A Modern Pharmacist

lee

Most of what gets called healthy is just normal. Normal is not the same as optimal.
I am Lee, a prescribing pharmacist working in the NHS. I also live with diabetes, so this is not theory for me. Every week I break down the tests, numbers and decisions that actually move the needle on long term health. The biomarkers I run on myself. The tests I cannot order on the NHS but wish I could. What it is really like navigating the health system as both the person prescribing and the person managing a condition every day.
No fluff. Just evidence, from a clinician who holds himself to the same standard

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S1 · E19
Yesterday · 29 min
Treating Hair Loss: What Actually Works
I'm going through my own hair loss treatment right now, so this episode is a bit more personal than usual. I walk through my own thinking on minoxidil and finasteride — the two main evidence-backed treatments — and why I've made the choice I have. Before we get to treatment, I cover what you need to rule out first: telogen effluvium from stress, iron deficiency, thyroid disorders, and B12/vitamin D deficiency. I also debunk the "check your mum's dad" myth for predicting hair loss — the real genetics are polygenic, not a single inherited trait. Then I get into the mechanisms: how minoxidil increases blood flow via vasodilation and why some people don't respond to it (a sulfotransferase enzyme issue), and how finasteride blocks the conversion of testosterone to DHT. I explain the genuinely strange DHT paradox — the same hormone shuts down hair growth on your scalp but promotes it on your beard and body — and why chasing a "zero DHT" target makes no sense clinically. Because this is a cosmetic rather than a life-or-death condition, I talk openly about how that should shift your risk tolerance around finasteride's side-effect profile, and why I've personally chosen to stick with topical minoxidil for now. Sources: Hamilton (1951, prevalence data via Endotext), Chumlea et al. 2004 (family history risk), Gupta et al. 2022 (minoxidil/finasteride hair count meta-analysis), Drake et al. 1999 (finasteride scalp DHT suppression data). This is informational purposes only, not medical advice. If you can't get seen by your own physician, by all means do so, but always speak to your own healthcare provider. New episodes every week.
S1 · E18
Sunday · 29 min
TRT: The Real Benefits, Risks, and When to Actually Use It
Testosterone replacement therapy is one of the most searched, most misunderstood treatments in men's health. I go through what the evidence actually shows: the genuine benefits, the real risks, the flawed studies that shaped 15 years of unnecessary fear, and exactly when treatment is justified. I start with the core diagnostic principle: the endocrine system is symptom-led, so a low number alone is never a diagnosis. True testosterone deficiency, once you require both a confirmed low level and real symptoms, affects only around 2% of men, mostly those over 60. I explain why free testosterone, not total testosterone, is the metric that actually matters, since only 1 to 4% of circulating testosterone is biologically active. On benefits, I cover the genuinely well-documented structural effects: lean mass gains, fat loss, and real increases in bone mineral density that surprised even leading researchers who assumed bone density couldn't be influenced this way. I also cover the metabolic benefits, including a 40% reduction in progression to type 2 diabetes in one major trial. On risk, I walk through the two badly flawed studies from 2013 and 2014 that wrongly linked TRT to heart attacks and strokes, including one that accidentally included women in a study meant to be all-male, and explain what the properly powered TRAVERSE trial actually found a decade later. I also cover the real prostate cancer picture, and go deep on fertility, including the mechanism behind why hCG and clomiphene work completely differently to preserve it. Studies and Sources: Prevalence and diagnosis: EMAS, the European Male Ageing Study. Structural and metabolic benefits: Amory et al., JCEM 2004, bone density; Page et al., JCEM 2005, body composition; Snyder et al., JAMA Internal Medicine 2017, bone density and strength; Cai et al. 2014, metabolic meta-analysis; Wittert et al., Lancet Diabetes and Endocrinology 2021, the T4DM trial; Yassin et al. 2016, continuous versus interrupted TRT. Cardiovascular controversy, the flawed studies: Vigen et al., JAMA 2013; Finkle et al., PLOS ONE 2014; Basaria et al., NEJM 2010; Xu et al., BMC Medicine 2013; Morgentaler et al., Mayo Clinic Proceedings 2015, critical re-analysis. Cardiovascular, the better evidence: Corona et al., JCEM 2018; Wallis et al., Lancet Diabetes and Endocrinology 2016; Lincoff et al., NEJM 2023, the TRAVERSE trial. Prostate cancer: multiple systematic reviews, 2004, 2008, 2009; TRAVERSE trial prostate sub-data. Fertility and HPG axis: classic hypothalamic-pituitary-gonadal axis physiology; intratesticular versus serum testosterone concentration data. Background and framing: Peter Attia, AMA number 28, All Things Testosterone and Testosterone Replacement Therapy, the Peter Attia Drive podcast, 2021. Informational only, not medical advice. New episodes of A Modern Pharmacist drop weekly.
S1 · E17
September 3 · 29 min
Statins, Diabetes, and Your Brain — What the Evidence Actually Shows
Statins are the most prescribed and most controversial medication on the planet. I am not debating whether they work, the evidence there is unambiguous. Instead I go deep on the two concerns patients raise with me most often: do statins cause type 2 diabetes, and do they harm your brain? On diabetes, I walk through a genuinely new mechanism discovered in 2024: statins alter specific gut bacteria, which reduces a bile acid called UDCA, which in turn lowers GLP-1 and worsens glucose tolerance. There is already a trial underway testing whether supplementing UDCA can fix this without losing the cholesterol lowering benefit. I also cover the real numbers, how many people develop diabetes per statin users treated, weighed against heart attacks and strokes prevented, and why higher intensity statins carry more risk than lower doses. On cognition, I explain why the brain being cholesterol rich does not mean statins starve it, since the brain has its own separate, protected cholesterol supply, and where the 2012 FDA warning about cognitive impairment actually came from versus what the trial evidence has consistently shown since. I also bring in the STAREE trial, published just days before recording this episode. Finally, I explain why this question just became more urgent: 2026 guideline changes now make statins a consideration from age 30, and what that means for an evidence base built on trials lasting a fraction of that exposure window. Studies and Sources: Mechanism, diabetes: She et al., Cell Metabolism 2024, 36(2), 408-421. NCT06684106, ongoing UDCA plus atorvastatin trial. Nature Reviews Endocrinology 2015, the diabetogenic action of statins. Diabetologia 2006, statins and adipocyte GLUT4. J Clin Invest 2011, adiponectin and AMPK pathways. J Cell Physiol 2019, mechanisms of statin induced new onset diabetes. Outcome evidence, diabetes: Sattar et al., Lancet 2010, 375, 735-742. Preiss et al., JAMA 2011, 305(24), 2556-2564. IPD meta-analysis, Lancet Diabetes and Endocrinology 2024. Ridker et al., Lancet 2012, JUPITER post-hoc analysis. Cleveland Clinic Journal of Medicine review 2023. NICE NG238 evidence review. Benefit versus risk: CTT Collaboration meta-analysis, 26 trials, over 170,000 patients, Lancet 2012. TheNNT.com, statins in low cardiovascular risk primary prevention. Collins et al., Lancet 2016, interpretation of statin efficacy and safety evidence. Outcome evidence, cognition: Cochrane review, statins for the prevention of dementia, HPS and PROSPER pooled. Zhou et al., JACC 2021, ASPREE trial. Ott et al., J Gen Intern Med 2015. Observational meta-analysis, European Journal of Preventive Cardiology 2022, 29(5), 804. Westphal Filho et al., Alzheimers and Dementia TRCI 2025. GeroScience 2026, brain, benefit or burden. STAREE trial, NEJM and ESC Congress 2026. PREVENTABLE trial, ongoing, Duke Clinical Research Institute. Guideline context: 2026 multi-society dyslipidaemia guideline, ACC, AHA and nine other societies, March 2026. Eligibility study, JAMA, July 2026, Pittsburgh and VA, NHANES data. LDL cumulative exposure hypothesis paper, 2024. Brain cholesterol mechanism: Tom Dayspring, Peter Attia podcast episodes 334 and 395, brain lipidology and cholesterol homeostasis. Informational only, not medical advice. New episodes of A Modern Pharmacist drop weekly.
S1 · E16
August 31 · 29 min
GLP-1s Are Approved for Way More Than Weight Loss
Everyone knows GLP-1 pens for weight loss and type 2 diabetes. What most people don't know is these drugs are now licensed — or being actively trialled — for at least eight other conditions, some of which genuinely surprised me while researching this one. I sort them into three categories based on how confident the evidence actually is. The first: conditions where the benefit tracks almost perfectly with weight loss — obstructive sleep apnea, MASH (fatty liver disease), and a specific type of heart failure. The second: conditions where weight loss explains some but not all of the benefit — cardiovascular risk reduction, which is already licensed in the UK, and chronic kidney disease, where the benefit stops making sense purely in terms of blood sugar control. The third and most interesting: two conditions — a rare brain pressure disorder and alcohol use disorder — where the evidence points to a completely separate mechanism, likely involving dopamine and reward pathways rather than weight or glucose at all. I also talk through a real patient case, a 27-year-old with a BMI of 46 and fatty liver disease, and where I think this field is heading next — including retatrutide and new drugs designed to protect muscle mass during GLP-1-driven weight loss. Studies & Sources: SURMOUNT-OSA (Malhotra et al., NEJM 2024); ESSENCE (Sanyal et al., NEJM 2025); STEP-HFpEF (Kosiborod et al., NEJM 2023) and SUMMIT (Packer et al., NEJM 2025); SELECT (Lincoff et al., NEJM 2023); FLOW (Perkovic et al., NEJM 2024); Mitchell et al. (Brain, 2023) on IIH; SEMALCO (Klausen et al., Lancet 2026); framework adapted from Peter Attia's "GLP-1 Medications Beyond Weight Loss" (2026). Informational only, not medical advice. New episodes of A Modern Pharmacist drop weekly.
S1 · E15
August 27 · 29 min
Insulin Resistance Is Way More Complex Than You Think
Insulin resistance gets thrown around online like it's simple. It's genuinely one of the most complex mechanisms in metabolic health, and in this episode I break it down properly using the two researchers whose work most of our current understanding is built on — Ralph DeFronzo and Gerald Shulman. I start with DeFronzo's "Ominous Octet" — the eight separate organs and tissues involved in insulin resistance, which is exactly why no single drug or intervention will ever fix it on its own. Then I go into the actual cellular mechanism: how fat builds up inside muscle cells specifically, physically blocking the pathway that lets glucose into the cell, and why your bloods can look completely normal for 10-15 years while insulin is quietly climbing behind the scenes to compensate. I cover the liver's surprising role in continuing to produce glucose even when there's already too much in the blood, why the kidney does the opposite of what you'd expect, and I share a personal example from my own continuous glucose monitor after a single bad night's sleep that genuinely surprised me. Finally, I go through what actually works: weight loss, cutting back refined carbs and saturated fat, prioritising sleep, zone 2 training specifically for improving fat-burning capacity, and building muscle mass as a genuine metabolic buffer. Studies & Sources: DeFronzo (2009, Banting Lecture, Diabetes journal); Gerald Shulman's body of work on diacylglycerol/PKC-mediated insulin resistance; classic research on brain glucose use during starvation; incretin (GLP-1/GIP) physiology; sleep restriction and insulin sensitivity research. Informational only, not medical advice. New episodes of A Modern Pharmacist drop weekly.
S1 · E14
August 23 · 27 min
The Cholesterol Test That's Been Sitting There Since 1994
Two years ago I barely knew what ApoB was. Now I think it's baffling we don't test it as standard — it's been a validated, standardised blood test since 1994, it costs next to nothing, and it may be the single most accurate predictor of cardiovascular risk we have. In this episode I explain what ApoB actually measures: one signalling molecule per lipoprotein particle, meaning it's a direct count of atherogenic particles rather than a measure of how much cholesterol mass those particles are carrying. I walk through chylomicrons, VLDL, IDL and LDL, and use a water-pipe analogy to explain why particle number — not just total cholesterol — determines how much damage reaches your arterial wall. I go deep on discordance: the phenomenon where someone can have a completely "normal" LDL cholesterol result and still be walking around with a dangerously high ApoB particle count, undiagnosed and under-treated. I also explain why your standard LDL-C result usually isn't even directly measured — it's estimated using an equation from 1972 that has real, well-documented limitations, especially at high triglycerides. I go through why the usual excuses — cost, lack of evidence, lack of standardisation — don't hold up, and where I sit on my own ApoB results. Sources: Marcovina et al. 1994 Clinical Chemistry (ApoB standardisation), Sniderman et al. 2024 European Heart Journal (UK Biobank discordance study), Sniderman et al. 2011 Circulation: Cardiovascular Quality and Outcomes (meta-analysis), Friedewald et al. 1972 Clinical Chemistry (LDL-C estimation equation). This is informational purposes only, not medical advice. If you can't get seen by your own physician, by all means do so, but always speak to your own healthcare provider. New episodes weekly — subscribe to stay on top of the biomarkers actually worth knowing.
S1 · E13
August 19 · 29 min
Lp(a) Levels: Do You Need to Get Checked?
One in five people carry a genetic heart disease risk factor most doctors have never mentioned to them — and I'm one of them. My own lipoprotein(a) came back so high the lab couldn't even calibrate it. In this episode I go deep on Lp(a): what it actually is (an LDL particle with apolipoprotein(a) covalently bound to it, forming a distinct and far more dangerous particle), and why it causes more damage than standard cholesterol. I cover the mechanism — how oxidised phospholipids drive arterial inflammation, and how Lp(a) mimics plasminogen to create a prothrombotic environment on top of the atherogenic one. I walk through the actual risk brackets used in the European guidelines (under 75 nmol/L low risk, 75–125 medium, above 125 high), why it's a test-once-in-your-lifetime marker since it's fully expressed by age 5, and the real hierarchy of complications — aortic valve stenosis first, then heart attack and ischaemic stroke, then chronic kidney disease and heart failure. I'm also honest about where treatment currently stands: statins don't lower it (and can slightly raise it), PCSK9 inhibitors only shift it 25-30%, but antisense oligonucleotide therapies in Phase 3 trials are showing reductions up to 98%. And I talk through my own approach — testing my dad, considering future therapies, and why I think this should be a routine paediatric test rather than something you have to go private to access. Sources: EAS 2022 Lp(a) Consensus Statement (European Heart Journal), Thanassoulis et al. 2013 NEJM (aortic valve calcification genetics), AHA/ACC 2018 Cholesterol Guideline, Capoulade et al. 2015 JACC (ASTRONOMER trial, statins and Lp(a)), Ionis/Novartis Lp(a) HORIZON Phase 3 trial data. This is informational purposes only, not medical advice. If you can't get seen by your own physician, by all means do so, but always speak to your own healthcare provider. New episodes weekly — subscribe to stay on top of the biomarkers actually worth knowing.
S1 · E12
August 16 · 29 min
Modern Healthcare Is Being Led By The Wrong People
This one's different — no script, no notes, just me thinking out loud for half an hour about where I think modern healthcare is actually heading. I recorded it on a Sunday evening because it had been building up after weeks of conversations with people who see health and medicine completely differently to me. I talk through why modern healthcare is genuinely excellent at reactive treatment but has barely moved toward prevention, despite having the data and tools to get there. I get into the "biohacker" problem — advice that works brilliantly for an already-healthy 1% being sold to everyone else as if it applies universally — and a real, slightly alarming conversation about someone self-dosing a peptide three times a week with no understanding of basic pharmacokinetics. I also talk honestly about why I don't think the NHS survives in its current form over the next decade, and share a genuinely serious real-world case of an unlicensed aesthetics practitioner causing permanent damage through a botched filler injection — a reminder of exactly why regulation and proper training exist. Studies & Sources: this episode is personal reflection rather than data-led, so there are no formal trials or statistics to cite. The one direct reference is Simon Squibb's book, What's Your Dream? (2025). Informational only, not medical advice. New episodes of A Modern Pharmacist drop weekly.
S1 · E11
August 13 · 29 min
We're Managing Blood Pressure Wrong in the UK
I believe we're managing blood pressure incorrectly in the UK — years behind the US, which itself still isn't being aggressive enough. In this episode I explain the physiology, the guidelines, and exactly how to monitor and improve your own numbers. I break down why UK targets (140/90 in clinic, 135/85 at home) are looser than the US (130/80), and the trial data that drove the US to change first — a landmark study that found a 25% relative risk reduction in heart attacks and heart failure by targeting a systolic pressure of 120 instead of 140, with the trial stopped early because the difference was so significant. I also cover why blood pressure matters far beyond just heart disease — particularly for kidney health, which is disproportionately vulnerable given how much blood flow it receives relative to its size — and I walk through exactly how to measure your blood pressure correctly at home, since small errors in technique can shift your reading by 10-20 points. Finally, I go through what actually moves the needle: weight loss, zone 2 exercise, sodium, sleep, and where medication fits in when lifestyle isn't enough on its own. Sources: SPRINT trial (NEJM, 2015); STEP trial (Zhang et al., NEJM, 2021); British Heart Foundation Know Your Numbers data; CDC NHANES 2017-2020; NICE NG136; Neter et al. 2003 (Hypertension); Cornelissen & Smart 2013 (JAHA). Informational only, not medical advice. New episodes of A Modern Pharmacist drop weekly.
S1 · E10
August 10 · 27 min
Your Surroundings Are Slowly Destroying Your Health
Do you know the average person globally is more likely to lose life expectancy to air pollution than to smoking? That stat is true — and it's also a bit of a play on words, which I unpack properly by the end of this episode. This week I'm covering the environment — air, noise and light pollution — three things I rarely give airtime to compared to diet, exercise, sleep and stress, but that quietly shape your cardiovascular health more than most people realise. I go through why 60% of air pollution deaths trace back to cardiovascular disease rather than lung disease, how researchers use "natural experiments" like the Dublin coal ban to study pollution without an unethical trial, and why particulate matter (PM2.5) slips past your body's usual defences entirely. I also introduce a principle that runs through all three pollutants: area under the curve — the idea that low-grade chronic exposure, the kind you've mentally tuned out, does more long-term damage than the odd loud night or bright evening. From there I cover noise pollution's effect on sleep even while you're unconscious, and why I think blue light blockers are less useful than just putting your phone down half an hour before bed. Finally, I come back to that opening stat and explain exactly what it does and doesn't mean — population averages versus individual risk, and why smoking still carries a far higher individual hazard ratio despite the lower population-average figure. This is informational purposes only, not medical advice. If you can't get seen by your own physician, by all means do so, but always speak to your own healthcare provider. New episodes every week — subscribe so you don't miss one. AQLI 2024 Annual Report (University of Chicago Energy Policy Institute) — 1.9-year global air pollution life expectancy figure WHO Global Air Quality Guidelines 2021 — PM2.5 thresholds, 99%-of-world-exceeds-limit stat Pope et al., Utah Valley steel mill closure study (1989) — natural experiment evidence Clancy et al., Dublin coal ban study, Lancet (2002) — natural experiment evidence WHO Ambient Air Pollution Fact Sheet — cardiovascular vs. respiratory death attribution WHO Environmental Noise Guidelines for the European Region (2018) — 30 dB bedroom guideline, RR 1.08 IHD figure IARC Monograph, Night Shift Work (2019 re-evaluation) — Group 2A classification, referenced for light pollution context Historical: Ministry of Health report, Great Smog of London (1952–53); Air Pollution Act 1956 (UK) Studies / sources for show notes
S1 · E9
August 5 · 25 min
HDL isn't good cholesterol (here's why)
"Your good cholesterol is high, so you don't need to worry about heart disease." You've probably heard this — I said it myself for years before researching this episode properly. I start with the basics: cholesterol is one molecule, full stop. "Good" and "bad" only describes how your body transports it, not what it actually is. I trace where the "good cholesterol" idea came from — the Framingham Studies, where low HDL turned out to be four times more predictive of heart disease than high LDL — and what happened when pharmaceutical companies tried to exploit that by raising HDL with drugs. It didn't go well. Then I get into the two ways your body actually clears cholesterol using HDL, why the marker used to "count" HDL particles is far less reliable than people think, and why genetic studies show a high HDL number doesn't reliably protect you at all. My conclusion: HDL should be treated less like a target number and more like HbA1c — a signal of what's happening elsewhere in your metabolism, not something to chase upward on its own. If a doctor or pharmacist has ever told you your HDL is "good" and left it there, this episode might change how you look at that result. Informational only, not medical advice. New episodes of A Modern Pharmacist drop weekly.
S1 · E8
August 2 · 24 min
Your Electrolyte Drink Doesn't Work
Electrolytes are now a $40 billion industry, expected to double within five years — and the marketing is good enough that it made me question basic physiology I've known for years. So I went and looked properly. I'll tell you upfront: I don't use electrolytes regularly myself, though I have in the past year or so on a few occasions — and this episode is me working through whether the evidence actually supports their use for the average person, with full study citations so you can check it yourself. I start with the physiology: how sodium, potassium, calcium and magnesium are kept within tight ranges in the blood, and why sodium behaves completely differently to the others. I bust the biggest myth in this space — sweat is hypotonic, meaning when you sweat, your blood doesn't get diluted, it actually becomes more concentrated. From there: a practical rule for under an hour of exercise on a normal diet (you likely don't need anything but water), where the evidence does support electrolyte drinks (prolonged exercise, heat, endurance events), how to actually read a sodium label and compare real products, and why morning salt water doesn't hold up. Then the context where electrolytes are genuinely life-saving: acute illness. I cover the research behind a 69% reduction in diarrhoea mortality with oral rehydration therapy, and why this is completely different physiology to a normal workout. I close with a quick tour of potassium, calcium and magnesium, and a clinical example from my own practice — patients on diuretic medications that directly block electrolyte reabsorption in the kidney, who very often still have completely normal blood results, which tells you a lot about how robust this system actually is. Physiology foundation: Hall JE & Hall ME (2020). Guyton and Hall Textbook of Medical Physiology, 14th edition. Key studies: McCubbin & Costa (2018, Int J Sports Sci) · Del Coso et al. (2016, Scand J Med Sci Sports) · Hew-Butler et al. (2006, Br J Sports Med) · Munos, Fischer Walker & Black (2010, Int J Epidemiol) · ACSM Position Stand on Exercise and Fluid Replacement · NDNS 2018/19 · CDC/NHANES 2021–2023 This is informational purposes only, not medical advice. If you can't get seen by your own physician, by all means do so, but always speak to your own healthcare provider. New episodes every week — subscribe so you don't miss the next one.
S1 · E7
July 29 · 27 min
Why Everyone Should Try a CGM (At Least Once)
I believe everyone should wear a continuous glucose monitor for 2-4 weeks a year — whether you're diabetic or not. In this episode I explain why, using both the evidence and my own data from a week of wearing one. I break down why average blood glucose, day-to-day variability, and glucose peaks all matter independently — and why fasting glucose and HbA1c, the tests the NHS actually uses, miss most of this picture. I also explain why the diabetic diagnostic threshold is a continuum rather than a finish line, using data showing a 4.5-fold difference in mortality risk between the lowest and highest HbA1c bands, even outside the diabetic range. Then I get into insulin — the part I think gets overlooked. A surprisingly small rise in insulin is enough to almost completely shut off fat-burning in the body, which is a big part of why chronically elevated glucose matters so much for weight and metabolic health, not just diabetes risk. I share what my own CGM has actually shown me this week: a coffee that spikes me to 9mmol/L, how a short walk brought that right down, and how sleep quality changed my glucose response the next day. Informational only, not medical advice — always speak to your own healthcare provider. New episodes of A Modern Pharmacist drop weekly.
S1 · E6
July 26 · 28 min
Using GLP-1s Without Losing Muscle or Bone
GLP-1 pens are transforming weight loss — but almost nobody using them is protecting their muscle or bone while it happens. In this episode, I go through how to use them properly, from both a prescriber's side and a patient's side. Everyone remembers the number from the STEP 1 trial: 40% of weight loss on semaglutide was lean mass. But newer data on tirzepatide shows that figure closer to 25% — genuinely comparable to a normal diet and exercise plan. I explain why DEXA scans, the standard way we measure this, can actually be misleading: lean mass isn't just muscle, and some of what gets flagged as "loss" might really be beneficial fat clearing from inside the muscle itself. I'm honest about the evidence gap too — no completed trials have yet controlled for protein intake and resistance training specifically in people on GLP-1s. Two studies, LEAN-PREP and STAY-LEAN, are running right now, but nothing's published yet. Everything I recommend is extrapolated from the wider weight-loss literature, not proven in this specific population — and I think that's an important distinction to be upfront about. I break down the two things that actually help: hitting 1.6-2g of protein per kilogram daily with a proper leucine threshold each meal, and resistance training — which can be as little as twice a week if you're just starting out. Then I go into the bone health risk nobody talks about: osteopenia, osteoporosis, the SELECT trial's fracture data, why postmenopausal women are especially vulnerable, and why the old 400-800 unit vitamin D guidance is now outdated. Informational only, not medical advice — always speak to your own healthcare provider. New episodes of A Modern Pharmacist drop weekly.
S1 · E5
July 22 · 27 min
Peptides | What's actually in the vial?
Peptides are having a moment right now — but almost none of what's flooding your Instagram feed is the peptide science that's actually transformed modern medicine. Insulin and GLP-1 drugs are peptides, and they're some of the most important therapies we have. This week I go through what's real, what's grey market, and what's just a good story. We start with the basics. What actually is a peptide — and why is it such a broad, almost meaningless category once you understand it's just a short chain of amino acids? I run through the UK-approved peptide drugs already sitting in mainstream medicine: insulin, the GLP-1 agonists, GnRH agonists like goserelin and leuprorelin, somatostatin analogues, teriparatide, desmopressin, and more. These are decades-old, rigorously trialled, and nothing like what's being sold in the wellness space under the same name. Then I lay out a five-question framework for evaluating any peptide — or honestly, any drug — before it goes anywhere near your body: is there a viable mechanism of action, do we have evidence of the intended effect in humans, what do we know about safety, how do the risks weigh against the benefits, and is there a legitimate approved alternative? From there, four case studies, in depth: BPC-157 — the murky "Body Protection Compound" origin story, the fact that over 80% of published data comes from a single lab with a direct commercial interest, and why zero peer-reviewed human trials exist for a compound that's been marketed for thirty years. I also cover the first real human RCT, which only began recruiting in early 2026. SS-31 (elamipretide) — approved for one rare disease, Barth syndrome, under the brand name Forzinity. I get into the actual trial data, which is more complicated than most marketing suggests: the primary endpoints in the blinded trial didn't reach significance, and I explain exactly what the approval was really based on. CJC-1295 — this leads into a proper breakdown of the growth hormone axis: how GHRH and growth hormone actually work, the real trade-off between visceral fat loss and blood sugar control, and the one clinical trial death that's part of this compound's history. Melanotan-II — the so-called "Barbie drug," its mechanism through the MC4 appetite pathway (which connects directly to how GLP-1 drugs work), and the adverse effects that don't get mentioned in grey-market marketing, including a genuinely dangerous one. Finally, where do these products actually come from? I break down the grey-market supply chain, what "Research Use Only" labelling actually means legally, and the specific public warnings the MHRA has issued — naming several of these compounds directly. This is informational purposes only, not medical advice. If you can't get seen by your own physician, by all means do so, but always speak to your own healthcare provider. New episodes of A Modern Pharmacist drop weekly — subscribe for evidence-first breakdowns of the tests, numbers, and decisions that actually move the needle on long-term health. No fluff, no fear tactics.
S1 · E4
July 19 · 29 min
Three Case Studies the System Got Wrong
This episode is three real patient case studies — anonymised except for one, which is my own dad — and they all show the exact same pattern: the data was there, the warning signs were there, and the system missed them anyway. The first is a woman in her thirties with chronic back pain and a raised hs-CRP, a more sensitive inflammation marker than the standard NHS test. Her result had doubled in three months. The GP's response was that it was still under the standard cutoff, so there was nothing to look at. I explain why that's the wrong way to think about a trend, not just a single number. The second is my dad. Since his heart attacks in his early fifties, he's had blood monitoring every three to four months — genuinely good, consistent care. But his HbA1c has sat in pre-diabetic range for three and a half years, and every single result was marked "satisfactory." I talk through the data on reversing pre-diabetes, including a well-known UK study putting patients into remission through a structured calorie deficit in just twelve weeks, and why nobody acted on his numbers until I did. The third is the hardest one: a 41-year-old man who'd been on unmonitored, black-market testosterone since he was eighteen. His bloods were abnormal when he first presented to the NHS, and nothing was done. Years later, he's in severe heart failure, with a heart pumping at roughly a tenth of normal efficiency. Throughout the episode, I try to work out where the responsibility genuinely sits in each case — patient, system, or somewhere in between — and land on something close to 60% system, 40% individual. I also talk about why so many clinicians default to "we can treat this later" instead of "let's stop this now," and what that says about how healthcare is actually structured around treatment rather than prevention. As always, this is for informational purposes only, not medical advice. If any part of this resonates with your own results, or someone in your family's, please speak to your own healthcare provider directly. New episodes of A Modern Pharmacist drop weekly — straight-talking, evidence-based health content from a pharmacist's perspective.
S1 · E3
July 16 · 29 min
Everything You Need to Know About Exercise (In One Episode)
Why is physical education so bad — in schools, in medical degrees, and in the NHS itself? In this episode I break down who's actually to blame for the exercise crisis, then give you the most efficient, evidence-based exercise plan I use myself. What's covered: • Who's failing you on exercise: guidelines, health degrees, healthcare professionals, and schools • UK & US inactivity stats — over 11 million UK adults classed as inactive, 25% of US adults doing zero activity • Baseline activity — why sitting less matters as much as training • The 4 pillars: Strength training, Zone 2, VO2 Max, and Mobility — how much of each you actually need, and how to do it • The Norwegian Method for VO2 max training • Why sarcopenia (muscle loss) matters more as you age, and how to protect against it This is informational only, not medical advice — always speak to your own healthcare provider before starting a new exercise programme.
S1 · E2
July 12 · 29 min
Modern Healthcare is Failing You
Why Modern Healthcare Is Failing You — and I mean that genuinely, not as clickbait. As an NHS pharmacist of 9 years, I break down three reasons: medicine moves too slowly, it's all about money (NHS budgets, QALYs, Mounjaro's £574m spend), and healthcare ignores what patients are actually doing — peptides, GLP-1s, biohacking. Informational only, not medical advice.
S1 · E1
July 9 · 22 min
Episode 1: No Nonsense Health
Welcome to episode one — the podcast I've been wanting to make for a long time. The aim here is simple: talk honestly about health. Not the sanitised, one-size-fits-all version, but what's actually true and actually useful. Healthcare isn't evolving fast enough, and people are more frustrated and more lost than ever about where to turn. I see this from both sides — I'm a prescribing pharmacist working in the NHS, but I also live with diabetes myself. That combination gives me a genuinely unusual view of the system: as the person prescribing, and as the person managing a condition every day. My goal is for this to become the place you come to for straight, useful information — no fluff, no filler, just what actually matters.

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