(side note, can a moderator inform me on the policy regarding citing with a scihub link?)
Sci-hub is cool.
I'm not entirely sure why taking suboxone 60 hours into a cold turkey is sending you into withdrawals, bupe shouldn't have this effect and theoretically the naloxone is added just as a deterrent for IV use (the naloxone isn't absorbed orally very well).
There have been some changes noted in the way that opioid receptors behave after using opioids chronically that may help explain what the OP has rather anecdotally reported, but I'm not sure exactly how.
Normally most opioid receptors couple to a signaling cascade element called a G protein, with activation of the opioid receptors resulting in different effects depending on what type of G protein the opioid receptor is coupled to.
Most of the opioid receptors in question (Mu Opioid Receptors) are bound to the G protein "Gi/o", which causes inhibition of cell firing and the desirable effects. But with chronic use of opioids, the MORs can switch coupling to excitatory "Gs" G protein coupling, stimulation of these Gs coupled MORs essentially produces withdrawal symptoms.
The reason why ultra low dose naltrexone/naloxone can help with opioid tolerance/withdrawal at very low doses is that naltrexone/naloxone can help reverse this aberrant coupling by binding to a high affinity site on the cytoskeleton that is involved in this G protein coupling switch, hence doses like 0.125mg naltrexone appear to help with opioid withdrawal and tolerance without blocking enough MORs to offset the beneficial effects on G protein coupling. If the naltrexone dosage gets too high, it becomes unhelpful.
Agonists display differential affinity for a G protein coupled receptor depending upon what G protein its coupled to, and its thought that opioid agonists tend to have higher affinity for Gs coupled MORs than Gi/o coupled MORs, thus leading to some facets of tolerance (the opioids tend to stimulate the Gs coupled MORs). The old theory of why ultra low dose naltrexone helped with opioid tolerance/withdrawal was actually that it preferentially bound to and blocked the Gs coupled MORs.
One explanation is that bupe is particularly good at stimulating the Gs coupled MORs that can still be present in acute WDs, but that stimulation of Gs coupled MORs will wear off and downregulation/desensitization of those Gs coupled MORs by bupe could mean that its only a matter of time until bupe no longer causes precipitated withdrawals.
The heroin used to negate precipitated withdrawals could simply be buying time while the Gs coupled MORs are endocytosed/downregulated.
So to recap the theory
1. Bupe stimulates lingering Gs coupled MORs, worsening withdrawals
2. Heroin use compensates and relieves
3. Gs coupled MORs are downregulated by bupe stimulation while heroin is buying time
4. Bupe eventually doesn't produce precipitated withdrawals after the heroin is gone because the Gs coupled MORs finally downregulated or reversed their coupling (maybe its possible the oral naloxone could be playing a role in this too?
sorry for the novel,
CY