Ever wondered how Vyvanse actually works in the brain?
Much information exists on the Web about Vyvanse’s side effect profile and its comparison to other drugs in the same class. But, little information is available on drug’s neurochemistry, and how it works in your brain and body. We’re here to solve that.
Vyvanse: The Basics
As mentioned in an earlier article, Vyvanse (lisdexamfetamine dimesylate) is made of d-amphetamines (dextroamphetamine).
The drug is officially labeled an amphetamine stimulant, and is most commonly taken orally (capsule form). Other examples of prescription amphetamines are Adderall, Evekeo, and Mydayis. To simplify things, amphetamines essentially speed up the messages between your brain and body. Hence, the street name “speed” for meth (methamphetamine).
Beginning in the Bottle
After swallowing, Vyvanse descends through the stomach and gets absorbed from the gastrointestinal tract and converted to dextroamphetamine, which is most responsible for Vyvanse’s activity (1).
As an amphetamine, dextroamphetamine readily crosses the blood-brain barrier to reach its main site of action: the brain.
Dextroamphetamine works by raising levels of neurotransmitters in your brain called dopamine and norepinephrine. These chemicals are what help you pay attention and focus in school and work, and are associated with feelings of motivation and euphoria.
Vyvanse, and other amphetamines, are able to act on dopamine because of their similar structure to dopamine and other neurotransmitters (2).
Vyvanse and Dopamine in the Brain
The two mechanisms Vyvanse uses to produce its effects are: 1) the blocking of the dopamine transporter (DAT), which typically clears dopamine, serotonin, and other neurotransmitters from the synapse (small gap at end of neuron). 2) the disruption of the vesticular storage of dopamine, which allows dopamine to accumulate in the cytoplasm (3).
Combined, these mechanisms cause an abundance of dopamine and norepinephrine in the synapse, and are what gives Vyvanse, among other amphetamines like cocaine, its “kick”. Lets look at these processes on a deeper level below.
Because of its structure, the dextroamphetamine is able to enter the terminal button of the presynaptic neuron via its dopamine transporters. The terminal button of the presynaptic neuron is just the end of the neuron where the neurotransmitters are released (4). Once inside the presynaptic neuron, Vyvanse pressures the dopamine molecules out of their storage vesicles and releases them into the synaptic gap by making the dopamine transporters work in reverse (i.e. more dopamine is transported into the synapse and extracellular space, as opposed to being forced out (5).
In simplest terms, Vyvanse works by preventing the cells that released dopamine and norepinephrine from absorbing them again.
A less understood mechanism that Vyvanse also uses is the exciting of dopaminergic neurons via glutamate neurons.
According to the National Institute of Health, Vyvanse “triggers the internalization of a glutamate transporter from the cell surface, which enhances the excitatory actions of amphetamine” (6). Glutamate transporters are simply neurotransmitter transporter proteins that move glutamate (another neurotransmitter) across cell membranes. As stated, the glutamate transporters essentially energize the amphetamine (and in turn triggering the dopaminergic neurons), giving Vyvanse its intensity so visible in its users.
Long Term Risks of Vyvanse Use:
As the drug is fairly new (approved by FDA in Jan ’15), no exhaustive long-term studies of the drug exist. Therefore, anyone should exercise caution and consult a medical professional before considering use. Preliminary trials suggest Vyvanse carries a host of long term negative health effects, such as reduced appetite , emotional instability, nervousness, and many more (7).
As always, we remain skeptical at Health & Life, particularly when dealing with novel medications with limited clinical observations.
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