For as long as I can remember, common medical knowledge has been that sugar causes diabetes. Indeed, everyone from parents to teachers to even medical health professionals (i.e., doctors) have told me to watch my sugar intake, lest I wind up with Type II diabetes. You’ve probably encountered some variation of the following folk wisdom: “Sugar is poison,” “Sugar causes diabetes,” or, my personal favorite, “Sugar is more addictive as cocaine”—a claim that really makes you wonder if the people saying this have ever tried real, genuine cocaine. I’m going with no, they haven’t.

The myth I’ve heard my whole life is that sugar is the biggest culprit in causing diabetes. The anti-sugar crusade has become so pervasive that we’ve collectively decided this sweet crystalline substance is basically the snake-in-the-garden villain origin story for every metabolic disease known to humanity. But when you dig into the research on whether sugar causes diabetes, the picture becomes a whole lot more complicated.

Buckle up, kiddos, because we’re about to wade through some fascinating science that suggests the relationship between sugar and diabetes is less “smoking gun” and more “accomplice who was maybe just in the wrong place at the wrong time.”

This is going to be a very long article…pass me the cocaine-laced sugar. 1

Let’s start with a few things to get the record straight. I’m not arguing that sugar doesn’t worsen diabetes and diabetes symptoms. This much is clearly true, just ask anyone painstakingly managing their blood sugar daily. But just because something worsens a condition, doesn’t mean it causes that condition. A distracting environment might make ADHD symptoms worse, but the cause of ADHD is mostly genetics. I’m also not arguing that sugary drinks and such are fantastic for your health. Even if all the sugary sodas in the world don’t cause diabetes, that doesn’t mean they’re great for you. 2

Next up, let’s talk about why nearly everyone thinks sugar causes diabetes in the first place. The folk logic goes something like this:

1. Diabetes is characterized by problems with blood sugar regulation.

2. Sugar raises your blood sugar.

3. Ergo, sugar must cause diabetes.

It’s beautifully, even intuitively, simple. It seems to make perfect sense to just about everyone at a glance. But it’s also wrong.

This is the same kind of reasoning that would lead you to conclude that firefighters cause fires because they’re always at the scene, or that doctors cause illness because sick people keep showing up at hospitals. Correlation, causation, yadda yadda—you know the drill.

The reality is that diabetes involves impaired insulin function and glucose metabolism, which means that yes, diabetics need to manage their sugar intake carefully. But managing a condition isn’t the same as what caused it. People with peanut allergies need to avoid peanuts, but peanuts didn’t cause their allergy—their immune system did that all on its own. 3

So, if not sugar, what actually causes type II diabetes?

The two biggest risk factors, by an enormous margin, are:

1. Your age: Your pancreas, like the rest of you, gets tired and cranky as you get older and can’t whoop ass like it once did

2. Obesity: Specifically, excess body fat, particularly around your organs

Other risk factors include genetics, physical inactivity, family history, ethnicity, and having had gestational diabetes. What’s conspicuously absent from this list is consuming sugar, even SSBs (sugar-sweetened beverages, AKA sodas), as well as other deliciously wonderful treats like cookies.

Now, let’s briefly get into the mechanisms of diabetes and how we understand all of this. The fundamental issue in type 2 diabetes is insulin resistance—your cells stop responding properly to insulin, so your pancreas has to produce more and more of it to get glucose into your cells, until eventually your pancreas can’t keep up. This process is heavily influenced by excess body fat, which affects how your cells respond to insulin.

So the question isn’t whether sugar affects diabetes (it obviously does—it’s literally sugar we’re talking about). The question is this: does sugar cause diabetes through some direct mechanism, or does it only contribute to diabetes by making you gain weight, which then causes diabetes?

In plain English, does sugar cause diabetes or does it make people obese, and it’s really the obesity that causes diabetes?

This distinction matters a lot, because these two aren’t the same. Other foods can make you obese. Fats are more than twice as caloric as carbs, including sugar, which means if obesity is the real culprit, fats would be more likely to cause diabetes than sugars in the long run.

Sweet, Sweet Research

Let’s start with the surpising stuff that blew my mind. When researchers started doing controlled studies where people consumed the same number of calories but different amounts of sugar, something unexpected happened: the diabetes risk didn’t really change.

A major 2017 review of cohort studies found that sugar-sweetened beverages (SSBs) didn’t affect glycemic control when total calories were kept equal (isocaloric conditions). No significant associations were found for added sugar or fructose when examined as nutrients.

Plain English: when you’re not gaining weight from the extra calories, the sugar itself doesn’t seem to be damaging your metabolism.

The comprehensive review found that when you control for total calorie intake, “intake of sucrose and other dietary sugars is not linked to type 2 diabetes.” That’s a pretty big deal. It suggests that sugar’s main crime isn’t being sugar—it’s being calories, just like all other foods.

It’s like drinking and driving. Whenever someone makes a painfully stupid decision and gets behind the wheel drunk, we don’t blame the car. It was just the vehicle for that person’s bad decisions. Similarly, sugar is just the vehicle for weight gain, and weight gain is the real culprit damaging people’s health.

Now, you may be wondering, “But do we know how much of diabetes is caused by excess weight?” Yes, multiple studies have examined precisely how much of sugar’s association with diabetes is explained by weight gain.

While BMI is an imperfect metric, it’s helpful for ruling things out. One study found that BMI mediates approximately 66% of the association between sugar consumption and diabetes prevalence. That means two-thirds of sugar’s apparent effect on diabetes is actually just working through weight gain. This study spanned 192 countries, so it was culturally independent and showed that, when you control for BMI, two-thirds of the link between sugar and diabetes goes away. It’s safe to say at least some of the rest that wasn’t erased by controlling for BMI may be a matter of BMI being an imperfect measurement. Which is exactly what was found in other research.

Plain English: if everyone was the same size, the link between sugar and diabetes disappears. This means it’s more likely that obesity is to blame than sugar, otherwise, you’d expect it in non-obese people.

Another study put it even more starkly: after adjusting for BMI, much of the association between sugar and type 2 diabetes simply disappears. A 2016 review concluded that “excess sugar can promote weight gain and thus diabetes through extra calories, but has no unique diabetogenic effect at physiological levels.”

Plain English: there’s absolutely, positively nothing unique about sugar that causes diabetes, any more than any other food.

Plot-Twist: Huge Counterpoint

Now, before the sugar industry reaches out to me offering to pay for my next vacation if only I’d drum up a write-up for them, or starts using this article in their marketing materials (please don’t, Big Sugar, I am not your shill), we need to acknowledge the story is complex.

Some studies have found evidence that sugar, particularly fructose, might have some direct metabolic effects independent of weight gain. One study found that while BMI mediated about 11.7% of the sugar-diabetes association, there was still a remaining association even in normal-weight individuals.

A study of 12,800 Chinese adults found a significant association between added sugar intake and the increased odds of diabetes, even when controlling for weight-related factors, suggesting a unique weight-independent diabetogenic effect. While BMI both moderated and mediated this association, the link didn’t completely disappear.

In plain English, this means that while weight and obesity play a role in diabetes, it doesn’t explain everything and the diabetes risk remained even in people in the average BMI range.

Fructose, Bastard Child of Sweetness

It turns out, the kind of sugar may (or may not) matter. Fructose specifically may be the troublemaker in the sugar family.

Table sugar (sucrose) is 50% glucose and 50% fructose. High-fructose corn syrup (found in some sodas) is roughly 55% fructose and 45% glucose (despite the scary name, it’s not that different from regular sugar). But fructose behaves differently in your body than glucose does. 4

When you eat glucose, it gets distributed throughout your body—your muscles, brain, and other tissues can all use it directly for energy. But fructose? Fructose takes a special detour through your liver, where it gets processed almost like alcohol.

Research has suggested that fructose specifically can promote hepatic insulin resistance—meaning it makes your liver less responsive to insulin. It does this through several mechanisms:

• Unregulated hepatic uptake: Your liver just gobbles up fructose without any real regulation

• Lipid accumulation: Fructose gets converted to fat in your liver more readily than glucose

• Impaired insulin signaling: Studies show that fructose, but not glucose, impairs insulin signaling in major insulin-sensitive tissues

But her’s the kicker. Some of these effects appear to be “independent of increased weight gain and caloric intake.” In other words, there might, maybe, possibly be some direct metabolic mischief happening beyond just calories.

One particularly interesting study found that fructose-related changes to insulin signaling were “related to fructose itself rather than the amount of calories ingested.”

Plain English: you might be able to eat all the table sugar you want, if diabetes is your worry, but stuff like soda may be the real culprit.

Based on this research, scientists have proposed a two-pathway model. It’s a lot more complicated than this, but here’s the simple version:

• Pathway 1 (Direct): Sugar, particularly fructose, causes dysregulation of lipid and carbohydrate metabolism independent of weight gain.

• Pathway 2 (Indirect): Sugar provides excess calories, leading to weight and fat gain, which then causes metabolic dysfunction.

The evidence suggests both pathways might exist, but, if so, Pathway 2 is doing most of the heavy lifting (pun intended), and this is still far from certain. It’s a hypothsis as of the time of this writing.

Population-Level Research: 175 Countries Can’t Be Wrong…Right? Right?!

Some of the most provocative research comes from large-scale population studies. One econometric analysis of 175 countries analyzed the country’s added sugar consumption and diabetes rates, and found that every 150 kcal/person/day increase in sugar availability was associated with a 1.1% increase in diabetes prevalence, and this association persisted even after controlling for obesity rates.

That sounds pretty damning for sugar, right? Not so fast. First, a 1.1% increase is extremely small. That means 98.9% of the populations’ diabetes were not explained by added sugars. On top of this, population-level correlations are ridiculously tricky to interpret. Countries with higher sugar availability (like the U.S.) might also have other factors that influence diabetes rate, stuff like:

• Different levels of physical activity

• Different healthcare systems

• Different diatary patterns overall

• Different genetic backgrounds

• Different definitions of what counts as “diabetes” and what does not

Population-level research can only show us more correlations. It’s suggestive, but not the smoking gun that other, stronger types of research are. 5

The Sugar-Sweetened Menaces: One Area of Real Concern

If there is one category of real concern regarding sugar consumption, one that consistently shows up in research conducted in different countries by people of different persuasions, it’s SSBs—your sodas, sweetened teas, high-sugar energy drinks, and fancy coffee. You know, any drink that has more sugar than the icing on your birthday cake.

Meta-analyses have found that each additional serving of SSBs is associated with higher diabetes risk, with “moderate certainty of evidence.” This makes sense for several reasons:

1. Liquid calories don’t fill you up: You can drink 500 calories of soda and still eat a full meal afterward, whereas 500 calories of solid food would make you feel pretty satisfied.

2. Rapid glucose spikes: Liquids are absorbed quickly, causing bigger and faster spikes in blood sugar and insulin.

3. Volume and frequency: People tend to consume SSBs regularly and in large quantities.

But even here, the question remains: is it the sugar in the beverages, or is it the way beverages deliver a massive metric fuck ton of a calorie payload without triggering satiety that’s the problem?

Weird, Whacky Findings About Sugar and Diabetes

Let’s dive into some super interesting findings that are really counterintuitive. Some studies have found that moderate intakes of total sugar and sucrose are actually inversely associated with type 2 diabetes. In other words, moderate amounts of sugar might be protective, and people eating moderate amounts of sugar had lower diabetes risk.

Now, before you go chugging that Canadian maple syrup with no chaser, let’s think about what this might mean:

• People who consume moderate amounts of sugar might be eating it as part of an otherwise healthy diet (fruit, for example, contains sugar along with fiber and nutrients)

• People who completely avoid sugar might be doing so because they’re already at high risk for diabetes

• The relationship between sugar and diabetes might be U-shaped: too much is bad, but too little might be a marker of other dietary restrictions or health issues

This is why nutrition science is so maddeningly, stupifyingly complex. The human diet isn’t a simple chemistry experiment—it’s a messy, interconnected web of foods, behaviors, genetics, and social factors. Lots of stuff to tease out. 6

Okay, Enough Science. What’s the Verdict?

After wading—nay, trudging with a high head and chests protruding out proudly—through all this research, here’s what we can reasonably conclude the following facts about sugar and diabetes.

What We Know for Sure:

• Obesity and age are the primary risk factors for type 2 diabetes. This isn’t controversial. Anyone who says it’s sugar or that sugar is the main cause is 100% misinformed. This should be the primary takeaway from this article, even if that doesn’t mean you should slam twelve sodas per day or chug the aforementioned maple sugar like you’re in a contest.

• Excess calories from any source can lead to weight gain, which increases diabetes risk. Sugar isn’t special in this regard—a calorie is a calorie when it comes to weight gain, and, considering this, fat is more than twice as destructive (but as long as you aren’t gaining weight, fats too aren’t a huge problem).

• Sugar-sweetened beverages are particularly problematic because they deliver gargantuan amounts of calories without triggering fullness, making overconsumption all-too easy peazy.

• Fructose has some direct metabolic effects on the liver that are independent of weight gain, though the clinical significance of these effects at normal consumption levels is still debated and we’re not sure how much of an effect it has on diabetes, but we can be pretty confident it will be very small compared with age and obesity. Unfortunately, the liver too, like the pancreas, just wears out with age.

What We’re Pretty Sure About

• Most of sugar’s association with diabetes (roughly 60-66%) works through weight gain, not through some unique diabetogenic property of sugar itself.

• When calories are controlled (isocaloric conditions), sugar doesn’t show the same associations with diabetes risk. This is a big deal and suggests calories matter more than sugar specifically.

• Context matters enormously: Sugar consumed as part of a healthy diet with adequate fiber, protein, and nutrients is very different from sugar consumed in isolation or as part of an ultra-processed, nutrient-poor diet.

What We’re Still Figuring Out:

• Whether the direct metabolic effects of fructose on the liver translate to clinically significant diabetes risk at the levels most people consume.

• Why some population-level studies show associations between sugar and diabetes even after controlling for obesity, while controlled intervention studies don’t.

• Whether individual genetic differences affect how people metabolize sugar and whether some people are more susceptible to sugar’s effects than others.

Wrapping it up like safe sex…

Okay, so ya boy kinda went ham with this one and I still wrote a ton more than I think would make this piece a slog, so, here’s what I’ve done. I’ve created an addendum piece to this, as I often do, discussing the implications of this research for those who really want to know how it should be interpreted. You’re the health and science superstars and I appreciate each and every one of you my beautiful little creatures.

Okay, so if you’ve wound up here, I trust you’ve already read the first episode of this duo, Debunking the Sugar-Causes-Diabetes Myth. If not, it’s right here:

Now, after reading that wall of text, you might be thinking, “Okay, so sugar might not directly cause diabetes, but it still contributes to obesity, which causes diabetes, so what’s the difference? Shouldn’t we still avoid sugar?”

Fair play. But the distinction matters for several reasons. First, we might be fighting the wrong battle. If we focus public health efforts (yes, that includes influencers, but I won’t hold my breath for a come-to-Jesus moment where they suddenly get on board with research) on demonizing sugar specifically, we miss the bigger picture that total calorie intake and physical activity are the real culprits. Someone can cut all the added sugars from their diets and still get diabetes through age or obesity alone.

You can eat a low-sugar diet and still gain weight if you’re eating too many calories from other sources (looking at you, Keto Kiddos inhaling sticks of butter like Bill Clinton most definitely inhaled marijuana).

This isn’t some strange fantasy. The obsessive focus on sugar has led to bizarre situations where people avoid fruit because it contains sugar but are happier than pigs in poop consuming gargantuan quantities of “sugar-free” foods that are still atrociously bad for them.

Individual Responsibility Vs. Bad Food Environments

Now, here’s where a lot of you are going to get on board with me. Telling people to “just eat less sugar” places all the responsibility on individuals, while painfully ignoring the food environment we’ve created. We live in a world (in the U.S.) where:

• Cheap, hyper-palatable, calorie-dense foods are everywhere

• Portion sizes have ballooned

• Physical activity has been engineered out of daily life

• Food companies spend billions making food as crave-able as possible

Blaming sugar specifically lets us avoid addressing these larger systemic issues. That’s exactly what they want us to do.

Next up, the nuance gets lost. When we say “sugar causes diabetes” people hear “sugar is poison” and start fearing all sorts of sugar equally. It’s like another boogeyman, “processed foods”—when scientists and health officials say “avoid processed foods” they don’t literally mean all processed foods. They mean sponge cakes, not peanut butter and yogurt.

Eating Vs. Exercise (is worth mentioning)

We also can’t out-exercise our forks (but exercise still matters). If you were to hop on a bike and ride as hard as you could for a half hour or so, you might burn 250–300 calories. Laudable, but that could easily be undone by a single candy bar. The idea that exercise is great and will undo poor eating habits just isn’t based in truth. I wish this weren’t so, but alas, the hardest part of maintaining a healthy body weight is the eating.

Practical Takeaways (because you probably want some actual advice):

Okay, so if sugar isn’t the demon we thought it was, what should you actually do with this information?

Still don’t go wild with the sugar bowl. This isn’t a license to start mainlining high-fructose sodas with a hypodermic needle. Sugar is still calorie dense and easy to overconsume. It lacks nutrients (I’m sure you’ve heard “empty calories”), is associated with weight gain when consumed in excess, and rough on your teeth (turns out, the dentist was telling the truth all along).

If there’s one clear takeaway from all this research, it’s that sugar-sweetened beverages are a uniquely problematic source of calories at the very least. They don’t fill you up, they’re easy to overconsume, and they’re consistently associated with negative health outcomes. Water is free, and your kidneys will love you for it.

Instead of obsessing over sugar specifically:

• Watch your total calorie intake: This matters more than the specific macronutrient composition

• Eat mostly whole foods: Fruits, vegetables, whole grains, lean proteins, and healthy fats

• Get regular physical activity: Both for metabolic health and for, you know, not dying prematurely

• Maintain a healthy weight: This is the single biggest modifiable risk factor for type 2 diabetes (unless you know the secret to age control)

A cookie at a birthday party is not a big deal. Three cookies every night while binge-watching Netflix, however, might be contributing to a pattern of excess calorie intake. The poison is in the dose, as some old alchemist once said (probably while eating a cupcake). Fruit is all good.

The Bigger Picture of Nutrition Science

This whole sugar-diabetes debacle is a perfect example of why nutrition science is so frustratingly complicated, and why headlines about food are constantly contradicting each other. Those problems include:

• Confounding variables everywhere: people who eat a lot of sugar might also be sedentary, smoke, drink alcohol, eat fewer vegetables, have lower incomes, experience more stress, and sleep poorly. Trying to isolate the effect of sugar alone is like trying to untangle a ball of black USB plug cables—in the dark—while wearing mittens.

• Different study designs show different things: population studies show associations, but they can’t prove causation. Randomized controlled trials can show causation, but they’re usually short-term and artificial. Long-term RCTs of diet are nearly impossible to conduct (and much of what we’d need to find out more would be wholly unethical today).

• Humans are terrible study subjects: We lie about what we eat (usually unintentionally), we can’t remember what we ate yesterday, and our diets change over time. Food frequency questionnaires—common research tools—are about as reliable as eyewitness testimony, which is to say, not very reliable at all.

• The food industry funds research: This doesn’t automatically make research invalid, but it does introduce potential bias, particularly in how results are interpreted and which studies get published. Personally, I address the research’s evidence, not who’s funding it. But I also take note of who’s funding it and researchers are forced to disclose that information and any conflicts of interest. However, other writers and especially influencers may not be so discerning.

• Nobody eats nutrients in isolation: You don’t eat “sugar” or “saturated fat”—you eat cookies, steak, pasta, and salads. These foods contain wildly complex mixtures of nutrients that interact with each other in ways we don’t fully understand.

• Individual variation is YUUUGE: Some people can eat a high-sugar diet and stay metabolically healthy. Others develop insulin resistance on a moderate diet. Genetics, gut microbiome, activity levels, stress, sleep—it all matters.

The Sweet Spot Between Panic and Permissiveness

Finally. We’ve made it to the end of this monstrous deep dive into the sugar-diabetes connection, and what, oh what, dear readers, have we learned?

First, sugar most probably isn’t the direct cause of diabetes that we’ve been led to believe it is. The evidence suggests that its primary sin is being an easy source of excess calories, which can lead to weight gain, which is the actual major risk factor for type 2 diabetes. Yes, fructose might have some direct metabolic effects on the liver, but the clinical significance of these effects at normal consumption levels remains unclear.

Does this mean sugar is fine, and we should all start eating candy for breakfast? No, obviously not. Sugar is still calorie-dense, nutrient-poor, and easy to overconsume, especially in liquid form. It’s just not the uniquely toxic villain we’ve made it out to be.

The real story is more boring and less clickable: Maintain a healthy weight through a balanced diet and regular physical activity, and you’ll dramatically reduce your type 2 diabetes risk regardless of whether those calories come from sugar, fat, or protein.

But alas, the truth is all-too-often less clickable than the internet-shitosphere bullshit. Until next time, remember: the dose makes the poison.

Stop and imagine for a moment that, before you were born, someone removed a gene from your body. By doing so, they made it so you couldn’t remember anything or your thoughts couldn’t finish. The moment you got close, the thought would vanish into thin air. Sounds like something straight out of science fiction, a Cory Doctorow sci-fi novella turned into a movie. But, as we’ll soon see, this is far from science fiction—it’s science fact. It’s possible to do just this, and it’s taught us a metric fuck ton about ADHD.1

Hold on to that thought experiment. It’ll come in handy.

This will no doubt make me unpopular online, but it’s time to debunk the abundant myths that swirl around the Internet shitosphere about ADHD. I see them constantly and it’s time to put a few of them to bed once and for all. A short, incomplete list of myths I have in my sights includes:

• ADHD is mostly a “social construct” and not a biological neurodevelopmental condition with a basis in the genes of the brain.

• ADHD is a modern condition, more a product of our modern world than genetics.

• ADHD is overdiagnosed and it’s hurting people because…

• The treatment of ADHD involves stimulants which are bad for you.

We’ll dig into the science-y stuff, but I’ll translate into plain English for anyone who doesn’t have a scientific background as we go along.

Now, if you spend enough time online discussing ADHD—or even the wealth of issues plaguing society—you’ll inevitably encounter skeptics who insist the above myths are true: that the condition is overdiagnosed, an unfortunate product of modern life to be treated by changing the surrounding society, or even that ADHD is a complete myth to be ignored. It’s tragic.

Opinions like these flourish online despite decades of meticulous scientific research demonstrating the precise opposite. They’re so rampant, I’ve created stock notes with details about the science that I can easily copy and paste when these myths inevitably crop up in conversation.

“No, actually,” I write, before pasting the note’s contents explaining what the actual science says. And the actual science says ADHD is not only real—it’s one of the most scientifically valid and strongly genetic conditions in psychiatry, with heritability rates comparable to physical traits like human height and eye color. Nobody’s arguing eye color is a societal failing and when they did, back in the 1930s, we rightly called them Nazis. 2

Any argument that we should change society and ADHD will just go away isn’t based in the vast body of scientific facts about the condition we’ve accumulated since the 1970s, and any such changes would be doomed to fail. 3 ADHD’s heritability has been well-established through extensive twin, family, adoption studies, studies that explored parents’ and teachers’ perceptions of their children and students, and even post-mortem studies.

We really, really, really know our shit when it comes to ADHD.

We’re talking absolutely massive studies of every variety. We’ve come at the question from every single angle imaginable and concluded, time and again, that ADHD is extremely genetic. The mass of research has shown that the heritability ranges between 70% and 90%, with the mean heritability across 37 twin studies being 74%, meaning that roughly three-quarters of variation in ADHD symptoms can be attributed to genetic factors. 4

For context: height is about 80% heritable, intelligence is about 55% heritable, and depression is around 35-40% heritable. ADHD sits right up there with the most heritable traits we know of—higher than conditions like bipolar and schizophrenia that nobody seriously questions as “real.” So when ADHD ranks in at about 74%-88%, it’s on par with the heritability of height.

In plain English, this means that it’s extremely fucking genetic. 5

When scientists say something is “heritable,” they mean it’s passed down through your genes. Twin studies—where researchers compare identical twins (who share 100% of their DNA) with fraternal twins (who share about 50%)—have consistently shown that if one identical twin has ADHD, the other twin is extremely likely to have it too. This pattern has been replicated across 37 different twin studies, in different countries, with different populations, and yes, different cultures. At this point, arguing that ADHD isn’t genetic is like arguing that eye color is just a matter of the kind of positive thinking you expect from the LinkedIn Bro who wants to sell you a success course.

Now, you might be thinking, “Okay, but have scientists actually found the genes?” Yes. Yes, they have, as a matter of fact.

One of the most significant discoveries is a gene called LPHN3 (short for Latrophilin 3, because scientists seem to really love making things sound like sci-fi weapons, clearly). Research involving over 6,000 participants worldwide has confirmed that certain variants of this gene are associated with ADHD. This isn’t some fringe study—this is large-scale, replicated science.

Here’s where it gets cool: LPHN3 is expressed specifically in brain regions that control attention, impulse control, and activity levels—the caudate, prefrontal cortex, amygdala, and cerebellum. When scientists knocked out this gene in rats, mice, zebrafish, and even fruit flies, guess what happened? The animals became hyperactive, inattentive, and developed the memory problems associated with ADHD. Every. Single. Time. Different species, same exact result. That’s about as solid as scientific evidence gets.

The thought experiment at the beginning wasn’t rhetorical. That gene exists, among others. Not only are people with certain LPHN3 variants are more likely to have ADHD, but they’re also more likely to have symptoms that persist from childhood into adulthood. Some variants even affect how well someone responds to ADHD medications. This gene isn’t just correlated with ADHD—it’s functionally involved in the biology of the condition.

And ADHD goes beyond just inattention and memory. These genes also influence behavior, so radical behavior, outbursts, and fixations are also a part of it. Sometimes, ADHD isn’t an inability to pay attention to anything, it’s an inability to pay attention to anything but the one thing you’re fixated on.

But wait…there’s more (genes)…

Before anyone gets too excited about a single “ADHD gene,” as the media often do, here’s the reality check: ADHD is polygenic, meaning it’s influenced by many genes, not just one. Think of it like baking a cake—LPHN3 might be the flour, but you’ve also got eggs, sugar, baking powder, and about fifty other ingredients all working together to create the final product. 6

Genome-wide association studies identified hundreds of genetic variants that each contribute a tiny bit to ADHD risk. About a third of ADHD’s heritability comes from these many common genetic variants, each having small individual effects but adding up to something significant when combined.

This complexity doesn’t make ADHD any less real or less genetic—it just means your DNA is more sophisticated than a simple on/off switch. (Take that, high school biology class!). I’ve covered this over on The Science of Sex, explaining that the whole point of having sex is to mix up the genes with every generation, like shuffling a deck of cards.

We shuffle a deck of cards to ensure fairness. We have sex to shuffle the genetic deck to ensure we’re not exact replicas of one another and that there’s random variation between generations. It’s why we’re not replicas of our parents; it’s also why we’re not all susceptible to the same diseases and conditions. Unfortunately, the other side of that coin is, we’re all susceptible to different diseases and conditions.

Now, genes aren’t the whole story. That 74%-88% heritability means that roughly 12%-26% of ADHD variation is influenced by environmental factors. This is important and shouldn’t be ignored. It means that things like sleep, stress, trauma, nutrition, and social support systems can all affect how ADHD manifests and how severe it is. But it also means that even if we maximized all of these things for every person with ADHD, the condition would persist.

Can environmental accommodations help? Absolutely. Should we provide them? Without question. But let’s stop pretending ADHD is primarily an environmental problem. The science is crystal clear that it’s fundamentally a neurodevelopmental condition rooted in brain biology.

Now, here comes the real juicy stuff. One claim I see people make over and over again, especially from the United States where trust in institutions is breaking down rapidly, is the claim that ADHD is overdiagnosed. “That’s all well and good,” they might tell me, “But it has nothing to do with the fact that doctors are handing out amphetamine pills like Jolly Rancher candies, and that’s a big problem that should be stopped.”

During the Adderall shortages of 2022, a viral tweet espoused outrage that 41 million prescriptions of Adderall were dispensed in 2021, basically rebranding people with legitimate conditions as meth users (evil as fuck):

This is the kind of disinformation I eat for breakfast.

Lifetime ADHD rates were 8.8% at the time, meaning 8.8% of the adult population suffered from ADHD. The U.S. population was 332.28 million people. 8.8% of 332.28 million is 28,908,360. So, roughly 28,908,360 people in the U.S. had ADHD. 7

Plain English: ADHD is woefully underdiganosed and treated by every metric.

But wait!

There’s more!

That doesn’t include narcolepsy!

That’s right. While the Internet shitosphere was busy worrying about overdiagnosis, here’s what’s actually happening: fewer than 20% of adults with ADHD are diagnosed and treated. Out of the millions of U.S. adults who have ADHD, less than one in five gets help for it. That’s the opposite of overdiagnosed. That’s underdiagnosed.

There’s a reason for this underdiagnosis from one of the more fascinating aspects of the research on ADHD. Some research wondered if parents and teachers could identify ADHD traits in children and students. They also asked the students if they had problems with those traits. The parents and teachers correctly identified ADHD in populations, even aligning with the aforementioned population-level research on heritability. But, get this. The kids and students couldn’t identify these problems in their own lives.

That’s worth repeating. When parents or teachers rate ADHD symptoms in kids, the estimates are very high. But when teenagers or adults rate their own ADHD symptoms, the estimates drop significantly. This is because people are unanimously bad at estimating their own symptoms. 8

The consequences for this massive underdiagnosis in the U.S. extend beyond, “Sorry, I fucked up.” Studies show untreated ADHD can reduce life expectancy by more than eleven years when it continues into adulthood. Eleven long years. 9 People shouldn’t have to suffer with a condition that’s disbelieved by the general public while this abundance of science is out there just because it doesn’t conveniently fit society’s narratives, or politics, or both.

Science should be informing our narratives and politics, not vice versa.

Those eleven long years? That’s because untreated ADHD is strongly associated with increased rates of substance abuse, accidents, relationship problems, unemployment, and other very serious life challenges that hamper human health and flourishing. Women are particularly underdiagnosed because their symptoms often look different—less obvious hyperactivity, more internal restlessness and overwhelm. Masking their symptoms through sheer willpower (and subsequent burnout) is common.

So when someone tells you ADHD is overdiagnosed, you can confidently respond with: “Actually, the problem is severe underdiagnosis, with less than 20% of people with ADHD getting diagnosed and treated; and people are literally dying because of it.” Nothing like some morbid statistics to kill a dinner party conversation in a split second.

Now, let’s talk about good ole’ fashion drugs.

Here’s another jolly little fact: the supposed “risks” of overdiagnosis are largely theoretical, while the risks of underdiagnosis and undertreatment are well-documented and destructive. We’re talking impaired educational achievement, lost career opportunities, increased risk of incarceration, substance abuse, depression, anxiety, and reduced quality of life.

This brings us to big bad stimulants, the first line of treatment. Hands down, without a doubt, stimulants—particularly amphetamine and methylphenidate—are the best treatments. There are non-stimulant medications that can work well, but stimulants are the gold-standard. This is as inarguable as the genetics itself. But what about risks of heart attacks and stuff?

Well, here’s the good news. The common-knowledge cardiovascular risks of ADHD medications like amphetamine and methylphenidate have proved more folk tales than concrete science, especially in recent years.

In 2022, a massive meta-analysis of 19 studies and more than 3.9 million participants concluded that there was “no statistically significant association between ADHD medications and the risk of cardiovascular events among children and adolescents, young and middle-aged adults, or older adults.”

The logic about stimulants and heart problems seems to follow the same logic as folk tales. It’s like, “Stimulants raise heart rate and blood pressure, therefore, they must be bad for your heart.” But exercise raises both heart and blood pressure and that’s good for your heart, so this layperson logic won’t do.

While the 2022 meta-analysis should’ve put the question to bed, later, high-quality research similarly found no link between cardiovascular events and ADHD stimulants. 10 Another study from 2022 concluded:

Attention-deficit hyperactivity disorder treatment has been shown to decrease antisocial behavior, poor academic performance, and mortality but to date, many individuals with cardiovascular disease continue to be deprived of ADHD medications because of overly cautious approaches unsupported by the evidence-base.

In plain English, even if the science has disproven fears about negative health outcomes from stimulants, myths persist. A 2024 study found that ADHD diagnosis and medication actually reduces the risk of dying:

Among individuals diagnosed with ADHD, medication initiation was associated with significantly lower all-cause mortality, particularly for death due to unnatural causes.

Meanwhile, another 2025 study found that while these medications increase blood pressure and heart rate, the effects are “negligible” in the grand scheme of things. Like the myth that sugar consumption causes diabetes, something we believed for generations without really testing it (it doesn’t), we’ve long believed that stimulants cause cardiovascular problems in healthy people without really testing it.

Fun fact: the biggest (accidental) experiment with this I know of came during WWII. The Nazis gave literally their entire army methamphetamine and, out of tens of millions of troops, there were less than a handful of negative cardiovascular events and only one person died (while swimming in the sea). We’ve seen what happens when you give unteseted stimulants—with zero knowledge of the risks of the dangers—to whole populations who are put in the most stressful situations imaginable. If they were really extremely dangerous, you’d have expected troops on both sides of WWII to have been dropping like flies from stimulants.

So the risk-benefit analysis here isn’t even close. As I’ve suggested before, though unpopular, what the “What if we’re treating people who don’t really have it” crowd are worried about are people using (or abusing) mind-altering substances. For the record, only about 1.3% of stimulant users misuse their prescrptions, and misuse is a much lower bar to hit than addiction or abuse. Basically, anyone who’s prescribed two pills per day, but they take three one day, has misused their prescrption. That’s an extremely minor risk.

Considering 4.8% of the U.S. population is allergic to cow’s milk, cow’s milk represents a much larger health risk than addiction to prescription stimulants. You’re about three-times as likely to have problems with the ordinary milk found in refrigerators across America as you are ADHD meds.

ADHD is as real and as genetic as the nose on your face. With heritability comparable to height, replicated findings across countless studies, identified genetic variants like LPHN3, and devastating consequences of underdiagnosis, the science isn’t up for debate.

The next time someone suggests ADHD is overdiagnosed, made up, or just needs some social construct, feel free to share the facts. Better yet, ask them if they think height is also a social construct that can be cured with a better attitude. When they look at you like you’re ridiculous, you can explain that’s exactly how ridiculous they sound to anyone who understands the science.

For the millions of people struggling with undiagnosed ADHD, proper recognition and treatment can be life-changing. It’s long past time we let evidence guide our understanding instead of myths, stigma, and outdated ideas about what ADHD “looks like.” And for those of you reading this who suspect you might have ADHD? Talk to a qualified healthcare provider. You deserve support, not skepticism. Your brain isn’t broken—it’s just wired differently. And thankfully, we have treatments that actually work.

Now, this part is pure educated prediction, not robust science (yet), but, considering the direction of the science (and the activism around this, which has been more than helpful), I think we’ll see the merger of ADHD and Autism along one long neurodevelopmental spectrum in the coming years.

We’ll see.

Thanks for reading.