Make rolling better.
Acetyl L Carnite
Acetyl L-Carnitine (ALCAR) synergises incredibly effectively with alpha-lipoic acid (below), working to remove the “fuel” for toxic oxidisation in the brain – these two substances can easily cross the blood-brain barrier, meaning that they can target oxidisation happening there while others, like vitamin C, will concentrate elsewhere.
Like acai berry, ginger is loaded with dozens of beneficial chemicals ranging from antioxidants to anti-inflammatories and antidepressants which can prove beneficial when fighting off oxidative stress and even the psychological effects of a comedown. As an added benefit for those of you who get queasy on the come-up, ginger is renowned for its ability to combat nausea (usually intended for when you’re ill, but it does the trick on a rough come-up too)..
One of the ways that the stimulant effects of MDMA work is by the opening of ion channels which flood calcium into the neuron. However, all this calcium interferes with the working of the neuron; magnesium blocks this channel to moderate the calcium influx and mitigate the harm caused. The bis-glycinate salt (a mix of magnesium and glycine) is among the most bioavailable forms of magnesium, meaning that the magnesium is absorbed into the body effectively.
Vitamin C works to enhance the overall antioxidant effect. In addition to scavenging reactive oxygen species in broadly the same manner as EGCG, donating a hydroxyl group to reduce the oxygen atom to a water molecule, vitamin C assists in the recycling of vitamin E to enhance its effects.
Like the ALCAR/ALA pair, co-enzyme Q10 (CoQ10) acts to prevent peroxidation of fatty acid chains, but tends to concentrate in the heart/liver/kidneys rather than the brain. It also works to manage calcium channels (like magnesium bis-glycinate below) where it resides and recycles vitamin E (also below), so that both the vitamin E in your RollKit and your dietary vitamin E are “in use” for longer and hence more effective.
Acai berry is rich in a variety of antioxidants, which are key in fighting off MDMA toxicity. It’s not a totally settled question yet, but the literature so far leads us to believe that this toxicity is the result of unstable, cell-damaging compounds called free radicals, which induce oxidative stress on the cell. Because this is a complex process, we use a stack of different antioxidants to interrupt it at several vulnerable spots, with acai providing a broad base for us to start from.
Alpha Lipoic Acid
Alpha-lipoic acid (ALA) combines with acetyl l-carnitine (above) to prevent MDMA toxicity in the brain. Together, these two substances are astonishingly effective in interrupting the processes of glutamate toxicity: promoting endogenous antioxidant enzymes and, this one is key, transferring and breaking down fatty acid molecules. This prevents the formation of reactive oxygen species, or ROS and in turn prevents any that slip through from “stealing” electrons from more fatty acids.
Green Tea Extract
Green tea is rich in a substance called epigallocatechin gallate, which we’ll refer to from here as EGCG for obvious reasons. In addition to its diuretic effects (counteracting MDMA, which makes it very difficult to pee), EGCG is also an antioxidant molecule which directly deactivates reactive oxygen species (ROS) by releasing a hydroxyl ion, which binds with the rogue oxygen to produce a molecule of water.
The research behind it
Numerous studies have been done using the same natural supplements in our kit, and below we have listed them for you to read through and gain a better understanding of the mechanisms and the role supplements can play in safety with MDMA use.
Ascorbic acid prevents MDMA‐induced hydroxyl radical formation and the behavioral and neurochemical consequences of the depletion of brain 5‐HT
Department of Psychiatry, Case Western Reserve University, Cleveland, Ohio
Acetyl-l-carnitine provides effective in vivo neuroprotection over MDMA-induced mitochondrial neurotoxicity in the adolescent rat brain
Toxicology Department, Faculty of Pharmacy, Univer- sidade do Porto (UP), Porto, Portugal
Division of Neurotoxicology, NCTR/FDA, Jefferson, AR, USA