AJ Martin

Share Your Story Get involved in BRP's new research project aiming to understand how we keep each other safe.

We're excited to announce the launch of our new research project in collaboration with @drkarenzamoore.bsky.social from Newcastle University & @crew2000.bsky.social! 🏴󠁧󠁢󠁳󠁣󠁴󠁿

We're looking for Scotland-based young people aged 16–30 who take #benzos to share your stories with us: brp.org.uk/ShareYourStory

Sign the Petition Stand with Ángel: urge Queen Mary University support a student left without funding

Please co-sign this open letter calling on @qmul.bsky.social to reinstate Angel and to change practices to stop any other student from being subjected to this kind of ordeal: c.org/kKdrfyLYy8

they’re always so waffly and dense, and the recognition that it’s not the voice of a human reduces my motivation to read it to 0

anyone who can spend months/years getting a paper published can surely spend a few mins writing a thread that is intriguing and concise?

also I imagine will.i.am can spend all that time working because he can afford to pay people to cook, clean, do laundry etc for him!

Even if you’re the most driven person, you still need rest. Some of my best ideas come when I’m not actively working. Also, people fought for us to have 40 h work weeks!

That said, I do enjoy spending some of my 5–9s volunteering at @brp.org.uk 🥰

Me sat by my poster after a long day of talking about alpha2delta and calcium channels, tired but still smiling!

Thank you for an amazing week @biophysicalsoc.bsky.social #BPS2025 already missing the sun back in London🥲

Screenshot of our poster details from the BPS Events conference app. Title: LB64 - UNCOVERING A NOVEL AUTOINHIBITORY DOMAIN OF α2δ SUBUNITS ESSENTIAL FOR FUNCTIONAL MATURATION OF VOLTAGE-GATED CALCIUM CHANNELS Session : Posters: Voltage-Gated Ca Channels (Late) Location : West Exhibit Hall Date : Tuesday, Feb 18 1:45 pm Duration : 2 hours Authors: Alexander J.L. Martin, Najoua Biba, Hannah J. Lee, Dario S. Linklore, Matthew Day, Annette C. Dolphin, Ivan Kadurin. Authors from Department of Biochemistry, QMUL, and Department of Neuroscience, Physiology and Pharmacology, UCL.

Counting down the days to #BPS2025 — my first intl conference and 2nd time leaving Europe ✈️

Stop by my poster for a chat about what our lab’s been discovering about α2δ and CaV channels 🧠

📍West Exhibit Hall, 1:45–3:45 pm Tues 18th Feb

Any fellow PhD students attending, it’d be great to link up!

"Biased" estimates.

"Excluded" outliers.

Controlled for "race and ethnicity" and "socioeconomic" "status".

"Inclusion" criteria for systematic reviews.

This is all basic, apolitical, technical science language. It would be standard in basically any empirical paper, on any topic.

Anyone concerned about UK universities (and you should be!) please sign this open letter to the government (the link goes to the letter itself, click through from that to sign)

Increasing London weighting to better fit the exorbitant cost of living here won’t address wider causes, but it would provide a survivable standard of living for students without additional income, and those with dependents.

An infographic summary of the 3 key findings from the 2019 report on London cost of living. 4 in 10 Londoners have an income below what is needed for a decent socially acceptable living standard. Up to 58% more expensive to reach a decent standard of living in London than in other urban areas of the UK, thanks to housing, childcare and transport costs. 1/3 of all pensioners in London now have incomes below the Minimum Income Standard, up from 1/4 in 2011.

A 2019 report from Loughborough’s Centre for Research in Social Policy found the cost of living to be 15–48% higher in London than the rest of the UK.

This seems to be at least partially driven by rents, taking up at least 40% of Londoners’ salaries vs 29% outside London.

Glad to see UKRI PhD stipends finally being brought in-line with the National Living Wage

There’s still a long way to go, as the measly £2000 London weighting puts students in the capital at a disadvantage

if you give a rat cocaine,
she will want jazz
doi.org/10.1037/a002...

TLDR: Pregabalin increases the effects of opioids when combined. Increases in analgesia, euphoria, and possibly also reversal of tolerance, may be desired. However, increased respiratory depression and tolerance reversal can increase risk of overdose and death. Carry naloxone in case of emergency!

I hope no one reading this has to respond to an overdose but, with the UK drug-related deaths emergency only getting worse, its good to be prepared.

Visit your local harm reduction hub (like @releasedrugs.bsky.social in London) or drug support service to get naloxone trained!

Stay safe 🫶

The aim of naloxone is to restore breathing, not necessarily to sober someone up — this can precipitate withdrawal symptoms. Wait with them until the ambulance arrives, and hand over your used naloxone so they know how much you administered.

If someone becomes unresponsive, call 999 (or your country's equivalent). Put them in the recovery position, check their breathing and administer naloxone. The operator will be able to talk you through this.

💊 Test your stuff: WEDINOS has a free anonymous mail-in drug checking service in the UK
💊 Stick with friends: Try not to use alone, and stagger doses between you so someone is able to respond if something goes wrong
💊 Carry naloxone: Naloxone is an opioid reversal drug that can save a life

💊 Start low, go slow: Take a small amount and wait to feel the effects before deciding whether to take more.
💊 Reduce the dose of each: As both increase each others effects, take less of each together than you would on their own
💊 Stagger doses: Wait to feel the effect of one before taking the other

How can people reduce harms relating to pregabalin and opioid co-use?

The simplest way would be to not mix them. But just telling people not to do something doesn't work! (see: the last 50 years of prohibition)

Some key harm reduction tips are below⬇️

With nitazenes emerging in the UK's opioid and benzo supplies, the risk of opioid-related harms is becoming even more pressing. Nitazenes are at least as strong as fentanyl, meaning co-use with pregabalin may further increase the risk of an overdose.

So is there more opioid and pregabalin co-use? Possibly, going by drug-related death statistics, but it's hard to measure prevalence.

Increasing homelessness and poverty, worsening mental health, among other things may lead people to use these drugs to cope in the absense of adequate support.

How does pregabalin do this, when its not an opioid?

The mechanisms underlying pregabalin and opioid-induced respiratory depression are still under investigation, and there are multiple ways this might happen. I might do another thread in the future on what we currently know.

Figure 4C, from Lyndon et al., Addiction. 2017 September ; 112(9): 1580–1589. doi:10.1111/add.13843. AUC analysis of the data in A & B [see ref 18] indicated that in morphine pretreated mice pregabalin + morphine induced significantly greater depression of respiration than morphine alone (P<0.05). N = 6 in each case.

In animal studies, pregabalin has been shown to reverse tolerance to opioids like morphine. Lyndon et al. found that morphine-tolerant mice experienced significantly depressed respiration when treated with morphine + pregabalin.

However, pregabalin also increases adverse effects from opioids. Gomes et al. found that higher doses (300 mg+) of pregabalin significantly increased the risk of opioid-related deaths.

One particular side effect is respiratory depression (slowed breathing) — a hallmark of opioid overdose.

Opioid and gabapentinoid co-use seems to be a significant contributer to this mortality.

Gabapentinoids taken alongside an opioid increases effects such as euphoria and pain relief. In a 2000 randomised-controlled trial, gabapentin significantly increased morphine's analgesic effects.

Pregabalin was approved in the EU in 2004, and has gone on to be prescribed to approx. 800,000 UK patients in '23/24.

There has also been an increase in non-medical use (i.e., without a prescription). But pregabalin doesn't seem to be solely responsible, as 97% of deaths also involved other drugs.

but there is a working model: Gabapentinoids block recycling of α2δ and calcium channels back to the synapse, thereby reducing overactive signals in pain, epilepsy, and anxiety.

This is why patients have to wait at least a few weeks for these drugs to work. So why are they involved in deaths?

That said, pregabalin and gabapentin don't mimic GABA's activity or activate GABA receptors. Instead, they bind to a voltage-gated calcium channel subunit called alpha2delta (α2δ).

There isn't complete consensus on how gabapentinoids interaction with α2δ leads to its effects,

The chemical structures of GABA, compared to gabapentin and pregabalin. Source: Patel and Dickenson, Mechanisms of the gabapentinoids and α2δ-1 calcium channel subunit in neuropathic pain. Pharmacology Research & Perspectives, 4:2 (2016). DOI:10.1002/prp2.205

First, what is pregabalin?💊

Pregabalin is a drug from the gabapentinoid class: used to treat neuropathic pain, epilepsy, and anxiety.

The gabapentinoids were designed to mimic GABA — the brain's primary inhibitory neurotransmitter (i.e., slows brain signals).