I always love going to PNIRS- great people, fabulous research. This year there is the added bonus of beautiful Halifax ⛵️ To all fellow PNI enthusiasts, seize the opportunity to submit an abstract by 5/20! #PNIRS2024

Incorporating CRP testing in psychiatric care can empower patients to address inflammation triggers like stress and poor diet, possibly easing depression. Catch our featured work on Your Fantastic Mind! #MentalHealth #Inflammation #Depression

Had a great time promoting immunometabolic approaches to psychiatry at #ACNP2023 and reconnecting with mentors! @BIEmory @AndyMillerLab @TyeLab

It's so cool when you cold email a potential collaborator and they say YES and show support every step of the way... Thanks @caseredoxlab for a fantastic collaboration!!

I'm very interested in this recently-published paper (link below) that details the remarkable improvements in #type1diabetes with GLP-1 agonists (#semaglutide; #wegovy/#ozempic). These drugs get a lot of attention for the improvements in #type2diabetes, but the improvements in #type1diabetes highlight what I believe is the main benefit in disorders of #hyperglycemia (i.e., #diabetes). Many claim that the benefit of GLP-1 agonism is the insulin-secretagogue effect (i.e., they stimulate insulin release; this idea is appropriately challenged). This study removes insulin from the equation because people with T1DM don't have sufficient beta cells to make sufficient #insulin. However, they DO have ample alpha cells producing FAR too much #glucagon. The late Dr. Roger Unger proposed that T1DM is as much a disease of too much glucagon as it is too little insulin, and was able to correct T1DM by simply inhibiting glucagon. (As a reminder, whereas insulin seeks to lower blood glucose, glucagon seeks to raise it.) That semaglutide is able to correct glycemia in people with T1DM while lowering insulin needs is evidence, to me, that the glucagon-inhibiting effect is the primary mechanism of improving glucose in people with diabetes. nejm.org/doi/full/10.1056/NE…

Emerging preclinical data suggest that our T cells may actually prefer ketones, molecules we produce when we're fasting, doing a strenuous workout, or following a ketogenic diet. This isn't just a minor quirk of biochemistry - it appears that T cells fueled by ketones may be more effective at fighting infection. Typically, fasting has been associated with a suppression of immune function, which seems contradictory to the idea that ketones, produced during fasting, could enhance T cell activity. It's an enigmatic area of biochemistry, and a reminder that our biological systems are complex and multi-faceted, often evading straightforward interpretations. cell.com/immunity/fulltext/S…

We don't often hear about a CURE in medicine, but today it's happening! Fantastic new work from @GavegnanoGroup @MonicaReece showing an estimated 99.99% (!) elimination of HIV-1 viral reservoir with treatment with a JAK inhibitor. Congrats to all involved in this important work!!

"it does not appear to cause anhedonia" theatlantic.com/health/archi…

How much energy do we waste by generating psychobiological stress responses? And does this accelerate biological aging? In human cultured fibroblasts, chronic stress increases the energetic cost by 60% of life and accelerate multiple aging biomarkers. doi.org/10.1016/j.psyneuen.2…

A mind-blowing paper has come out today in @Nature In 2016, JC Venter Institute scientists trimmed a bacterial genome to its barest minimum required for life to synthesize what they called a "minimal genome" (science.org/doi/10.1126/scie…). Today, a group of scientists from Indiana University reports how that minimal genome evolved over 2000 generations in comparison to the non-minimal genome. The authors found that even when you reduce a bacterial genome to its absolute minimum where every nucleotide matters, the genome undergoes mutational events generation after generation as much as the non-minimal genome. One simply cannot stop the evolution. Just over 300 days of evolution (equivalent to 40,000 years in humans) the minimal cell has gained everything it lacked in fitness on day one in comparison to the non-minimal cell. When comparing the evolved traits between the minimal and non-minimal cells, the scientists found something striking. The evolutionary process increased the cell size of non-minimal cells but not that of the minimal cell. But that is not the striking part. The scientists were able to identify the key mutation that resulted in cell size evolution. And it turned out that the mutation that helped the non-minimal cells to grow bigger is the same that helped the minimal cells to stay smaller. Growing bigger had a survival advantage for non-minimal cells and not growing bigger had a survival advantage for minimal cells. So, the mutation had a context-dependent effect. This just demonstrates that the evolutionary effects on traits have no absolute direction. All that matter is what is beneficial for the organism's survival. The conclusion of the paper is metaphorically a quote from the Jurassic Park movie: “Listen, if there’s one thing the history of evolution has taught us is that life will not be contained. Life breaks free. It expands to new territories, and it crashes through barriers painfully, maybe even dangerously, but . . . life finds a way". (scienmag.com/artificial-cell…) nature.com/articles/s41586-0…

So excited I get to attend my first in-person @ACNPorg meeting as a travel awardee! A big thanks to my mentors @BIEmory for their support!!

Increasing evidence suggests that cardiometab and mental health are deeply intertwined in many levels (behavioral, biological incl genetic). Treatments that target this on a behav and/or pharmacol level could help. RCTs like this one will be crucial to provide answers.

My colleague just trashed my grant in the most helpful way possible, and I am so excited to use their feedback to make this proposal even stronger!!!! Senior PIs, take time to bless a junior PI with your critical eye. We love it!

Calprotectin is a pro-inflammatory protein that leads to negative consequences, right? NOT SO FAST!!! Our new accepted paper shows calprotectin appears to be protective after psychological trauma! bpsgos.org/article/S2667-174… But how???

Negotiating a faculty position can be confusing. Here, as a group of new faculty members, we pull back the curtains to explain nuances, identify negotiable components, and build a framework for the process of negotiation based on our recent experiences. authors.elsevier.com/a/1gDYR…

Time to wake up and smell the coffee. The field of Immunopsychiatry (and psychiatry) is in jeopardy if we don't change our clinical trial designs and our mind sets. One size does not fit all! Read "Burning Down the House" rdcu.be/c0RCv #acnp2022

Congratulations to @ParianteLab for winning the 2022 @ACNPorg Media Award for the digital magazine Inspire the Mind! Run by scientists @SPILabKCL, @inspirethemind_ brings accessible & accurate mental health research views to a broad audience (>200k views!) youtube.com/watch?v=E3YaC3j_…

Our next immunopsychiatry meeting will be on MONDAY 7th Nov at 4pm UK time! We will hear from @MandyBekhbat on #immunometabolism as biomarker of #anhedonia and from @JBrasanac on #immune signature of #MultipleSclerosis associated with #depression (link on the day)