes, and heart disease. Although reducing our sugar consumption can be challenging, the health and well-being benefits may be worth the effort [14].
References
1. Faruque, S., Tong, J., Lacmanovic, V., Agbonghae, C., Minaya, D. M., & Czaja, K. (2019). The Dose Makes the Poison: Sugar and Obesity in the United States - a Review. Polish journal of food and nutrition sciences, 69(3), 219–233. https://doi.org/10.31883/pjfns/110735
2. DiNicolantonio, J. J., & Lucan, S. C. (2014). The wrong white crystals: not salt but sugar as aetiological in hypertension and cardiometabolic disease. Open heart, 1(1), e000167. https://doi.org/10.1136/openhrt-2014-000167
3. Yang, Q., Zhang, Z., Gregg, E. W., Flanders, W. D., Merritt, R., & Hu, F. B. (2014). Added sugar intake and cardiovascular diseases mortality among US adults. JAMA internal medicine, 174(4), 516–524. https://doi.org/10.1001/jamainternmed.2013.13563
4. DiNicolantonio, J. J., O'Keefe, J. H., & Wilson, W. L. (2018). Sugar addiction: is it real? A narrative review. British journal of sports medicine, 52(14), 910–913. https://doi.org/10.1136/bjsports-2017-097971
5. Avena, N. M., Rada, P., & Hoebel, B. G. (2008). Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neuroscience and biobehavioral reviews, 32(1), 20–39. https://doi.org/10.1016/j.neubiorev.2007.04.019
6. Colantuoni, C., Schwenker, J., McCarthy, J., Rada, P., Ladenheim, B., Cadet, J. L., Schwartz, G. J., Moran, T. H., & Hoebel, B. G. (2001). Excessive sugar intake alters binding to dopamine and mu-opioid receptors in the brain. Neuroreport, 12(16), 3549–3552. https://doi.org/10.1097/00001756-200111160-00035
7. Avena, N. M., Long, K. A., & Hoebel, B. G. (2005). Sugar-dependent rats show enhanced responding for sugar after abstinence: evidence of a sugar deprivation effect. Physiology & behavior, 84(3), 359–362. https://doi.org/10.1016/j.physbeh.2004.12.016
8. Colantuoni, C., Rada, P., McCarthy, J., Patten, C., Avena, N. M., Chadeayne, A., & Hoebel, B. G. (2002). Evidence that intermittent, excessive sugar intake causes endogenous opioid dependence. Obesity research, 10(6), 478–488. https://doi.org/10.1038/oby.2002.66
9. Gosnell B. A. (2005). Sucrose intake enhances behavioral sensitization produced by cocaine. Brain research, 1031(2), 194–201. https://doi.org/10.1016/j.brainres.2004.10.037
10. Avena, N. M., Carrillo, C. A., Needham, L., Leibowitz, S. F., & Hoebel, B. G. (2004). Sugar-dependent rats show enhanced intake of unsweetened ethanol. Alcohol (Fayetteville, N.Y.), 34(2-3), 203–209. https://doi.org/10.1016/j.alcohol.2004.09.006
11. Falbe, J., Thompson, H. R., Patel, A., & Madsen, K. A. (2019). Potentially addictive properties of sugar-sweetened beverages among adolescents. Appetite, 133, 130–137. https://doi.org/10.1016/j.appet.2018.10.032
12. Lenoir, M., Serre, F., Cantin, L., & Ahmed, S. H. (2007). Intense sweetness surpasses cocaine reward. PloS one, 2(8), e698. https://doi.org/10.1371/journal.pone.0000698
13. Ahmed, S. H., Guillem, K., & Vandaele, Y. (2013). Sugar addiction: pushing the drug-sugar analogy to the limit. Current opinion in clinical nutrition and metabolic care, 16(4), 434–439. https://doi.org/10.1097/MCO.0b013e328361c8b8
14. Vreman, R. A., Goodell, A. J., Rodriguez, L. A., Porco, T. C., Lustig, R. H., & Kahn, J. G. (2017). Health and economic benefits of reducing sugar intake in the USA, including effects via non-alcoholic fatty liver disease: a microsimulation model. BMJ open, 7(8), e013543. https://doi.org/10.1136/bmjopen-2016-013543