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.

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.

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.

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.

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

"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.

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.

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.

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.

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.