A few years ago, a patient with early Parkinson’s disease asked me something that stopped me mid-sentence. He was not asking about tremor control or sleep. He wanted to know whether cannabis might change the trajectory of his brain.

Not the symptoms. The direction.

That question feels especially timely now. Just this month, researchers analyzing more than 26,000 adults aged 40 to 77 in the UK Biobank reported that individuals with a history of cannabis use tended to show larger volumes in several brain regions and performed better on certain cognitive measures compared with non-users. The authors were careful, emphasizing that these findings are associative, not causal. They do not tell us whether cannabis produced those differences, nor do they clarify dose, potency, or lifetime exposure patterns.

Even so, the signal forces us to revisit assumptions we have held for years. For decades, …

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If you only have a minute: This paper examines hospital coding for cannabis use disorder in patients already hospitalized with advanced metabolic liver disease. It shows an association with documented myocardial infarction during admission. It does not measure cannabis dose, route, or causality. The rest of this essay explains why that distinction matters.

The headline lands before the method does

There is a particular kind of quiet that settles in a room when someone says the words heart attack and cannabis in the same breath. I have seen it in clinic, in hospital consults, in family conversations where no one wants to sound alarmist but everyone can feel the ground shift a little. The body already knows what those words mean, even before the mind catches up and asks the obvious question, is this a real signal or just another headline that will be replaced by the next o…

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When clinicians read the JAMA cannabis review closely, one thing becomes immediately clear. Most of the weight of its conclusions rests not on experimental certainty, but on the limits of the data it had available to summarize.

That doesn’t make the review wrong. But it does mean the conclusions need to be handled with care.

A large share of the evidence cited is observational, cross-sectional, or retrospective. Cannabis exposure is usually self-reported. Often it’s reduced to simple categories like “use” or “no use,” or “daily” versus “non-daily.” Details that matter clinically, dose, potency, route, formulation, timing, are rarely captured with much precision.

That matters because even sophisticated statistical adjustment cannot fully correct for what isn’t measured. Residual confounding remains substantial. Exposure misclassification is almost guaranteed. And as every epidemiologist knows, associations generated this way are hypothesis-generating, not proof of causality.

From a clinica…

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🍼 The Question Every Parent Asks

If you’ve ever been pregnant—or loved someone who has—you’ve probably heard the age-old advice: “Just take Tylenol. It’s the safest thing you can use.”

But what if the “safe” option isn’t quite as simple as we’ve been led to believe? A new systematic review published this year takes a hard look at the connection between acetaminophen (Tylenol) use during pregnancy and neurodevelopmental disorders (NDDs) like ADHD and autism.

Current Controversy: RFK Jr. Steps Into the Spotlight

Just as this systematic review lands, U.S. Health Secretary Robert F. Kennedy Jr. (RFK Jr.) is expected to release a controversial report suggesting a link between prenatal acetaminophen (Tylenol) use, low folate levels, and autism. The Wall Street Journal reports that the forthcoming study, led by HHS with NIH involvement, will also spotlight folinic acid (leucovorin) as a potential treatment for autism symptoms—even though it’s based solely on existing literature, not new clinic…

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The Cannabidiol Curveball No One Saw Coming

July 7, 2025. JAMA Internal Medicine drops a tightly designed, placebo-controlled, double-blind trial titled:
“Cannabidiol and Liver Enzyme Level Elevations in Healthy Adults: A Randomized Clinical Trial” by: Jeffry Florian, PharmD; Pablo Salcedo, PhD; Keith Burkhart, MD; Aanchal Shah, PhD; Lakshmi Manasa S. Chekka, PhD; Dro Keshishi, PhD; Vikram Patel, MD; ShanChao Yang, MD; Melanie Fein, MD; Ryan DePalma, MD; Murali Matta, PhD; David G. Strauss, MD; Rodney Rouse, MD. (Here’s the PDF)

The premise? Measure liver enzyme elevations in healthy adults taking high doses of pharmaceutical-grade CBD isolate (up to 1600 mg/day) over 28 days.

The outcome? Some enzyme elevations—ALT and AST primarily—but no symptoms, no liver damage, and all values returned to baseline once CBD was stopped.

That’s it. That’s the study.

But here’s the kicker: the internet (and eventually the media) is about to l…

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🍃 The Perils of Big Claims in Blurry Studies

This week, when you scan headlines like “Cannabis May Harm Your Heart,” your pulse might quicken—for reasons having little to do with science. Especially if you’re one of the tens of millions using cannabis for stress, sleep, …

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This post is for everyone who’s heard the scary headline but sensed something was missing. Spoiler: you’re right. Let’s talk about what’s really going on behind the numbers.

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🫀 Is Cannabis Bad for Your Heart?

A JAMA Study Got the Headlines—But Not the Full Story

TL;DR:

This week’s JAMA Cardiology study sparked big headlines linking cannabis to vascular damage. While it raised valid questions about endothelial function, it overreaches in ways that risk reinforcing stigma over science. In this post, I’ll explain what the study did well, where it loses scientific footing, and why we keep repeating this cycle of sensational cannabis stories that don't match the complexity of the plant—or its real-world use.

💡 For an even deeper clinical + scientific breakdown, including image guides and literature comparisons (and the full text PDF), see my full-length review on CEDclinic.com: https://cedclinic.com/cannabis-and-cardiovascular-health-jama-study/

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High Hopes, Low Data

Sometimes all it takes is a single ER visit to launch a thousand headlines.

This month, JAMA Neurology published a study linking cannabis-related emergency visits with later-life dementia diagnoses. And predictably, it got spun like a Lazy Susan of panic: “Weed causes dementia!” shouted the headlines.

But let’s slow down for a second. Because buried in the fine print—and the ICD-10 codes—is a very different story. If you’ve ever wondered whether cannabis really messes with memory, or whether that ER visit five years ago means your brain is doomed, you’re in the right place.

Let’s walk through what this study actually says (and what it absolutely doesn’t).

Spoiler: It’s not about joints. It’s about judgment.👇

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1️⃣ Correlation ≠ Causation – Just because two things happen together doesn’t mean one caused the other. Example: Ice cream sales and shark attacks both rise in summer—coincidence, not cause.

2️⃣ Media Loves Misleading Headlines – Words like “linked to,” “associated with,” and “tied to” are red flags. They suggest causation where none exists.

3️⃣ Studies Can Be Flawed – Small sample sizes, confounding variables, and biased funding often skew results. Most headlines don’t mention these details.

4️⃣ Cannabis & Heart Disease? – A recent study claimed a link but failed to control for smoking, diet, or stress—making the results questionable at best.

5️⃣ How to Protect Yourself – Don’t trust a single study. Look for absolute vs. relative risk, study replication, funding sources, and dose-response relationships before believing a claim.

Read on for the full breakdown.

The Causation Illusion: How Your Brain (and the Media) Trick You

You’ve seen the headlines. 📰

📢 “Eating Chocolate Linked to Higher Intelligence!”

📢 “Owning a Cat Comes with Increased Risk of Schizophrenia!”

📢 “Wearing Yellow Tied to Financial Success!”

Sounds compelling, right? Eye-catching, clickable, maddeningly misleading.

Welcome to the wild world of causation vs. association, where correlation—a statistical relationship between two things—masquerades as cause. And everyone from the media to your well-meaning Aunt Linda on Facebook is eager to tell you that one thing must be causing another because, well… just look at the numbers!

It’s an easy trap to fall into because our brains love simple explanations. We crave neat, cause-and-effect relationships. It rained because I washed my car. My phone slowed down because Apple wants me to buy a new one. More people are getting tattoos, and the economy is getting worse—coincidence? I think not.

But here’s the truth: most studies don’t prove causation. They rarely can. Most of what you read is just an association—two things happening at the same time, not one causing the other. But thanks to slippery phrasing and click-hungry headlines, we’re left thinking otherwise.

Let’s fix that.

Wait, What’s the Difference?

Causation:

Causation means A directly makes B happen. There’s a proven, repeatable, demonstrable mechanism at work.

Example: Drinking poison causes death. No arguments there. No “linked to” needed.

Example: Dropping your phone into a pot of boiling water causes it to break. (Sorry, no headline necessary.)

Association:

Association means A and B tend to happen together, but that doesn’t mean one causes the other. Maybe A causes B. Maybe B causes A. Maybe C causes both. Maybe they’re just statistical roommates, coexisting by pure coincidence.

Example: People who carry lighters are more likely to get lung cancer. But lighters don’t cause cancer—smoking does.

Example: People who own more books tend to be smarter. But buying books doesn’t make you a genius—reading them might, or maybe smart people just buy books.

Example: Ice cream sales and shark attacks both rise in the summer. Because it’s summer. Not because sharks have suddenly developed a craving for mint chocolate chip.

Correlation: A Statistic, Not a Cause

If sales of organic food and autism diagnoses both rise in the same decade, that’s a correlation. But one doesn’t cause the other—they just happen to be increasing at the same time. Yet, this kind of data is often twisted into misleading claims, especially when the media is involved.

👉 Example: Autism diagnoses have risen, and so has the number of childhood vaccines. Some people jumped to the conclusion: ‘More vaccines = more autism’

🚨 The reality?

1. Autism awareness and diagnostic criteria have changed, leading to more kids being identified—but that doesn’t mean autism itself is increasing.

2. Some children who would have previously been labeled as “developmentally delayed” are now correctly diagnosed with autism spectrum disorder (ASD).

3. The original study that falsely linked vaccines to autism was retracted, and further research found no connection—but the damage was already done.

4. People still believe the myth because misinformation spreads faster than corrections.

The Media’s Favorite Trick: Misleading Phrasing

The media knows causation sells but association is easier to find. So, what do they do? They fudge the language—just enough to imply causation without actually stating it outright.

Once you recognize the patterns, you’ll start seeing them everywhere. Here’s the cheat sheet for spotting the worst offenders in science reporting:

🚩 “Linked to” – Translation: We found two things happening at the same time, and we’re going to pretend they’re related!

– This was the phrase that helped fuel the vaccine-autism myth. A now-debunked study wrongly claimed a connection between vaccines and autism, and even though it was retracted, the “linked to” phrasing stuck.

🚩 “Comes with” – Translation: These things tend to exist together, but we have no clue why.

🚩 “Tied to” – Translation: We noticed a pattern and we’re gonna make it sound dramatic!

🚩 “Heavily correlated with” – Translation: Statisticians found a relationship, but that doesn’t mean one thing is making the other happen.

🚩 “Associated with” – Translation: These two things co-exist, but we’re not saying one causes the other (even though we really want you to think so).

Each of these phrases allows sensationalized headlines to suggest something far more dramatic than what the research actually found. Next time you see a headline throwing these phrases around, assume they’re twisting the data—because they probably are!

Case Study: The Cannabis & Heart Disease Study That Got Overhyped

Let’s take a real-world example: a 2025 study published in JACC: Advances examined whether cannabis use increases the risk of heart disease . [PDF to read it here]

Here’s what the study actually found:

🔹 They compared cannabis users and non-users who were already “relatively healthy” (no prior history of heart disease, high cholesterol, or diabetes).

🔹 Cannabis users showed a slightly higher risk of heart attack over several years. But here’s how the numbers were twisted:

• The ‘absolute risk increase’ was just 0.47%—less than half a percent.

• But the ‘relative risk’ looked big, which makes for scarier headlines.

It’s like saying, ‘Eating ice cream doubles your risk of shark attack!’ If the original risk was 1 in 10 million, doubling it still makes it only 2 in 10 million. The risk is real, but does it actually matter for more than just a headline?

🔹 The absolute risk increase was tiny. Even though the relative risk looked big, the actual increase was just 0.47% higher in cannabis users.

🔹 The study did not control for confounders like diet, exercise, stress, or other drug use. This means that cannabis users in the study may have been more likely to smoke cigarettes, have different stress levels, or eat differently—any of which could have contributed to the slightly increased heart disease risk. Without accounting for these factors, the study can’t isolate cannabis as the cause. Yet, that didn’t stop the headlines from claiming cannabis ‘causes’ heart attacks

🚨 The Reality: This study showed a weak association, not causation. But how do you think the media reported it?

📢 “Smoking Weed Causes Heart Attacks, Study Finds!”

📢 “New Research Reveals Major Cardiovascular Risks of Cannabis!”

In reality? The study was observational, didn’t prove causation, and had major confounders. But none of that made the headlines.

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…BUT… Perspective Matters!

Don’t Lose Sight: The Science Isn’t Always as Pure as It Seems

Let’s get real: researchers are not neutral robots dedicated to a holy pursuit of absolute truth. They are people—highly trained, highly ambitious, and very aware of the impact of their findings. Many of them want their research to be noticed, cited, and talked about. Most of them also enjoy being continuously employed. So what happens?

🔹 They frame their results in ways that sound as profound as possible.

🔹 They highlight connections that seem significant—even if causation isn’t proven.

🔹 They may overstate implications, knowing that funding, prestige, and career opportunities can hinge on the perception that their research is groundbreaking.

And if scientific researchers—who are supposed to be methodical, critical, and cautious—can get carried away in how they present their data, imagine what happens when that data gets handed off to journalists.

One year eggs are deadly, the next they’re a superfood. This cycle repeats with fat, sugar, salt, and coffee—because most of these claims come from weak correlations, NOT causation

Sound familiar? The same scientific flip-flopping happens with cannabis, vitamin D, cholesterol, red meat, exercise, fasting, carbs—you name it. If you follow science news, it’s impossible to avoid the whiplash of ever-changing trends crashing into each other.

Science evolves, but headlines often make it seem like research is constantly contradicting itself—when in reality, the details matter most.

If you want information that will stand the test of time, you have to read with skeptical glasses on. If you don’t, you’re likely going to fall prey to the confirmation bias I wrote about last time, and be lulled into lapping up what supports your preexisting views, and makes you feel like you’re perfect just the way you are.

Or, at the very least, align yourself with someone who has the nerd goggles firmly strapped on—someone who will sift through the noise, read between the lines, and tell you when the hype is real and when it’s just another round of scientific hot potato.

That’s me. And that’s one of the points of this newsletter, for a least this small community to share skepticism and educated critical reading with others who aren’t sheep to be duped.

So the next time you see a “New Study Finds [Insert Scary Thing Here] Tied to [Insert Common Thing Here]” headline, take a deep breath. Ask:

🔹 Did this study actually prove causation, or just an association?

🔹 Who was studied? Were they lifelong heavy users or casual consumers?

🔹 Are there other confounding factors that could explain the findings?

Chances are, the headline isn’t telling the whole story.

And in the world of health, science, and cannabis research, that makes all the difference.

Related Reading | Nature Publication | Catalogue of Bias | Intro to Data Science

Mastering the Science of Causation—How Not to Be Duped

When Correlation Starts to Look Like Causation

The next half of this post is not for the casual reader. This is for those who want to think like a scientist, avoid getting misled by research hype, and truly understand how causation is determined in the real world.

It’s one thing to know that correlation isn’t causation—it’s another to spot the tricks, understand the deeper science, and cut through the noise like a pro.

If you’ve made it this far, congratulations. You’re better armed than most clickbait readers these days.

The goal so far has been to break down how science gets misrepresented. But… how do researchers actually determine when something is truly causal? Now we move beyond the media tricks and dive into the real science of causation. What follows is RED pill territory:

By now, we’ve seen how association can masquerade as causation, and how the media twists that confusion into clickable but misleading headlines. But does that mean we can never identify causation? Not at all.

Some research findings do point to a true cause-effect relationship—so long as we evaluate them with the right criteria. This is where epidemiology, critical thinking, and scientific rigor come in.

The Red Flags: How Researchers Signal (or Fake) Causation

A study isn’t automatically worth believing just because it appears in a peer-reviewed journal. Many studies are designed to look more impressive than they actually are—often in subtle, strategic ways.

Here’s what makes a study’s findings seem more profound than they really are:

1. The Strength of Association is Exaggerated

A legitimate causal relationship usually shows a clear, strong link—like smoking and lung cancer. The risk isn’t just slightly higher; it’s dramatically higher. But a weak correlation (like “Cannabis Linked to Slightly Increased Risk of Heart Disease”) can be framed as alarming, even if the effect is minuscule (remember above, “if the original risk was 1 in 10 million, doubling it still makes it only 2 in 10 million.”)

🚩 Red Flag: If the risk increase is less than 50%, it’s usually statistical noise or confounded by other factors.

2. The Study Has Never Been Reproduced

Real science relies on replication. If only one study ever found a link, but no one else has been able to replicate it, it’s probably just noise in the data. Yet, that one study can still become a media sensation.

🚩 Red Flag: If no follow-up studies confirm the findings, be skeptical.

3. The Timing is Backwards (Reverse Causation)

If A causes B, then A must come before B. But many studies fail to prove that order.

Example?

🚩 A study claims that cannabis use causes depression—but if depressed people were more likely to use cannabis in the first place, then the causation might be reversed.

Many cannabis studies suffer from this exact flaw, but it doesn’t stop them from making bold claims.

4. No Dose-Response Relationship

A true causal effect usually follows a dose-response curve—the more exposure, the greater the effect.

🚩 If a study finds that both heavy and light cannabis users have the same schizophrenia risk, that contradicts the idea that cannabis itself is causing the issue. Without a dose-response curve, causation is less convincing.

🤔 Current evidence suggests that high and frequent doses of THC may increase the risk of schizophrenia. However, for the vast majority of consumers using low to moderate doses, the risk appears to be negligible.

5. The Study is Based on Self-Reported Data

Many studies on cannabis rely on surveys—where participants self-report their cannabis use, their mental health, and their habits.

🚩 People lie. Or forget. Or misremember details. Or just want to get through the time-wasting questionnaire. they’re given. Self-reported data is notoriously unreliable, yet many studies treat it as hard science. And, most of the cannabis research we have relies on self-report.

Example?

🚩 A study claims that people who smoke cannabis daily have lower IQs. But… are they actually smoking daily, or just guessing when asked? One step further: who is ever smoking the same exact products every day, and in the same way?

6. No Mechanism is Explained

Even if a study finds a strong statistical association, causation is far more believable when there’s a known biological mechanism.

🚩 If a study claims eating bacon causes violent behavior, but there’s no biochemical explanation, it’s probably just statistical noise.

Want to discuss this with other like-minded readers? 👇

Take A Deeper Look At The Game of Scientists At Work.

We expect journalists to sensationalize research, but here’s what most people don’t realize:

🔹 Scientists are also under great pressure to make their studies sound more important than they really are. Now more than ever before (looking at you, DOGE)

🔹 Getting published in a top journal requires novelty, drama, and big claims.

🔹 Null findings (no significant links) rarely get published—even though they are just as scientifically important as studies that do find a link. This is known as the “file drawer effect”—because studies that find no dramatic results often get tucked away in the research equivalent of a bottom drawer, never seeing the light of day. As a result, the published literature is biased toward studies that report strong correlations, making it seem like links are everywhere, when in reality, many studies that found no connection simply never made it to press.

So what happens?

Researchers frame their findings to look more significant—usually not by faking data, but by choosing words carefully:

Instead of: “We found no strong evidence linking cannabis to schizophrenia.”

They write: “Our findings suggest a possible connection that warrants further investigation.”

See the difference? One is honest. The other keeps the door open for misinterpretation.

And once that study lands in a journalist’s hands… well, you know what happens next.

How to Read Science Without Getting Scammed

Want to cut through the noise and actually understand if a study is legitimate? Here’s how:

🔹 Ignore the Headlines – Journalists sensationalize everything. Don’t trust them.

🔹 Find the Original Study – Don’t just read an article. Go to the source.

🔹 Look for Confounding Variables – Ask: Did they actually control for other factors that could explain the association?

🔹 Check for a Dose-Response Relationship – If more exposure doesn’t lead to more effect, it’s probably not causal.

🔹 See If the Study Has Been Repeated – If no one else has replicated it, be skeptical.

🔹 Ask If It Even Makes Sense – If a study says, “Drinking green tea prevents heart disease,” but there’s no biological explanation, question it.

🔹 Trust Nerds With Strong BS Detectors – If you don’t have time to dissect research, align yourself with someone who does.

Causation: How Do We Actually Prove It?

Science is obsessed with causation—because it’s the only thing that really matters. Finding an association between two things is easy—proving one actually causes the other? That’s the holy grail.

Here’s how real causation is determined (and how you can tell if a study is actually onto something—or just hyping a correlation).

1. Causal Inference: The Hardest Part of Science

To say A causes B, we need to prove that:

✔ A comes first. (No reverse causation.)

✔ More A leads to more B. (A dose-response relationship.)

✔ Other variables aren’t responsible. (No confounding factors.)

✔ Removing A makes B disappear. (Experimental evidence.)

✔ There’s a logical reason why A would cause B. (Biological plausibility.)

If a study doesn’t meet these standards, it’s not proving causation—it’s just pointing out a pattern.

2. The Causation Pyramid: Ranking Scientific Evidence

Not all studies are created equal. Some barely tell us anything, while others come close to proving causation.

Here’s how to rank research quality from weakest to strongest:

🟥 Case Reports & Observational Studies (Weakest)

• Example: “We found 100 people who use cannabis and noticed some had heart issues.”

• 🚩 Lots of confounding variables. No proof of causation.

🟧 Cross-Sectional & Cohort Studies

• Example: “We followed 10,000 people for 10 years and saw cannabis users had slightly higher rates of heart disease.”

• 🚩 Better than case reports, but still just an association.

🟨 Longitudinal Studies

• Example: “We tracked cannabis use before heart issues developed to confirm timing.”

• 🚩 Better control of causation, but still missing key proof.

🟩 Randomized Controlled Trials (RCTs) (Strongest)

• Example: “We randomly assigned 1,000 people to use cannabis and 1,000 people not to, then measured heart disease rates.”

• ✅ Now we’re talking! This is real science, but still not perfect.

🟦 Systematic Reviews & Meta-Analyses (Gold Standard)

• Example: “We analyzed 50 high-quality studies and found consistent results across all of them.”

• ✅ This is the best type of evidence—but only if the included studies were well done.

Most cannabis studies are observational, meaning they cannot prove causation—but that won’t stop the media from pretending they can.

3. The “Cause Mirage”: How Science Can Trick You

Even strong studies can be misleading. Here’s how causation can still be faked—even when a study looks rigorous:

🚩 The Hidden Third Factor (Confounding) – Example: “Coffee drinkers live longer.”

➕ Maybe coffee doesn’t make you live longer—maybe coffee drinkers exercise more, eat better, or have other habits that increase lifespan.

⚠️ Some studies have found that autistic children have higher levels of inflammation in the brain. This has led some people to wrongly assume that inflammation must be the cause of autism (and remember, the point of vaccines is to cause an immune response = inflammation reaction. There is tempting logic there, although an incomplete picture ). But correlation does not mean causation—autism could lead to immune changes, or both autism and inflammation could stem from a deeper underlying factor like genetics or environmental exposures.

🚩 The Timing Trick (Reverse Causation) – Example: “Cannabis use is linked to schizophrenia.”

➕ What if people predisposed to schizophrenia are more likely to use cannabis? That would mean schizophrenia risk is driving cannabis use—not the other way around. Many people struggling with mental health face a treatment system that fails to meet their needs. Seeking their own solutions—like exercise, diet, and sleep—is not only adaptive but actively encouraged by medical professionals. Yet, when individuals turn to cannabis for relief and find it effective, research will inevitably frame this as cannabis being associated with mental health disorders, rather than recognizing it as a response to inadequate care.

🚩 The “Just a Little Bit” Effect (Small Sample Size) – Example: “We found 15% higher risk of heart disease in cannabis users.”

➕ That sounds significant, but if the actual increase is 0.1% to 0.12%, that’s not enough to mean anything. At least to the wise group of readers who look beyond the headlines.

🚩 The “Not Really Significant” Trick (P-Hacking) – Example: “Cannabis increases cancer risk (p=0.049).”

➕ The magic p<0.05 threshold means “statistical significance”, but many results barely make the cut and may not be repeatable.

🚩 The Selective Reporting Game – Example: “7 out of 10 studies show cannabis is harmful.”

➕ What if 30 studies found no harm, but those weren’t published? This is called publication bias, and it happens all the time.

4. The Final Test: When Should You Actually Believe a Study?

When you see a new “science says” headline, don’t just believe it—run it through this Causation Checklist:

🔲 Is it an observational study, or an actual experiment?

🔲 Did they control for confounding variables?

🔲 Did they show a dose-response relationship?

🔲 Did they prove that A came before B?

🔲 Was it replicated in multiple studies?

🔲 Does it actually make biological sense?

🔲 Is the effect size large enough to matter?

🔲 Are journalists hyping it up, or is it really solid science?

🔲 Has the study been debunked? Some studies get retracted after new evidence proves them false—but once a claim spreads, it’s hard to erase. The best example? The vaccine-autism myth. The original study was retracted decades ago, but misinformation lingers, proving that science’s biggest enemy isn’t just bad research—it’s what people choose to believe long after the science has moved on

If a study fails even one of these tests, be skeptical.

🔲 Does the research match the clincal reality?

One unique opportunity—often overlooked in research—is the intersection of clinical reality and scientific findings. Healthcare providers witness conditions unfold in real time, offering a raw, unfiltered perspective on how exposures and outcomes play out in daily life. While this view has its limitations—since only certain individuals seek medical care, creating a built-in selection bias—high patient volume can reveal patterns that research alone might miss.

This is one of the key advantages of CED Clinic’s approach to cannabis care. With thousands of patients under ongoing care and longitudinal tracking, we have a unique opportunity to observe how cannabis impacts health in real-world settings, complementing the insights gained from lab studies and clinical trials.

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Summing it Up: The Relentless Pursuit of Truth

The world is drowning in bad science, misleading media, and half-baked conclusions. Sensationalized headlines push overhyped findings, and even peer-reviewed research isn’t immune from bias, spin, and selective reporting.

If you want real, future-proof information, you have to look beyond the headlines, beyond single studies, and deep into the logic, methodology, and motivations behind the research.

That takes time, patience, and a relentless commitment to the truth.

Most people won’t do that work—they’ll take the easy answers, the bold claims, the viral soundbites.

But you will.

Because you’re still reading.

And if you stick with people who actually care about truth—not just clicks, ideology, or attention—you’ll always be ahead of the game.

🔹 Truth isn’t a quick fix.

🔹 It’s not a single study.

🔹 It’s the patient, skeptical search for patterns that hold up over time.

Want truth that stands the test of time? You won’t find it in single studies, media hype, or the latest health scare du jour.

It’s in:

✔ Recognizing patterns across years of research—not cherry-picking single studies.

✔ Skeptical analysis of funding, biases, and methodology.

✔ Looking beyond what’s being said, to why it’s being said.

So next time you see “New Study Finds…”, don’t just take the bait.

Ask the harder questions.

Next time you see a ‘Science Says’ headline, don’t just take the bait.

🚨 Stop. Ask yourself:

🤔 Does the study prove causation or just an association?

🤑 Who funded it? Who benefits from the conclusion?

🫣 What’s the absolute risk vs. relative risk?

😶‍🌫️ Has the study been debunked, or is it part of the ‘file drawer effect’?

Most people won’t bother to ask these questions. They’ll just share the clickbait headline and move on.

But if you’ve made it this far, you’re different. You’re someone who thinks from top to bottom and probably thinks before believing. That’s what separates hype chasers from truth seekers.

And if you stick with people who actually *care about truth—not just clicks, ideology, or attention—you’ll always be ahead of the game.

For an even deeper dive, The Doctor-Approved Cannabis Handbook explores bias in cannabis in even greater detail. The book encourages readers to critically evaluate claims and look for well-designed clinical trials rather than relying solely on personal experiences or observational studies.

Causation vs. Correlation

Page 102: This is in the section where I break down how to interpret cannabis research responsibly.

“Just because two things happen together—such as cannabis use and symptom improvement—does not mean one caused the other. This is a common mistake in both media reports and personal testimonials.”

Page 104: You address how media headlines can misrepresent cannabis studies, leading people to assume causal relationships where none exist.

“A study might find that people who use cannabis report lower levels of anxiety, but that doesn’t necessarily mean cannabis caused the reduction—it could be that people who are naturally less anxious are more likely to use cannabis.”

Confirmation Bias

Page 55: I discuss how patients and even some healthcare providers may unconsciously focus on positive experiences with cannabis while overlooking studies that show mixed or negative results.

“Many people approach cannabis with strong beliefs—either positive or negative. This can lead to confirmation bias, where we selectively notice and remember information that supports what we already think.”

Page 57: You discuss how people who believe cannabis is a “miracle cure” may only seek out success stories while ignoring studies that show mixed results or potential side effects.

“If someone is convinced that cannabis cures insomnia, they might only remember the nights when it helped them sleep while forgetting the times it didn’t.”

More: confirmation bias

Talking about cannabis and pregnancy can feel overwhelming, with strong opinions and mixed messages coming from all directions. This post cuts through the noise with an honest, evidence-based look at what we actually know. It’s not here to push an agenda—no glorification, no scare tactics—just a clear, thorough discussion of the science, the concerns, and the real questions people are asking.

You’ll find perspectives from both medical professionals and patients, along with research-backed insights to help make sense of a complex topic. The goal isn’t to tell you what to think, but to give you the best information available so you can engage in informed conversations—whether with your doctor, your patients, or your loved ones.

If something here sparks a question or a thought, jump into the comments. Share your experiences. Let’s have a real discussion. And if you know someone who could benefit from this, feel free to pass it along—because knowledge is most powerful when we share it.

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TL;dr — Cannabis has long been hailed for its pain-relieving properties, but until now, skeptics have dismissed it as anecdotal or unproven. A groundbreaking Yale study changes that, confirming that CBD, CBG, and CBN directly inhibit Nav1.8, a key protein responsible for amplifying pain signals. This isn’t just theory—it’s molecular validation of what patients have reported for decades. Meanwhile, Suzetrigine, a pharmaceutical Nav1.8 blocker, was fast-tracked for approval, raising the question: Will cannabis finally be accepted as legitimate medicine, or will it be sidelined in favor of more expensive, patentable drugs? Science is no longer the barrier—policy, profit, and access are.

A Moment of Clarity in the Fog of Pain Management

Pain has shaped human history—often in tragic ways. From the opium dens of ancient civilizations to the modern opioid epidemic, our attempts to manage it have led to both breakthroughs and devastating consequences.

For years, millions have reported relief from cannabis, but skeptics dismissed their experiences as anecdotal, unproven, or even dangerous.

Now, a landmark Yale study provides indisputable molecular proof that cannabinoids deliver real, measurable pain relief at the nerve function level. This is terra firma—not speculation, not theory, but a demonstrated biological mechanism.

And if there were any lingering doubts? The pharmaceutical industry just approved Suzetrigine, a drug designed to do precisely the same thing that cannabis has been doing all along.

The difference? One is a plant, historically stigmatized and restricted. The other is a patentable, profit-driven pharmaceutical.

So, where do we go from here? And why does this change everything?

The Molecular Mechanism: Why This Isn’t Just Another “Cannabis May Help” Study

For decades, the medical community has dismissed cannabis-based pain relief as vague or anecdotal.

“It reduces inflammation.”

“It interacts with the ECS.”

“It changes pain perception.”

All plausible, but none provided the precise molecular mechanism needed to satisfy clinical skeptics.

This study changes that.

At its core, pain is an electrical signal, transmitted from the site of injury or dysfunction to the brain. Nav1.8, a voltage-gated sodium channel, amplifies pain signals—keeping them firing and making them harder to ignore.

The Yale study confirms that CBD, CBG, and CBN directly inhibit Nav1.8, silencing excessive pain signals before they reach the brain.

Of these, CBG emerged as the most potent inhibitor—suggesting it may be one of the most powerful cannabinoids for next-generation pain management.

This isn’t a vague benefit or a general anti-inflammatory effect. This is direct evidence of cannabis blocking a primary pain pathway—a game-changing confirmation of what patients have known all along.

Culturally, This Is a Tectonic Shift in Pain Management

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For over a century, cannabis has existed in a strange paradox. Despite overwhelming anecdotal and observational evidence that it helps with pain, medical institutions, regulatory agencies, and pharmaceutical companies have been reluctant to fully embrace it.

The go-to response? “We need more research.”

That response was always frustrating—because it is evident that the people clamoring for more research never seemed to read the research currently available, and it was never applied evenly. Opioids, for instance, were pushed into the mainstream without the same level of scrutiny (no long-term studies), despite their catastrophic consequences. (And look at the catastrophic epidemic that came by way of FDA approved channels!)

Now, with Suzetrigine approved—a synthetic drug designed to block Nav1.8, just like cannabis does—we’re forced to confront a deep inconsistency in our approach to medicine.

If blocking Nav1.8 is an exciting breakthrough for pharmaceutical pain relief, then why has cannabis, which does the same thing, been ignored for so long?

This study makes one thing clear:

The argument that “we don’t know enough” about cannabis is now scientifically indefensible.

We know. We understand the mechanism. We have the evidence.

The real question is whether the healthcare system will continue to sideline cannabis in favor of pharmaceuticals that do the same thing—but with a prescription and a higher price tag.

The Historical Context: What Pain Management Looked Like Before This Moment

Let’s take a step back and appreciate just how big this shift is.

For most of human history, pain relief has been a messy mix of trial and error, often with devastating consequences:

- Opium & Morphine (1800s – Present): Highly effective but highly addictive, leading to cycles of dependence.

- NSAIDs (Aspirin, Ibuprofen, etc.): Useful for mild pain but can cause gastrointestinal, renal (kidneys), and cardiovascular damage with prolonged use.

- Opioids (OxyContin, Fentanyl, etc.): Hugely successful at relieving severe pain—but also responsible for nearly 1 million deaths and the modern addiction crisis.

- Antidepressants & Anticonvulsants (for neuropathic pain): Help some people but come with side effects like fatigue, dizziness, and mood disturbances.

And then there was cannabis—available, effective for many, but dismissed because it lacked a clearly defined mechanism of action.

Now, for the first time, we can put cannabis alongside mainstream pain medications not just as an “alternative,” but as a scientifically validated treatment.

This isn’t about personal belief, political ideology, or outdated stigma. It’s about evidence.

What Concerns Still Exist?

No discovery, no matter how groundbreaking, comes without its fair share of unanswered questions, skepticism, or the occasional bureaucratic roadblock. The Yale study confirms that cannabinoids block Nav1.8, making it a clear molecular player in pain relief—but like any major shift in medical understanding, it leaves a few loose ends that will need tying up.

1. How do cannabinoids compare to other Nav1.8 inhibitors?

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Cannabis research always seems to be something of a maze, doesn’t it? One study says it’s a miracle for healing, another warns it’s the harbinger of doom for your brain.

Enter the latest from JAMA Psychiatry, a study that attempts to link cannabis use with reduced synaptic density—a measure of how well-connected your neurons are—and, in the same breath, this paper, like a magician showing the rabbit in one hand and the top hat in the other, ties reduced synaptic density to psychosis. The dots are left dangling, inviting readers to connect them in a way that casts cannabis as the villain (for those paying attention, this is par for the course for JAMA)

It’s a clever/sly move, but also deeply problematic. This narrative misses the forest for the trees, focusing on a narrow slice of data without considering the …

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A growing number of patients are turning to medical marijuana (MMJ) as a solution to chronic pain, anxiety, and other debilitating conditions—and now we have some impressive numbers to back up what people have been feeling (and saying) for years. A recent study from Pennsylvania offers important insights into how MMJ impacts health-related quality of life (HRQoL) over the first three months of use. Conducted by Lent et al. and published in the *Journal of Cannabis Research*, the study tracked 438 patients, all first-time medical marijuana users, and found significant improvements across several domains of HRQoL, including physical functioning, emotional well-being, social engagement, and pain levels. But, as with any medical intervention, the findings are nuanced—MMJ isn’t a magic wand, though for some, it might sure seem to come close.

Reporting on this study

The Study PDF

A Study Rooted in the Right Questions

At the heart of this research lies a simple yet compelling inquiry: Can medical marijuana meaningfully improve quality of life for patients suffering from chronic conditions? The researchers followed the participants for three months, assessing their HRQoL using the well-validated Short Form-36 (SF-36) tool. The study showed improvements across all HRQoL domains, with the most striking gains in emotional well-being and social functioning.

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Picture it: people who may have once felt trapped by anxiety or pain suddenly find themselves re-engaging with life—perhaps even joining in at family dinners rather than opting for the couch.

But how does this study fit into the broader literature? Previous research has often been inconclusive or limited to specific conditions like chronic pain or anxiety. What makes this study stand out is its prospective design, following patients from their very first introduction to medical marijuana (no "been-there-done-that" crowd here). It also covers a broader spectrum of conditions, from anxiety disorders to neurodegenerative diseases. And compared to other treatments—analgesics, antidepressants—the HRQoL gains from MMJ are not only competitive, but in some areas, superior. It’s as if medical marijuana just walked into the classroom and scored higher on the test than the teacher’s favorite student.

This type of research signals an important shift, especially with cannabis about to be rescheduled by the federal government. When the science shows cannabis can offer substantial benefits to quality of life—and with fewer side effects than some pharmaceuticals—policymakers are beginning to recognize that maybe it’s time cannabis had a more formal place in the medicine cabinet. Now, if only the healthcare infrastructure (payers, providers, and patients too) could get on board too.

Unpacking the Numbers: What Did the Study Find?

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The core findings of the study are compelling. Over three months, participants showed significant improvements across eight HRQoL domains: physical functioning, role limitations due to physical health, emotional well-being, social functioning, energy/fatigue, bodily pain, and general health. For example, participants’ ratings of their role limitations due to emotional problems improved by a striking 29%, which is more than just a good day at the office—it’s a fundamental shift in how they felt about their mental health. Physical functioning improved by a more modest 6.5%, which is a little less jaw-dropping, but still meaningful for those living with chronic pain.

Statistically, these findings are solid. Improvements across all domains were highly significant, with *p*-values less than 0.001. The study also found that age was a significant predictor of how much benefit patients would experience. Older patients reported less improvement in physical functioning and pain relief, which may not surprise anyone who's had a backache that decided it wanted to "stick around for a while." But it also highlights an important area for further research—can MMJ be tailored for better results in older adults?

As promising as these findings are, it's worth noting that the study did not include a control group. Without one, it’s impossible to rule out placebo effects. Participants’ excitement about trying MMJ for the first time, or simply the natural improvement of their conditions, could explain some of the positive outcomes. A few patients might just have experienced the equivalent of "new shoes, new me." But… for anyone who hasn’t read The Cannabis Handbook, I raise the theory that perhaps the placebo effect may be rooted in the endocannabinoid communication system - so is including consideration for the placebo effect itself a confounder, in cannabis research? Why have we simply accepted the “fact” of a placebo effect, without hunger to tease it apart and flush out its origins? A topic for another day!

Limitations: The Devil in the Details

As exciting as the results are, there are limitations here—big ones. First, the sample was predominantly White (94.5%) and female (66.4%), raising questions about the generalizability of the findings. Would the same results hold true for men, people of color, or those with different socioeconomic backgrounds? Given the diversity of cannabis users in the real world, this demographic imbalance is like asking a group of turtles to test-drive a car—not exactly representative of the full population.

Second, the study only followed participants for three months. We have no idea if these benefits stick around for six months, a year, or longer. That’s like reviewing a movie after watching just the first 15 minutes—it could be great, but without seeing the whole picture, it’s hard to tell. The study doesn’t touch on the potential long-term effects of MMJ either—positive or negative.

Additionally, this was an observational study, so it can’t establish cause and effect. Sure, participants’ HRQoL improved, but can we definitively say that MMJ was the reason? Without an RCT (randomized controlled trial), there’s always the possibility that other factors were at play, like a new diet or lifestyle changes. Nevertheless, it’s nice to see some good press for cannabis.

How Does This Impact You?

(Summary, Tables Below the Paywall)

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Let’s face it—menstrual pain is no joke. For millions of women, cramps and discomfort take a real toll. But what if there’s an unexpected solution that’s been flying under the radar? Enter CBD, the trending wellness ingredient making waves in everything from anxiety relief to skincare. Now, it’s being explored as a way to soothe period pain.

Sound too good to be true? Let’s break it down.

Why Should You Care About Menstrual Pain Solutions?

Period pain doesn’t just mean feeling a little “off.” For many, it’s debilitating. What if there were a way to reduce cramps, bloating, and fatigue without constantly popping painkillers? That’s where CBD suppositories might step in, and the results are worth knowing.

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The intersection of cannabis and COVID-19 has led to some fascinating discoveries, with a recent study showing that cannabis users had MUCH better outcomes compared to non-users when battling severe COVID-19. But as with any promising headline, there’s more to the story. Let’s break down the facts, the takeaways, and what this means for patients and healthcare professionals navigating the complexities of COVID-19 and immune health.

For those who like to read the full study, here it is

Here’s the news report in Forbes

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As the popularity of CBD continues to skyrocket, so does the number of ways people choose to consume it. Vaping has emerged as the fast & easy choice for many, touted for its quick onset and convenience. BUT, a study at the Roswell Park Comprehensive Cancer Center in Buffalo, New York, USA, led by Dr. Yasmin Thanavala and her colleagues, between January 2022 and January 2023, loudspeakers some new findings and concerns to the forefront, and they suggest, from a mouse model, that the very method designed for ease of use could be causing more harm than good, especially to your lungs.

This post peels away some layers of the onion, probing into the study's findings, breaking down what they really mean, and then takes a critical magnifying glass to examine the study's methods and serious limitations. At the end, I commnt on how these findings stack up against the real-world experiences of CBD users, and why more…

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Say, What?

Imagine this: you’re ready for your big day—the one where you finally get that tummy tuck, nose job, or lift you’ve been dreaming about. You’ve followed all the pre-op instructions to the letter, but there’s one thing you might not have thought twice about: your occasional puff of marijuana. No big deal, right? After all, it's legal now, and you're just using it to relax, nothing harmful in that. Well, think again.

A recent study titled "Patterns of Marijuana Use and Nicotine Exposure in Patients Seeking Elective Aesthetic Procedures" has turned up some unexpected findings that could seriously a…

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Recent headlines have swept through mainstream media, proclaiming a significant link between cannabis use and an increased risk of head and neck cancers. These findings, drawn from a new study published in JAMA by Tyler J. Gallagher, BS¹; Ryan S. Chung, BA¹; Matthew E. Lin, MD²; et al, have been widely circulated without much scrutiny, leading to widespread concern. However, a closer examination reveals that the study’s conclusions may not be as solid as they appear. The numerous limitations and potential biases inherent in the study suggest that we should be cautious about accepting these findings at face value.

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Here are the bold, bottom line claims made by this study:

• Cannabis Use Linked to Higher Cancer Risk: The study suggests a significant connection between cannabis use and an increased risk of developing certain head and neck cancers, particularly laryngeal and oropharyngeal cancers.

• Cannabis as a Possible Cause of Cancer: The study implies that cannabis use might directly lead to the development of these cancers, hinting at a cause-and-effect relationship.

• Increased Cancer Risk for Cannabis Users: According to the study, people who use cannabis, especially those diagnosed with cannabis-related disorders, have a higher risk of developing these cancers compared to non-users.

• Cannabis Compared to Other Carcinogens: The study suggests that the cancer risks associated with cannabis might be comparable to those linked to other known carcinogens like tobacco and alcohol.

• Potential Public Health Concerns: The study raises concerns about the broader public health implications, suggesting that these findings might warrant stricter regulations or caution around cannabis use to prevent potential increases in cancer cases.

  

Medical research is essential for advancing our understanding of health and guiding us toward better treatments and prevention strategies. Researchers work hard to ensure their findings are solid and contribute to the bigger picture of what we know about health. But it’s also important to remember that no single study tells the whole story, especially when it comes to complex issues. Analyzing data and making it comparable across different studies is tough— it involves a lot of careful work, assumptions, and sometimes indirect estimates. Scientific progress happens gradually, by building on many studies and perspectives. With that in mind, let’s take a closer look at the recent study linking cannabis use to cancer, and see how it fits into the broader landscape of research and what might get overlooked in the headlines.

Science, and the publication of results, is a fragile and evolving process, not the sweeping, dramatic revelations that headlines often suggest. The reality is that human health and diseases are incredibly complex, and clear-cut answers or dramatic epiphanies (take, for example, OMG - cannabis causes head and neck cancers) are rare, if not unheard of. Most scientific discoveries shine light on just a small, specific aspect of a much bigger picture. All findings published by a small handful of scientists need to be viewed with careful consideration and skepticism, as they often come rich with the hopes/wishes and biases of the team conducting the work , and most often, the work reflects a unique situation that might not apply universally. The strength of science comes from its ability to question, adapt, and continually refine our understanding, rather than offering final, absolute answers.

Scratch The Record, Please: Let’s Peel Away the Smoke & Mirrors

It's important to take a magnifying glass to the findings of any study, and certainly one that suggests a significant link between cannabis use and an increased risk of any relatively common disorder. While this study “adds to the conversation,” the numerous limitations it contains should make us cautious about how much we trust its conclusions.

Read Between the Lines and The Twists of Academic Demonization

Many in modern culture have been brought up to see cannabis as evil. Some were made to believe it was a stepping stone to terrible things, others may have had a lousy experience themselves and simply swore it off as all bad, all the time. A study reporting a significant association between cannabis-related disorders and certain head and neck cancers, such as laryngeal and oropharyngeal cancers, is all too juicy a morsel of meat for both the researchers and the publishers at JAMA to let go of, no matter how much the tasty superficials may hide a little rot inside. But, there are enough critical issues with the study's design and how the data were interpreted for an astute reader to raise serious questions about the reliability of these findings and their leaps to conclusions. There’s enough here to raise polite, academic red flags. Hopefully shedding bright light on the failures will be enough to calm the exaggerated reports and unwarranted conclusions!

The Issue of Reverse Causality

A major concern is reverse causality—the possibility that people who are developing or already have undiagnosed cancers might be using cannabis to manage symptoms like pain or discomfort. The study doesn't adequately account for this, which means it can't reliably tell us whether cannabis use is a cause or simply a response to these cancers that had existed before the person decided to consume some cannabis.

Moreover, our bodies naturally produce cancerous cells as part of normal processes (read this post all about the 5000 cancers we produce every single day - gulp!) , and our immune system typically works to eliminate them before they become a problem (this is the whole point of having T-cells in our body). The endocannabinoid system, which helps regulate our immune function and maintain balance in our cells, could be involved in cases where this natural defense fails. Those who are prone to cancer might turn to cannabis for relief, leading to a misleading association between cannabis use and cancer when cannabis isn't actually the cause. Ironically, as the world slowly begins to discover that there are many elements of cannabis that appear to kill and prevent the growth of cancers, more than it having mere usefulness in treating symptoms, associations like the ones found in this study are likely to become more popular. (Murphy’s law, isn’t it?)

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Missing Mechanism of Action

Another major flaw in the study is that it doesn't propose a clear mechanism of action—a plausible biological explanation for how cannabis could cause these cancers. Even though there ARE studies and literature on the mechanisms of action by which cannabis can stop cancer growth (see here), somehow the importance of postulating HOW this stuff actually works is a blatant omission here. In medical research, understanding how something works is key to proving that it actually does. Without this, the association the study found remains speculative - a wink and a hope. The endocannabinoid system, which plays a crucial role in maintaining cellular health, doesn't naturally suggest a pathway leading to cancer. In fact, some research shows cannabinoids might even help protect against certain cancers by promoting the death of cancerous cells. This lack of a clear mechanism suggests that the association might be due more to reverse causality than cannabis being a direct cause of cancer.

Flaws in the Study's Design and Interpretation

Several other flaws in the study's design and how the data were interpreted further weaken its conclusions:

1. No Control for Reverse Causality: The study doesn't account for the possibility that people might be using cannabis in response to early cancer symptoms, rather than cannabis causing the cancer.

2. No Dose-Response Analysis: The study doesn't tell us if the risk increases with more cannabis use, which is crucial for determining if cannabis is actually causing the cancer.

3. Detection Bias: People who use cannabis, especially those diagnosed with a cannabis-related disorder, might be more closely monitored by doctors, leading to higher rates of cancer detection. This could falsely inflate the association between cannabis use and cancer.

4. Ignoring Pre-Existing Conditions: Many cannabis users may have other health conditions that make them more likely to develop cancer. The study doesn't fully consider these factors, which means the association it found could be due to these other health issues, not cannabis use.

Coding as a Source of Participant Identifiers

In the context of building a study population for this article, the researchers rely on ICD-10 codes as a way to pick participants, and this presents a huge limitation. These codes are inherently subjective and often do not reflect the nuances of a patient’s cannabis use. Physicians documenting cannabis use are constrained by the limited options available to them in their electronic chart system, which are typically focused on diagnosing problems or disorders, and not merely adding interesting commentary about a patient’s choices, preferences, or personal liberties they take when dealing with medical challenges. This can easily lead to an inaccurate representation of someone’s cannabis consumption, where cannabis is marked as a problem even if it is not causing any harm to the patient, or in fact may be there to help the patient improve. Furthermore, these codes fail to capture essential details such as the amount, potency, or duration of cannabis consumption—factors that are crucial for assessing its true impact on health. As a result, these diagnoses can linger in a patient’s medical chart for years, potentially without proper context, which in the case of the current study, would powerfully skew the study’s findings. The presence of these codes, without an accurate and detailed record of cannabis use, may contribute to misleading associations between cannabis and cancer, undermining the study’s conclusions.

Unspoken Issues and Contradictions

The study also misses several important factors that could significantly change how we interpret its findings:

• Changing Social and Legal Context: As cannabis becomes more accepted and legalized, the profile of cannabis users and the associated health risks might change, something this study doesn't consider. Where products are not legal and regulated, it’s easy for confounding variables to slip into studies unaccounted for.

• Polydrug Use: The interaction between cannabis and other substances, like tobacco and alcohol, could affect cancer risk. The study doesn't thoroughly explore this, which is a big oversight.

• Genetic and Environmental Factors: Differences in genetics and environmental exposures, which can significantly impact cancer risk, aren't accounted for in the study. This limits how applicable the findings are to different groups of people.

Putting Relative Risk in Perspective

Another important point is understanding the difference between relative risk and absolute risk. The study talks about an increased relative risk of cancer among cannabis users, but it’s important to translate that into real-world terms.

• Relative Risk: This compares the risk between two groups (e.g., cannabis users vs. non-users). Even a high relative risk doesn’t necessarily mean the absolute risk is high.

• Absolute Risk: This is the actual chance of developing a disease. For example, if the baseline risk of developing a certain cancer is 0.1% and cannabis use increases this by 3.5 times, the new absolute risk is still only 0.35%—a small increase in real terms.

In context, while the study reports an increased relative risk, the absolute risk of developing these cancers remains low for most people, especially those who use cannabis infrequently or for medical reasons.

Relative Risk, In Real Terms:

In the study, the relative risk of developing certain head and neck cancers among cannabis users might be reported as a multiple—say, 3.5 times higher than in non-users. To put this in perspective, imagine you're walking through a neighborhood where typically, 1 out of 1,000 homes experiences a small kitchen fire each year. If you suddenly decide to cook more often, and your relative risk of a kitchen fire increases 3.5 times, it now means you have a 3.5 out of 1,000 chance—still quite small. The difference feels more significant when expressed as "3.5 times higher," but in absolute terms, your risk has only increased by a tiny margin, much like the way the study's relative risk might sound alarming, but the actual increase in absolute risk could be very modest.

Absolute Risk, In Real Terms:

When you suspect a broken bone, getting an X-ray is a common first step in confirming the diagnosis, and most people wouldn’t think twice about it. While it’s true that an X-ray exposes you to a small amount of ionizing radiation—around 0.1 millisieverts, compared to the 3 millisieverts you receive from natural background radiation each year—the absolute risk increase of developing cancer from a single X-ray is minuscule, approximately 1 in 1,000,000. This risk is so small that it hardly registers in our everyday decision-making, especially when weighed against the immediate need to accurately diagnose and treat a potential injury. Similarly, flying in an airplane also exposes you to slightly higher levels of cosmic radiation due to the higher altitude. For instance, a typical long-haul flight might add around 0.05 millisieverts of radiation exposure—another small fraction of your annual background radiation dose. Yet, just like with X-rays, this increase is so minimal that it’s not something people typically worry about, particularly given the necessity and convenience of air travel.

For another example, consider the use of low-dose aspirin, which until very recently (until 2021-2022) was commonly recommended to reduce the risk of heart attacks and strokes in adults. While taking aspirin daily does slightly increase the risk of gastrointestinal bleeding—about 2 additional cases per 1,000 people over 5 years, or a 0.2% absolute risk increase—most doctors didn’t hesitate to prescribe it, and most people felt comfortable taking it. The small increase in bleeding risk is generally outweighed by the significant benefit of preventing life-threatening cardiovascular events. These examples show how minor risks are often accepted in the face of clear and substantial health benefits, reminding us that not all risk increases are cause for alarm.

A Table of Other Meaningful Limitations of This Study

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Hopefully everyone has heard that sunlight is bad for you. But it is more than just about looks and aging skin. It’s also about cancer and preventing serious damage to our bodies. With the increasing awareness of the harmful effects of ultraviolet-A (UVA) radiation on skin health, the search for effective protective measures has become crucial. (If you didn’t read my recent post about all the options we have available for Sunscreen Protection - check it out!) This month, a study "Topical Nanoencapsulated Cannabidiol Cream as an Innovative Strategy Combatting Ultraviolet A-Induced Nuclear and Mitochondrial DNA Injury" looks into the amazing potential of cannabidiol (CBD) to mitigate the dangerous effects of UVA sun exposure. Here, I’ll share a brief overview of the study, highlight the key patient-relevant findings, and discuss the implications of these findings for everyday life and personal skincare routines.

Who does this study benefit?

Individuals with sun-sensitive sk…

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