Can’t stop yourself from going online? Then you are not alone. We shop online, we communicate online, and we learn online, and with all of the applications that the World Wide Web has to offer, most people could not spend a whole day without the Internet. Think about it, what are you doing right now?
As a busy university student, I find myself constantly online. However, I’ve never felt truly addicted to the Internet, so I have always questioned the existence of “Internet Addiction Disorders”. After researching this disorder, it turns out that it is quite real and it affects almost 4% our world’s population. Luckily for me, I received a low score on Kimberly Young’s Internet Diagnosis Test (a national test to diagnose Internet addictions), which suggests that I am not an addict.
Internet Addiction Disorder (IAD) is a new term that is being reviewed for entry into the American Psychiatric Association’s DSM1. Internet abusers are known to have certain addictive behaviours such as euphoric1 sensations when spending time online, and even withdrawal symptoms when they are away from the net such as feeling lonely and angry from deprivation and lying about their Internet habits. National statistics suggests that approximately 1 in 8 Americans have been diagnosed with IAD, but little research has been conducted to characterize the molecular basis of this addiction. However, over the past decade, several studies2 have suggested that non-drug and illicit drug addictions both work by affecting the dopamine reward system1. These findings concluded that there may be genetic pre-dispositions correlated to Internet addictive behaviours.
You heard me right. You’ve spent your whole life escaping addictions by staying away from illegal substances, and you find out your genes might make you more prone to IAD. Great. How are you suppose to know if you are more susceptible to this addiction, and how are you going to keep yourself away from the Internet? Today, people are diagnosed with IAD when they develop anxiety from being away from social media, and Internet websites. Before I explain to you why your genes can make you more susceptible to the Internet addictions, you’ll have to understand the brain’s chemical rewards system.
Basically, the brain’s reward pathway is controlled by dopamine, which sends our “happy feelings” to the limbic system1, and tells our brains to adopt a “feel good” behaviour. The brain has several parts involved in the reward pathway including the mesolimbic dopamine system1, which transmits dopamine from the ventral tegmental area1 (VTA) of the brain to the limbic system through the nucleus accumbens region1 (Figure 1). Dopamine is a neurotransmitter that is released into the VTA when you feel pleasure, and it is dopamine that activates the euphoric signal to be sent from the VTA to your prefrontal cortex1. Without dopamine release and neural stimulation, we would never develop pleasurable feelings. However, like everything else in our bodies, dopamine must be regulated to control the activity of the reward pathway.
Typically, in a normal brain, dopamine is released from a presynaptic neuron into the synaptic area between dopaminergic neurons. While in the synapse, dopamine will bind to dopamine receptors (D2 receptors) on the post-synaptic neuron causing the activation of the receptors by a conformational change. The D2 receptors are G-protein coupled receptors1, and when they are activated, they activate a G-protein that directly stimulates adenyl cyclase1 to produce cAMP1 in the cell, thus causing a signal transduction pathway. This conduction will continue the signal transmission to the prefrontal cortex, until a sense of euphoria is released. After this signal transmission is sent, the dopamine molecules in the synapse must be removed to regulate neural signaling. Several proteins in the synaptic area are involved in sequestering dopamine from the synapse including dopamine re-uptake pumps, which bring dopamine back into the pre-synaptic neuron, dopamine transporters that carry the dopamine to the re-uptake pumps, and enzymes involved in dopamine cleaving (Figure 2A). An example of an enzyme that degrades dopamine in the synapse is the catecholamine-o-methyltransferase enzyme.
But how is the dopamine pathway involved in addiction? Almost all recreational drugs affect the dopamine pathway in a similar manner. Drugs cause high concentrations of dopamine to accumulate in the synaptic areas of the dopaminergic neurons for long periods of time. With high dopamine present in the synapse, the reward signal to brain becomes more intense and continuous for the drug user, thus giving them a euphoric high. Different drugs cause high dopamine accumulation in different ways by interacting with the proteins responsible for dopamine degradation and removal from the synapse. Stimulants, like Cocaine, bind to the dopamine re-uptake pumps on the presynaptic neurons and stop dopamine from being removed from the synaptic region thus increasing its concentration in the synapse and prolonging the high (Figure 2B). After a couple of hours, cocaine concentrations decrease, and dopamine re-uptake will resume.
Drug addictions are characterized by their ability to sensitize your brain and to cause tolerance. Drug sensitization occurs when users feel a high euphoric feeling after they take a drug that stimulates their reward system; however, when a user takes a drug over and over again they develop drug tolerance. Your neurons are smarter than you think, so when you’re ready to use the drug for a second time, your cells will try everything they can to reduce the continuous dopamine transmission in the synaptic area to regulate the reward pathway. One way they try to decrease this activation is by reducing the number of dopamine receptors on the postsynaptic neuron. With fewer receptors available, a reduced signal is transmitted. Hence, the user develops tolerance towards the drug and needs more concentrations of the drug in the future to feel the same reward.
Following me so far? Here comes the interesting part: People with Internet Addiction Disorder seem to have similar addiction symptoms as drug users, and this may be because high levels of dopamine has been seen to accumulate in the synaptic areas of the reward pathway after Internet use. However, there have been many studies on non-drug addictions, such as gambling and food addictions that suggest that these non-drug addictions may only develop in people who have certain genetic pre-dispositions that can stimulate an addictive pattern. Therefore, unlike drug addictions that can affect anyone who uses drugs, non-drug addictions only affect people with certain genes that make them more susceptible to becoming an addict.
In hopes to determine if there was a genetic susceptibility to IAD, Han et al2 from Harvard Medical School, did a study focusing on Internet addictions in video game play in 2007. In their studies, they found two conserved single nucleotide polymorphisms in the D2 dopamine receptor and in the catecholamine-O-methyltransferase genes, respectively, in people who were addicted to Internet games compared to those who do not game online excessively. Single nucleotide polymorphisms1 are small changes found in a genetic code compared to a norm group. Why is this so interesting? These exact polymorphisms are also correlated to gambling addictions.
When comparing Internet addicts and a norm group, they found high variations in the Taq1A1 locus of the D2 receptor gene in excessive Internet users alone. They also found that most Internet addicts were homozygous for this allele. They suggested that this conserved change among addicts might lead to a decrease in the density of the D2 receptors on the post synaptic neurons; consequently, decreasing pleasure transmittance and increasing the users tolerance to achieve reward. They also found a conserved SNP in the catecholamine-o-methyltransferase gene in Internet users alone. They suggested that this SNP may impair the enzyme’s activity to degrade dopamine in the synapse. This would allow for increased dopamine concentration in the synapse for longer periods of time causing a longer high.
Furthermore, in 2012, Hou et al2 at the University School of Medicine in Zhejiang, China, used a radioactive label to label dopamine transporters in the synapse and found that there is was a large reduction in the amount of dopamine transporter proteins in people with IAD compared to a norm group. This transporter protein binds to dopamine and carries it to the neural presynaptic terminal after signal transmission to help decrease dopamine from the synaptic area. Thus, fewer transporters would increase dopamine concentrations in the synapse.
So, next time someone tells you that the Internet can’t be truly addictive, you can tell them they’re wrong. These findings suggested that there might be genetic predispositions correlated with Internet addiction disorders. See Figure 2C for an overview of how dopamine concentrations may be accumulating in the dopaminergic neural synaptic areas of people with IAD.
Although this is still all new science and no major conclusion about IAD has been made, many researchers are beginning to focus their addiction studies in this field as the Internet is so prominently used in our society. Because our generation runs on the World Wide Web, some pharmacologists have already begun running clinical trials on the use of the FDA approved drug Bupropion, a drug used to treat nicotine addictions, on Internet users. How fascinating is it that both substance and non-substance dependent addictions show common biological backgrounds and perhaps may be treated the same way? So, what do your genes say about you? We are the most active generation of Internet users and without proper caution into how much time we spend online; this addiction disorder may take over faster than we think.
Thinking you might have Internet Addiction Disorder?
Check out Kimberly Young’s Diagnosis Test to see where you fall with respect to IAD. This is the standard test to diagnose IAD, and ironically it’s online!
1: See Blog Definitions Page for full definitions of scientific terms
2: See Recent Literature Page for references used in this blog and additional papers regarding IAD