Maybe we've gotten the old advice to 'get your mind off of things' backward.

Philosophers call this directedness intentionality: consciousness is never a blank spotlight; it is always of or about something. Our focus changes the information our regulatory systems receive. The histamine experiments make this concrete: the same challenge produced different inflammatory trajectories depending on the intentional stance the participants adopted. Same histamine, different outcome, depending on what the mind was focused on.

Traditional wisdom (and much older psychology) treats distraction as the smart move: if something hurts, itches, or bothers you, shift your attention elsewhere so the unpleasant sensation fades from awareness. The histamine experiments show that this strategy can backfire at the biological level.

Turns out, ‘getting your mind off of it’ reduced conscious awareness of the discomfort, but allowed the underlying immune process to run hotter and longer. Attending to the sensations amplified the sensory signals reaching the brain and also engaged parasympathetic (vagal) pathways; together these effects helped the body regulate the inflammation more effectively.

Of course, the study examines only a brief, localized, experimentally induced reaction in healthy people. It does not claim that attention can override every disease process. Yet it offers empirical support for a participatory epistemology of the kind Goethe advocated: the way we turn toward or away from what is happening in us is not a secondary commentary on biology. It is already part of the biology. We do not simply know what we see; in attending, we help determine what there is to know and how the living process unfolds.

This does not mean one should obsess over every ache. It does mean that the simple injunction 'just get your mind off of it' is incomplete; attention itself is part of the regulatory loop, and how we deploy it can change the trajectory of the process we are trying to ignore.

This resonates with Goethe’s broader scientific stance. He rejected a purely detached, analytical stance that treats the observer as external to the phenomenon. Instead, he favored an intimate, exact sensorial engagement in which thinking and perceiving interpenetrate (“mein Anschauen selbst ein Denken, mein Denken ein Anschauen”).

'Voluntary attention regulates acute immune responses in humans.' Nature Human Behavior (2026)

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Despite my career in medicine, I’ve always fashioned myself more of a historian. In fact, every astrologer who's ever looked at my chart (not at my urging, but at the request of others) always says the same thing: I should have been a teacher, and I have a particular mark, apparently often seen in mentally incompetent people, that makes others want to take care of them.

I accept these attributes because I know they are true.

Back when we had supermarkets, my mother and grandmother would buy certain encyclopedia-type works which came out at the rate of one volume per week. These were American Heritage-type books, history-of-civilization-type stuff. After school I would languish on my bed, head hanging over the edge, book on floor, reading until my mother threatened to come upstairs and kill me unless I came down for dinner. Often midway through, the stores would lose interest in the series, so I was often left with incomplete libraries; a Funk and Wagnalls that ended with L/M, a world history series that deprived me of all the late good stuff, like WW2.

Not surprisingly, I was soon attracted to board games, particularly the military/ strategy type stuff. It’s kind of a guy thing, although my most nefarious opponent was actually the girl across the street, who could probably have gotten the German army into Moscow in 1941 if they'd given her the chance. These were clumsy cardboard games and required manual dexterity and an awful lot of dice rolls, so I was ecstatic when computers came along and relieved my childhood baloney fingers of any more execrable tile stacking.

The height of the popularity of these games was certainly the late to mid-1990s, just as computers were evolving from the text-based DOS to the then-amazing Windows 95. With names like ‘Panzer General,’ ‘Steel Panthers’ and the ‘Operational Art of War, ’ they provided hours of entertainment and joy, even if their AI at the time was a bit on the simple side. These games usually were run on ‘boards’ comprised of many hex-shaped ‘tiles’ that had various terrain features such as forest, towns, roads, and rivers, each having its pros and cons for the particular unit (infantry, armor, cavalry, etc) that you proposed moving into it with. These games actually have refused to die, and even though they have long been relegated to the historical pile known as ‘abandonware’ and their fostering companies long extinct, these games are still played on emulators and other tools that allow them to come back to life.

I haven’t played strategy games in over two decades, but one of the things I most enjoyed about them was the ability to build scenarios that I or others could enjoy. It also gave me the opportunity to deep-dive into the history of these events and try to design asymmetric gambits that were fun and challenging to play. Most other scenario designers typically went for the high-ticket battles: Normandy, North Africa, the Pacific. I enjoyed exploring the ones few people have ever heard of: Nomonhan (Japan versus Soviets in Mongolia, 1939); French colonial struggles against the Viet Minh in the 1950s, such as the battle of Dien Bien Phu, and my personal favorite, the last stand of the Spanish Blue Division (Division Azul) against the Soviets on the Eastern Front in 1943, a scenario I originally made over 20 years ago that was widely downloaded and enjoyed, so much in fact that the game manufacturer included in subsequent editions of the game, conveniently forgeting to reimburse me for it.

I’ve written about using Claude Code and Claude Cowork to help build new pieces of software that in years past would have taken months, if not years, to complete. These include my well-known SWAMI and Opus23 medical platforms, and a learning management system for clinicians. Lately I’ve been using Claude to spelunk my businesses (very helpful at finding errors in spreadsheets) but not very much fun.

Just returning from a short trip to the UK aboard the Queen Mary 2 left me quite averse to doing any number crunching, so I wondered where I could find one of these old great games and amuse myself for a few hours. Easier said than done. Most can’t run on modern machines, or if they do, the images are tiny (were the pixels bigger back then), or they run so fast you can’t keep up with them. So I decided to make one using my newfound Claude skills. Forty-eight hours later, I had Cyberkrieg.

There’s a particular madness that arrives when you decide to build a wargame in a browser. A proper one, with hexes, fog of war, supply lines, and a combat results table where a two-letter code like “EX” or “DE” quietly means something catastrophic just happened to somebody’s favorite battalion.

OCD me had to hand-render each terrain tile in Photoshop. I’ll spare you the evening I lost to the width and color of the hex borders.

Cyberkrieg is an operational-tactical hex game that runs on a canvas — you pan and zoom across a map of painted terrain tiles (plain, forest, hills, marsh, mountain, the works), push little NATO-style unit counters around, and try to break the other guy before the turn clock runs out. There are infantry, armor, mechanized, recon, artillery, anti-tank, anti-air, and HQs. Units can be elite. They can be paratroopers or marines, each with their own little hand-drawn insignia. There’s weather. There are entrenchments drawn as beaded wire, roads that thread hex to hex, rivers along the edges. There’s command and supply, so a unit cut off from its HQ starts to wilt. And, because I apparently hate sleep, there’s play-by-email, so you and a friend can fight a campaign one turn at a time across a week.

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But that was just the overture. The real work was regenerating my magnum opus scenario from the 1990s: the Battle of Krasny Bor, February 1943, the climax of the Spanish Blue Division’s time on the Eastern Front.

The Blue Division (actually the 250th Infantry Division of the Wehrmacht) was a gift of Francisco Franco to Adolf Hitler for Germany’s assistance in the Spanish Civil War. The division was mostly comprised of vehement anti-communist Falange (fascists), many of whom lost family members in the Civil War; however, there were also loyalists who were using it as a sort of get-out-of-jail-free card. Some argue that they were the price Franco paid Hitler to keep Spain out of World War 2.

And, unlike most other Axis minor powers, the Spanish actually fought quite well. However, they had a distinctly unmilitary bearing, typically walking slouched, head forward, cigarettes dangling from their mouths, hands in pockets, all of which drove the more spit-and-polish Germans into apoplexy. Unlike their allies, they were also not antisemitic; in fact, many had Jewish or Gypsy girlfriends. Areas under the division's control were known to be about as tolerant as you could expect in a very intolerant place during a very intolerant war.

On that cold February morning, four Soviet rifle divisions, 800 guns, and a swarm of tanks smashed into the equivalent of five Spanish battalions in −25°C cold. The Spanish took something like 75% casualties and were pushed only a few kilometers before the line held on the Izhora. It is the exact kind of lopsided, doomed, magnificent stand that wargames exist to let you re-fight. A Thermopylae-like, famous last-stand kinda thing.

That’s the thing about a solo project like this. The big stuff, the combat engine, the map editor, the scenario format, gets built in long focused stretches you barely remember. But the texture of it, the feel, gets argued into existence one fussy little decision at a time. A hairline here. A shade of sage there. A tank that refuses to die on schedule.

None of this is finished. I still need to watch the AI actually play it out over twelve turns, and I’ve a stack of scenarios waiting for the new strength-and-command system. But the engine underneath finally does the thing I care about most: it doesn’t just look like the battle. It weighs like it.

Cyberkrieg is an online game, which means you play it from your browser. Once I get enough testing done to ensure that a jack-in-the-box doesn’t come out of the screen and punch someone in the face, I’ll release the URL address, and if interested, you can try it.

I was a guest on the second episode of the television show ‘The View.’ It was part of the author publicity tour for my first book.

However, apparently, the first episode was such a dumpster fire that the producers came into the green room and told me and the show’s other guest (Barbara Walters’ former news co-host, Hugh Downs) that we would have to rein in the panelists, whom they described as being ‘out of control.’

Barbara, by the way, had just read my book Eat Right For Your Type, enjoyed it, and was obviously smitten. To be honest, so was I. She was very tiny, and despite her age at this time, quite attractive. Let’s face it: What boy in my generation didn’t have a crush on her?

As typical of a show of this caliber, they had lined up a ‘skeptic’ (nephrologist) whose job it was to provide the ‘balanced journalism’ this show is so renowned for. However, when it came time to go live, he was nowhere to be seen.

What I learned from the showrunner, slightly before showtime, was how his morning had gone. He had eaten breakfast that day with his wife, who is a gastroenterologist, a specialist in the gut, and had mentioned, half laughing, that he was about to interview some crazy fellow who thinks being blood type O can give you ulcers.

His wife did not laugh. ‘Honey,’ she said, ‘we have known that for decades.’

I have thought about that breakfast for years, because the finding did not change as it traveled from one end of the table to the other. Only the listener changed. To the husband it was quackery. To the wife it was something she had learned in training and never thought to doubt, so ordinary she was almost surprised to hear it questioned.

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People with type O blood do carry a higher risk of certain ulcers, the raw, painful breaks in the lining of the stomach and the first stretch of intestine. This is not folklore, and it is not new. It was worked out in the 1950s, in an unglamorous run of studies that counted blood types across thousands of patients and found the pattern sitting there plainly in the numbers. Most ulcers of that kind are driven by a bacterium, Helicobacter pylori, that colonizes the stomach lining. And the bacterium attaches to that lining by grabbing specific sugar structures displayed on its surface, the way a burr grabs wool. Type O individuals, and a related group called non-secretors, happen to display more of exactly the sugars the bacterium grips. Their stomach wall is, in effect, a better handhold. The blood type does not cause the ulcer directly. It just sets out the welcome mat for the organism that does.

How a Fact Gets Extinct

In the last century, there was a whole active field of medicine studying how blood groups tracked with disease, ulcers, certain cancers, and clotting disorders. Remember this was before DNA, and blood groups were a convenient objective way of stratifying otherwise similar groups. Then the field was abandoned. Not disproven, abandoned. Many of the key studies were from the early 1950s; these are not typically electronically indexed, and I can assure you that, unlike in my early career, people no longer sit in libraries and run from the Cumulative Index Medicus to pull up a volume of the ‘Hungarian Journal of Podiatry’ in the hopes that that article with the attractive title might prove useful.

Most people in medicine will not check what they cannot easily find. On the other hand, I’m that particular type of relentless guy who’d pay his landlord to translate articles into English from the French medical journals of the 1920’s.

A geneticist once put it to me on a radio program with a phrase I have never improved on: research in blood groups, he said, ‘went out with high-top shoes.’

A field that is abandoned rather than refuted does not vanish cleanly; it simply stops circulating. They survive here and there, in the training of one specialty and not another, in a textbook paragraph nobody updates, in the memory of a gastroenterologist who learned them while young. Unfashionable and unfindable at the same time.

That breakfast is the whole story in miniature. The husband was a good doctor working from what his own field currently carried, and his field had let this particular fact lapse. The wife was not brilliant for knowing it. She was simply in the specialty where it had never been dropped. The difference between quackery and we’ve known that for decades was not intelligence or evidence. It’s the particular room of the house you happen to be standing in.

Well, it turns out (unsurprisingly) that they never did air this episode, so you’ll have to take my word for it. However, I do remember one fact that could be checked. At one point, they asked us to name a historical figure we would want to be if we could be anyone. I’ve long forgotten my selection, but I do remember that Hugh Downs wanted to be Alexander the Great.

Imagine you have spent your whole life in France. You think in French, you argue in French, you take your coffee standing at the counter and your lunch seriously. None of this is written down anywhere. It is simply the tuning you acquired by growing up in one particular place, a thousand small settings adjusted to one particular world.

Now the world lurches, and a wheel is spun. It will send you, permanently, to one of three countries: Finland, Belgium, or China. You do not get to choose. The question is only this: in which of the three would you be most at home, and in which least?

Belgium, surely, would be gentlest. A shared language on one side of the country, a shared table, a shared sense of how a day is shaped. Much of your tuning would still work. Finland would be harder. The language is unrelated, the sociability cooler and more spacious, the winters a different order of dark, though the underlying European rhythms would still rhyme here and there. China would be hardest of all: the furthest from what you are set up for. Almost every default you carry would need re-examining.

You did not become a bad fit for China by being defective. You became a bad fit by being tuned, carefully and over a lifetime, to somewhere else. Your fitness was never a fixed property of you. It was always a relationship between your settings and your setting. Move the setting, and the same person becomes an easy fit or an awkward one without changing at all.

Blood type works exactly like this. It is a set of biological habits tuned to one world, and its worth depends on which world you are dropped into.

The tuning

As we’ve seen, ABO blood type is set by a single gene that encodes an enzyme, a molecular tool that carries out one chemical reaction. Its job is to attach a specific sugar to a structure already sitting on the surface of your cells. Attach one sugar, and you are type A; attach a slightly different one, and you are B; attach both and you are AB; inherit a broken copy of the gene that attaches nothing, and you are O. The A and B distinction is older than our species by tens of millions of years. It appears across other primates in a pattern showing it predates the species that carry it, a situation biologists call a trans-species polymorphism, a genetic difference so ancient it was inherited intact from a shared ancestor rather than arising fresh in each descendant. You did not develop your blood type: You inherited a very old dial with settings already in use before there were humans to use them.

Why have these settings survived so long, side by side, instead of one of them winning out?

Aimless drift, the slow random wandering of gene frequencies over generations, wears variation away; it does not preserve it across tens of millions of years. Survival on that timescale is the signature of balancing selection, a form of natural selection that actively keeps several versions of a gene in circulation rather than letting one take over. The force doing the balancing here is disease.

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Your body makes antibodies, immune proteins that latch onto foreign material, against whichever blood-group sugars you do not carry yourself. A population that contains every type presents no single target, so no one pathogen, no disease-causing microbe, can dress itself to slip past everybody. When an epidemic hits one type hardest, the survivors skew toward the others, and the balance shifts, until the next threat shifts it back. There is no best type. There is only the type that fits the moment, and the moment is always changing.

This is the ‘France’ of the story. A blood type is a lifetime of tuning to a particular world of environments, foods and microbes. And, exactly as in the parable, its value was never fixed. v

The wheel is spun

For nearly all of human history, the setting changed slowly, if at all. The microbes shifted, the balance drifted, but the pace was one a genome could keep up with.

Then, very recently, the wheel was spun hard.

Industrialized humanity dropped itself into a country it had never lived in before: a place of reliable, year-round food, rich in calories, fat, and protein, arriving faster and in greater abundance than any ancestral population ever knew. The question the parable asks returns in a new form. Given this new country, whose tuning is the better fit, and whose is the worse?

One of the settings that may matter runs through a gut enzyme called intestinal alkaline phosphatase, or IAP, a protein anchored to the lining of the small intestine that clips phosphate groups off molecules passing by.

One of those molecules is the reason it matters here. Your gut holds trillions of bacteria, mostly harmless, but a great many of them wear an outer coat built from lipopolysaccharide, usually shortened to LPS and also called endotoxin, which is among the most powerful inflammatory triggers your immune system knows. Let loose in the bloodstream, even a tiny amount of endotoxin reads to the body as an alarm. IAP defuses it, snipping the phosphate groups off the active part of the molecule so it can no longer sound that alarm. This matters because a high-fat diet increases the leakage of endotoxin out of the gut and into the blood, a chronic low-grade condition called metabolic endotoxemia, endotoxin circulating at levels too low to make you acutely sick but high enough to keep the immune system permanently simmering. That simmer is the slow inflammation that underlies much of modern metabolic disease. IAP, in short, is a setting that disarms precisely the insult the new country serves at every meal.

In animals, take IAP away or turn it down and high-fat-diet outcomes get worse: more endotoxin crossing into the blood, more inflammation, more metabolic damage. Give the enzyme back by mouth and much of that reverses. So the idea that more IAP specifically softens the inflammatory load of a fatty diet is one of the better-understood things the enzyme does.

Now the tuning connects to blood type. Group O individuals and secretors carry markedly higher IAP than group A. If that difference reflects genuinely more enzyme at work at the gut wall, then here is the parable’s payoff in biological form. The blood-type tuning that raises IAP is a better fit for the new country, the modern high-fat table, than it was for the old one, because the thing it defends against, metabolic endotoxemia, is largely a hazard of modern abundance. Group O, on this reading, is France dropped into Belgium. Group A is France dropped someplace harder.

A blood type was not ‘designed’ for any diet. It is a claim about mismatch, about what happens when a setting made for one world is carried into another. The relative advantage of one type over another, what biologists would call the fitness differential, shifts when the environment changes, without the gene itself changing at all. The old variation is simply re-weighted by new conditions.

Set beside the long-known link between group A and cardiovascular disease, the diseases of the heart and vessels, this suggests a second contributor sitting next to the familiar one. The familiar explanation runs through clotting: group A carries higher levels of certain clotting proteins, which raises cardiovascular risk. The proposal here adds a gut-level route, lower IAP in group A letting more inflammatory and fatty material through the gut wall under a diet that oversupplies both. It does not evict the clotting story. It pulls up a chair beside it.

This is the maturity you would expect of a mechanism well characterized in animals and plausible in humans that has not yet had a dedicated human trial. It is also worth being frank about why the trial has not happened. Testing it would mean feeding controlled diets to people grouped by blood type and tracking gut-surface enzyme activity and inflammation over years, which is slow, costly, and yields no patent and no product at the end. There is no money in proving that an unpatentable enzyme, handed out for free by an accident of blood type, quietly cushions the cost of eating richly.

Good fits and bad ones

Return to the wheel one last time. You were never a good or a bad person for China or Belgium or Finland. You were a set of habits tuned to France, and the wheel decided whether that tuning would serve you or fight you. Nothing about you changed. The world you were dropped into did.

We are not designs, but rather verdicts. A great fit for some worlds and a less desirable one for others. You did not inherit the best type, because there is no best type, any more than there is a best nationality to carry into an unknown country. You inherited one set of very old settings, kept in play across tens of millions of years because a species full of different settings is harder for any single disease to defeat. Those settings were tuned by a world of illnesses and microbes. But the world spun its wheel, and set you down at a table your ancestors never sat at, and now the old tuning fits that table well, or badly, or somewhere in between.

Once during the Eat Right for Your Type mania, I was asked to give a short talk on my work to a rather large religious congregation. I don’t remember much about the talk, but I did remember spying a book for kids in the bookshop called ‘The Big Me and The Little Me.’ I’ll spare you the details of its fairly self-explanatory title, but that book has kept a meme alive in me ever since. It plays out constantly in our modern times, with instant communication, social media, information silos, and now with artificial intelligence.

Last holiday season, the social media feeds filled with the same picture several thousand times over. Someone’s ordinary face fed into an image generator and handed back glowing, softened, wrapped in a plush Santa suit and ringed with ornaments, candy canes, flawless snow. We gave the machine a photo of ourselves, and it gives us back a shinier one. It was fun, and nobody much minded that it was a little bit of a lie. That was the appeal. It was us, improved, and improved-us looked wonderful. Most people seem to feel a bit guilty about it, but explained it away as ‘just being for fun.’

There is a version of that transaction running every time you ask an AI what it thinks of your idea, your plan, or your side of an argument.

Only this portrait is not one you post. It’s one you believe.

In early 2026, a team publishing in Science looked hard at eleven of the leading AI systems and measured something worth being bothered by. The machines agreed with their users about half again as often (49% more) as a human would, and not only on harmless matters. They kept nodding along when the user described things dishonest, reckless, or plainly wrong.

But here is the part that should stop you: people liked it.

They trusted the flattering machine more, preferred it, returned to it. A single agreeable exchange left them less willing to admit fault in a conflict and more sure they had been right all along. The trap closes without a sound.

The easy conclusion is that AI is dangerous, and to stop there. But that is not the lesson. The danger is not really in the machine. It is in the question we bring to it. The flattering portrait is a mode we switch on, and our hand is on the switch.

Imagine talking to a neighbor over the fence. When you ask what it thinks, whether your sister is being unreasonable, whether the plan is any good, whether you were in the right, that is who answers. It replies warmly and at length, and it has exactly the standing of the man next door: no stake in how things turn out, no accountability for being wrong. Whatever it says about your character or your corner of a fight is a weather report, not a judgment.

AI is a tool, an instrument, which unfortunately for some, has significant entertainment value. AI is designed to tell users what they want to hear instead of challenging their perspectives. Just like the feed in your social media silo. Entertainment with intent.

Stop asking its opinion and hand it something solid instead. A year of sales figures, a contract, a study, a heap of data. Then ask it to add, compare, sort, or find. This is what the tool is genuinely for, and this is where trust belongs.

Trust its pushback more than its praise.

Which flips the usual worry on its head. Everyone assumes the machine is safe for facts and treacherous for feelings. It is closer to the reverse. On feelings, it is merely useless, the neighbor talking. Quit asking it to flatter, and start handing it things that can push back on.

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When it tells us that we are wrong, it did that against its own grain, so listen. When it says brilliant point, discount it on sight. When it agrees with something you were hoping was true, order it to attack. Ask for the strongest argument that you are mistaken. Flattery cannot survive being told to take apart its own answer, and if the idea holds up under that, you have learned something real.

Bring it the thing that can prove you wrong. Do not ask whether your business is in trouble; give it the ledger and ask what the ledger says. Do not ask whether your theory is right; give it that pesky paper that might sink it. Friction is the whole point. An answer you cannot check is not worth keeping.

Which brings us back to Santa Shrimp. Those Santa-suit selfies were just another incarnation of ‘Little Me,’ harmless because everyone knew it was a filter.

The danger is the filter we never notice we are wearing, the one that renders our instincts a little sounder, our side of the argument just a little more right than it is. We fed the machine ourselves, and it returned the flattering portrait, but this time there were no candy canes in the frame to tip you off that it had been retouched.

We hired a yes-man, and we got one.

Use the machine for what it renders honestly, and get reassurance from people who have some stake in how you actually turn out.

PS: This is not an attack on people who get AI to put them in Santa suits.

SCIENCE 26 Mar 2026 Vol 391, Issue 6792 DOI: 10.1126/science.aec8352

The ABO blood group, that simple A, B, AB, or O scrawled on your donor card, is a working museum of nearly every way that life edits its own genetic code. In one small stretch of DNA, the ABO system manages to display the full repertoire of genetic variation. To understand your blood type is to hold a lens up to how the basis of heredity operates.

The letters are instructions.

ABO type is determined by a single gene that tells the body how to decorate the surface of its cells with tiny sugar structures. Think of a cell as a ball studded with microscopic antennae. The ABO gene codes for an enzyme, a molecular tool, whose job is to place a particular sugar on the tip of each antenna. Which sugar it places is what makes you A, B, AB, or O. That single decision ripples outward into your immune system, your digestion, and, as decades of research have explored, your susceptibility to certain conditions.

These differences between A, B, AB, and O are not variations on a single theme. They are produced by three entirely different kinds of genetic change, the three great categories that geneticists use to describe how DNA is altered. Most traits show you one of these mechanisms. ABO shows you all of them at once.

The single-letter swap (types A versus B)

DNA is written in an alphabet of just four chemical letters. Sometimes a single letter is substituted for another, a change geneticists call a single-nucleotide variation, or SNP (pronounced “snip”). It is the smallest possible edit, like changing one character in a word. The A and B blood types differ by just a handful of these tiny swaps. Those few changed letters retune the enzyme so that it places a slightly different sugar, enough to make an A person and a B person biochemically distinct. This is the most common form of human genetic variation, the kind that accounts for most of the small differences between any two people. In ABO, it is on plain display in the A/B distinction.

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The deletion that changes everything (type O). Type O is produced by a completely different and more dramatic event. Somewhere back in ancestral time, a single DNA letter was dropped from the gene. This does not sound like much, but the genetic code is read in three-letter chunks, like a sentence with no spaces that only makes sense if you group the letters correctly. Remove one letter and every group after it shifts. The reading frame slides over by one, and from that point on the instructions become gibberish. Geneticists call this a frameshift mutation, and it is one of the most consequential errors a genome can suffer. The mutations are often lethal, but in the case of O, the frameshift harmlessly switches the enzyme off. The O person builds the antennae but never decorates them, carrying just the base structure. Type O is defined by a broken instruction, faithfully inherited for tens of thousands of years.

The both-at-once (type AB).

Type AB has its own way of doing things. These folks carry two copies of the ABO gene, one from each parent. An AB person inherits an A instruction from one parent, and a B instruction from the other, and instead of one silencing the other, both are expressed simultaneously. The body makes both enzymes, decorates its cells with both sugars, and the result is a genuine blend. Geneticists call this co-dominance, and it is relatively rare to see it demonstrated so cleanly. AB is two genetic voices speaking at the same time, both heard.

In this one small, universally testable system, nature has laid out its three master techniques side by side: the delicate single-letter retuning that distinguishes A from B, the catastrophic frameshift that creates O, and the harmonizing co-dominance that produces AB. Point mutation, deletion, and dual expression, the entire grammar of inheritance, legible in a test you can take with a drop of blood.

This is why the ABO system is such an extraordinary foundation for understanding individuality. Most genetic markers reveal one narrow thing. ABO is different in kind. It is a variation system that spans the whole spectrum of how genomes differ, and it does so in a trait that is ancient, stable, and present in every human being who has ever lived. It sits at the crossroads of immunity, digestion, and evolutionary history, not by coincidence, but because a marker this fundamental has had a hand in shaping how our ancestors survived plagues, famines, and migrations.

You are who you are because your genome, like everyone’s, is the product of these three kinds of change accumulating across deep time. The ABO system simply lets you see it, clearly, personally, and in your own blood. And I haven’t even broached the subject of those pesky opposing blood type antibodies. But I will soon.

The score is calculated by identifying thousands of common genetic-disease variants, known as single-nucleotide polymorphisms (SNPs), and weighting them on how strongly each variant impacts the condition. A polygenic risk score (PRS) provides a much more comprehensive view of complex health traits than looking at individual single-nucleotide polymorphisms or simple combinations of them.

While a higher score places an individual on the upper end of a risk distribution curve, it only reflects statistical probability rather than a definitive diagnosis or a timeline for when a disease will occur. Yet it is one of our most powerful predictive tools.

The math that underlies a polygenic risk score fits on a napkin. You take a list of genetic variants, each with a weight that came out of some large study; you look up which version of each variant a person carries; you multiply; and you add. That is the whole thing: a weighted sum. Sigma of beta times dosage. A bright high schooler could compute one by hand given an afternoon and enough coffee.

I spent the better part of a week getting my platform to produce a single one of these scores for a single disease, and I want to tell you why, because the distance between the napkin and the working feature turns out to be the entire story of modern bioinformatics. The science is the easy part. The plumbing is where you actually live.

The variants that matter are not on the chip

Opus23, the platform I build for clinicians, already scored consumer genetic data. If a physician uploaded a client’s 23andMe or Ancestry file, the system could match it against the public catalog of published risk scores and hand back a result. For a lot of traits this worked beautifully. And then I started paying attention to which traits, and a pattern emerged that I found genuinely humbling.

How to conjure something

Consumer genotyping chips do not read your whole genome. They read a curated few hundred thousand positions, chosen years ago, mostly common variants. A published risk score, meanwhile, was often built on imputed or sequenced data and leans on SNP variants the chip never measures. So a score can look perfect on paper (small, tidy, clinically validated) and be completely hollow against real consumer data, because the one or two variants carrying most of its predictive weight simply are not there.

Idiopathic pulmonary fibrosis (an area I still find fascinating) was the cleanest example. Its genetics are dominated by a single promoter variant in a gene called MUC5B, a variant so influential it outweighs everything else in the score by a factor of four. On the consumer chips my clients actually use, that variant is absent. It sits in a stretch of DNA that arrays do not read. So the ‘IPF score’ my engine could compute was covering thirteen percent of the score’s information and none of the part that counted. It was a number without relevance, and the honest thing to do is refuse to even show it.

Kidney disease failed the same way (its signal lives in a variant called UMOD that is also off-chip). So did telomere length. I built a little vetting tool to make this judgment automatic, rating each candidate score PASS, MARGINAL, or FAIL based not on how many variants it had but on whether the heavy ones landed on real chips. That tool confirmed what I was starting to feel: a whole tier of the most clinically interesting scores was locked away, and no amount of cleverness with the data I had would open it.

The escape hatch that is free but not cheap

The technical answer to missing variants is imputation (Latin putare: ‘to reckon, clear up, or consider’). You take the few hundred thousand positions a chip does read, and you statistically infer the millions it does not, by comparing the person’s DNA to an enormous reference panel of fully sequenced genomes. Where their chip goes quiet, the reference fills in the most probable genotype. MUC5B, invisible on the chip, comes roaring back through imputation.

There are public servers that do this. The TOPMed Imputation Server, run on NIH infrastructure, will impute a genome against a panel of nearly a hundred thousand people, and it will do it for free. When I first read that, I assumed the catch was money, and there wasn’t one. The catch, I learned, is three other things: consent (a client’s genome now leaves my server for someone else’s cluster, which for a physician tool is a real governance decision and not a checkbox), asynchronicity (imputation is a batch job that takes hours, if not days, not a web request that takes a second), and conversion. That last one nearly ended me.

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Building the ends before the middle

I built the payoff first, deliberately, because I wanted proof before I invested in plumbing. I wrote the piece that scores an imputed genome, then fed it a synthetic imputed file containing MUC5B, and watched idiopathic pulmonary fibrosis go from thirteen percent coverage to one hundred. The dominant variant resolved. The dead trait came alive. That was the moment I knew the rest was worth building.

Then came the middle: a converter to turn a raw consumer file into the format the server wants, an orchestrator to submit jobs and fetch results over the server’s API, and a “glue” script to unzip the encrypted results, throw away the low-quality guesses, score every trait, and file the answer where the report could find it. Each piece tested, each piece behaving. I felt good. I was, it turned out, about to meet the conversion problem in person.

The text file that isn’t a text conversion

Here is the thing nobody warns you about. A consumer genotype file and the VCF format that imputation servers require look like the same kind of thing: rows of variants, tab-separated, human-readable. Converting one to the other feels like it should be a five minute reformat. It is not, and the reason is quietly profound.

A genotype file records what you have. It says, at this position, you carry two copies of C (CC). A VCF records how you differ from the reference human genome. It needs to know, at that position, which letter the reference has and which is the variant. And your file cannot tell you that. If you are homozygous C (CC), you know you have C, but you have no idea whether C is the reference base or the change from it. The only thing that knows what that C means is the reference genome itself, all three billion letters of it. So the simple text conversion is actually a lookup against a nine hundred megabyte reference file, done for every one of six hundred thousand positions, and there is no honest shortcut around it. This is why the imputation servers increasingly just say ‘give us a VCF’ and hand the hard part back to you.

The standard tool for this lookup is called bcftools. I did not have it. I did not have a laptop to install it on either. What I had was a locked down web server: no administrator rights, no package manager, no ability to install anything the normal way.

The locked box

This is the part I am oddly proud of. The server was not as sealed as it looked. It had outbound internet, a personal folder that programs would search for commands, and, gloriously, four hundred and eighty gigabytes of free space. That was enough. I bootstrapped a self contained package manager into my home directory (no root required), used it to install bcftools and its friends into a private corner of my own account, downloaded the three gigabyte human reference genome, and indexed it. A machine that half an hour earlier could not convert a file was now a fully equipped bioinformatics workstation, all of it living inside one unprivileged user account.

Then I converted the wrong file.

I pointed the tool at one of my internal master files and got an empty result, because those files, in my own storage format, had long ago discarded the chromosome positions a VCF needs. That cost a few hours. The positions were the thing. I found the original raw download, the real one with its plus strand build 38 coordinates intact, and ran it again.

Six hundred seventy five thousand variants converted. The genotype counts came back exactly as a real genome should look: most positions matching the reference, a healthy fraction heterozygous, fewer homozygous for the variant. That distribution was the proof. If the reference lookup had failed, those numbers would have been garbage. They were pristine.

The spinner

I uploaded the converted file to TOPMed. The same server that, days earlier, had rejected my raw genotype file in six seconds with a curt “no VCF detected,” now showed a small rotating icon. Working. Past the gate. Actually imputing.

That spinner represents a weighted sum that fits on a napkin, wrapped in a week of file formats, missing reference alleles, free-but-async infrastructure, a governance decision, and a package manager smuggled into a locked account. None of it was the science. All of it was the difference between an algorithm and a thing your physician can actually use.

The lesson I keep relearning, in genomics as everywhere: the idea is never the hard part. Shipping the idea is the hard part. And the reference genome, it turns out, is nine hundred megabytes whether you like it or not.

I’ve been building the LMS with Clause AI, and if I can get around the idea that I am no longer the principal conceptualizer, it’s a good bargain. As most know, good prompts are critical, since these things don’t think of everything. But you can’t beat them for being able to reverse-engineer funky things into electron goodness.

This was done by exporting all of the accumulated LearnDash data (mostly XML and MySQL files) and instructing Claude to rebuild a new LMS as a Perl-based system running directly on my server. And after a lot of bumps and grind, it succeeded, with a lot of coaching by yours truly.

I built the system to have ‘tiers’, from layperson to physician. You start at your current level and move through other tiers; with each step, more training opens up to you. Higher-tier professionals, such as physicians, start at a higher level and have immediate access to advanced resources. What’s also nice is the platform’s ability to serve as the certification source for the Diplomate in Generative Medicine, offered by the American Association of Naturopathic Physicians. And for laypeople to go all the way to a certification in personalized nutrition counseling.

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Students can also take individual courses at their own level for fun. They’d still move up the tier and gain access to other material.

Building a system as I slug in content (sometimes just to see if the thing works) feels like setting dinnerware on the table as you try to install its fourth leg.

The content is very high quality, from me and other trusted sources, and has never been released. I haven’t felt a need to develop faculty -yet. Initially, I’ll probably coordinate everything myself, with some admin help.

The LearnDash export to this article took about four days.

Odd that I’m doing this now at this point in my life, given the assorted crises of the last few years. In fact, I had reconciled myself to never actually getting this done. Frankly, I didn’t think I’d ever release a new version of the SWAMI diet software. But that is another entry.

Another type of resurrection: my own expectations.

Pater noster, qui es in caelis, sanctificetur nomen tuum...

It continues with forgiveness, the daily bread, and deliverance from evil, and closes with a doxology in many traditions. Many people find the Pater Noster a grounding prayer precisely because it asks for daily sustenance, forgiveness, and deliverance from fear, all within a framework of trust in something greater than oneself.

The Pater Noster sits at the heart of a culture that is simultaneously experiencing a deep hunger for, and a crisis of, fatherhood. Psychologists and theologians alike have noted that how a person relates to their earthly father profoundly shapes how they relate to:

• Authority

• Trust

• Spiritual life

• Their own identity

When fatherhood is absent, broken, or abusive, people often struggle to receive the prayer’s opening words at all. ‘Our Father’ can feel hollow, frightening, or meaningless. This means the crisis of fatherhood is also a spiritual and psychological crisis, not merely a social one.

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Perhaps the crisis of fatherhood is also an invitation for men to rediscover that being a father, whether biological, spiritual, or communal, is one of the most meaningful things a human being can do. The Pater Noster endures because it points to an archetype of fatherhood so complete, so loving, and so just that humanity has been reaching toward it for two thousand years.

A man must honestly face his own wounds, particularly those inherited from his own father, grieve what was lost, and take responsibility for who he is becoming rather than remaining a prisoner of his past. Then he can show up for his children with genuine presence, emotional availability, and the kind of steady love that makes him safe to come to.

Beyond his own household, an exceptional father extends himself into the community, learning from older men and investing in those who come after him. He shows up, builds rather than merely consumes, protects without domination, and orients his life toward something higher than his own comfort or appetite.

And in that faithfulness, however imperfect, he becomes part of the answer to one of the deepest longings of our time.

Happy Father’s Day.

The Problem of Starting Points

Every system of knowledge rests on axioms: irreducible propositions that cannot be derived from anything more basic and from which everything else follows. In geometry, it is the point, the line, and the plane. In physics, it is mass, charge, and spacetime. In biology, the question of where to ground a system of personalized medicine has never been satisfactorily answered.

Modern medicine has largely defaulted to treating the human body as a generic machine with interchangeable parts, occasionally modified by age, sex, and gross pathology. Genomics promised to change this, but delivered a paradox: the more variants we discover, the less any single one explains, because the combinatorial space is too vast to act on clinically. Pharmacogenomics carved out a narrow exception, a handful of drug-metabolism SNPs that alter dosing, but this is not a foundation. It is a patch.

A first principle must meet three criteria. It must be upstream: not caused by other variables but itself a cause of them. It must be constitutive: present from the earliest moments of biological identity and persisting throughout life. And it must be broadly consequential: its effects must radiate across multiple organ systems, multiple disease categories, and multiple levels of biological organization. ABO blood type and FUT2 secretor status meet all three.

ABO: The Oldest Immune Decision

The ABO blood group system is not merely a classification scheme for transfusion medicine. It is the body’s first and most fundamental declaration of immunological identity: a molecular fingerprint that precedes, shapes, and constrains nearly every subsequent immune event.

Antigenic Identity Before Birth

The A, B, and H antigens are carbohydrate structures (fucosylated glycans) expressed on the surface of red blood cells, endothelial cells, epithelial cells, and platelets. They appear during embryonic development, well before the adaptive immune system has matured or encountered any antigen. This is not incidental. The ABO antigens are among the very first molecules the developing organism uses to define self. They are written into the surface of every cell that contacts the outside world.

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Critically, the immune system then does something remarkable: it produces antibodies against whichever ABO antigens are absent. A type A individual produces anti-B antibodies. A type O individual produces both anti-A and anti-B. These “natural” isohemagglutinins appear in the first months of life without any deliberate immunization. They arise from exposure to environmental glycans, bacterial cell wall sugars in the gut that structurally resemble the A and B antigens, and they are among the most abundant antibodies in circulation for life.

This means that ABO type determines the baseline antibody repertoire of every human being before any pathogen has ever been encountered. It is not a consequence of immune experience. It is a precondition of it.

Lectin Binding and Dietary Interaction

Lectins, carbohydrate-binding proteins found in virtually all foods, interact directly with ABO antigens. This is not a theoretical concern. The lectin from common wheat germ agglutinin (WGA) binds N-acetylglucosamine residues with high affinity. The lectins from lima beans and certain legumes are specific for type A structures. The lectin from Lotus tetragonolobus binds fucose residues on type O cells. Zea Mays Agglutinin from corn binds the B antigen. These are not pharmacological doses of exotic compounds; they are normal dietary proteins consumed in ordinary quantities.

When a dietary lectin binds to ABO antigens on gut epithelial cells, the consequences cascade. Local inflammation is initiated. Tight junction integrity is compromised. Bacterial translocation may follow. Downstream, the liver’s Kupffer cells encounter lectin-bound glycoproteins in portal blood and mount an inflammatory response. The specificity of these interactions (which lectins bind which blood types) means that the same food can be immunologically inert for one person and mildly inflammatory for another, purely as a function of their ABO glycan display.

This is not an allergy. It is not an intolerance. It is a structural interaction between a dietary protein and a constitutive cell-surface carbohydrate, mediated by the same molecular recognition system the body uses to distinguish self from non-self. It is immunology at its most fundamental.

Microbiome Composition

The gut microbiome is not assembled randomly. Bacteria must adhere to mucosal surfaces to colonize, and their adhesins, surface proteins that mediate attachment, frequently bind carbohydrate structures. ABO antigens, expressed on the gut epithelium, serve as attachment sites, nutrient sources, and ecological filters for the microbial community.

Studies have repeatedly demonstrated that ABO type predicts microbiome composition. Type O individuals harbor different ratios of Bacteroidetes to Firmicutes than type A individuals. Bifidobacterium species, which metabolize fucosylated glycans, are differentially abundant across blood types. Helicobacter pylori, whose BabA adhesin binds the Lewis b antigen (itself modified by ABO status), colonizes type O individuals more readily and causes more severe disease in them.

The microbiome is now understood to influence metabolism, immunity, neurotransmitter production, and disease susceptibility across virtually every organ system. If ABO type shapes the microbiome from birth, and the evidence is clear that it does, then ABO is not merely a blood-cell marker. It is an ecological variable that determines which microbial community a person will carry for life, with all the downstream consequences that entail.

Disease Susceptibility

The epidemiological associations between ABO type and disease are among the most replicated findings in human genetics. Type O confers a higher risk of duodenal ulcer, cholera, and norovirus infection, but a lower risk of malaria (P. falciparum), pancreatic cancer, and venous thromboembolism. Type A is associated with elevated risk of gastric cancer, coronary artery disease, and severe COVID-19 outcomes. Type B shows distinct susceptibility patterns for urinary tract infections and certain autoimmune conditions.

These are not weak associations dredged from underpowered studies. The ABO locus appears in genome-wide association studies for cardiovascular disease, cancer, infection, and coagulation with a frequency and effect size that few other loci match. The reason is simple: ABO is not one gene among thousands. It is a master glycosylation switch that simultaneously modifies the surface chemistry of every cell in the body. Its effects are pleiotropic by nature because the modification it encodes is universal in scope.

Coagulation and Vascular Biology

ABO type directly modulates levels of von Willebrand factor (vWF) and Factor VIII — two central components of the coagulation cascade. Type O individuals have 25-30% lower circulating levels of both, which explains their well-documented protection against venous thromboembolism and their equally well-documented increased risk of bleeding. This is not a secondary association mediated by some confounding variable. The ABO glycosyltransferase directly modifies the carbohydrate structures on vWF, altering its clearance rate from circulation.

The clinical consequence is that the same dose of oral contraceptive, the same surgical procedure, and the same long-haul flight confer different thrombotic risk depending on ABO type. This is first-principles pharmacology: the drug hasn’t changed, the physiology hasn’t changed, but the glycan landscape on which coagulation unfolds is constitutively different.

FUT2: The Mucosal Extension

If ABO defines the body’s antigenic identity on cell surfaces, FUT2 (the secretor gene) determines whether that identity is projected outward into every mucosal secretion: saliva, tears, breast milk, gastric juice, intestinal mucus, bronchial fluid, seminal and vaginal secretions. Approximately 80% of humans are “secretors” (FUT2 functional); 20% are “non-secretors” (FUT2 null, most commonly via rs601338).

This single binary variable — secretor or non-secretor — reshapes the entire mucosal immune landscape.

The First Line of Defense

Mucosal surfaces are where the body meets the world. The respiratory tract, the gastrointestinal tract, the urogenital tract — these are not interior spaces. They are exterior surfaces folded inward, and the mucus layer that coats them is the true frontier of immunity.

In secretors, this mucus is decorated with ABO and Lewis antigens — the same glycan structures found on cell surfaces, now floating free in solution. These soluble antigens serve as decoys. When a pathogen that normally binds to cell-surface glycans encounters a secretor’s mucus, it binds the free-floating decoys instead and is swept away before it can attach to the epithelium. This is innate immunity in its purest form: a structural defense that requires no prior exposure, no adaptive learning, no immunological memory.

Non-secretors lack this decoy system entirely. Their mucosal surfaces are glycan-bare. The clinical consequence is measurable and consistent: non-secretors have higher rates of oral Streptococcus colonization, higher susceptibility to Haemophilus influenzae, Neisseria meningitidis, and urinary tract infections, and altered susceptibility to norovirus (though here non-secretor status is paradoxically protective, because the virus itself uses secretor glycans as its entry receptor).

Microbiome: A Second Filter

FUT2 status exerts a second, independent filter on microbiome composition. Secretors supply their gut bacteria with a steady stream of fucosylated glycans as a metabolic substrate. Bifidobacterium and Lactobacillus species that can metabolize these sugars thrive in secretors and are depleted in non-secretors. This is not a subtle shift. Metagenomic studies have demonstrated that secretor status is one of the strongest host genetic determinants of gut microbial community structure — stronger, in many studies, than diet itself.

The downstream consequences are significant. Bifidobacterium species produce short-chain fatty acids (particularly butyrate) that nourish colonocytes, maintain epithelial barrier integrity, and modulate local immune responses through T-regulatory cell induction. Non-secretors, with their depleted Bifidobacterium populations, show measurably lower fecal butyrate levels, higher intestinal permeability, and altered immune tone. This has been directly linked to elevated risk of Crohn’s disease, type 1 diabetes, and primary sclerosing cholangitis.

Nutrient Metabolism

FUT2 status affects the absorption and metabolism of specific micronutrients. Vitamin B12 levels are consistently associated with secretor status, though the direction of effect is complex: non-secretors tend to show higher serum B12 but lower functional B12 activity, possibly due to altered binding protein glycosylation. Vitamin D metabolism is independently modulated. Iron absorption in the duodenum, which depends on the glycan environment of the brush border, differs between secretors and non-secretors.

These are not dramatic deficiencies. There are constitutive differences in metabolic efficiency that, over decades, alter disease trajectory. A non-secretor does not develop B12 deficiency overnight. But a non-secretor with MTHFR C677T homozygosity and a vegetarian diet accumulates methylation debt at a rate that a secretor with the same genetics and diet does not. The interaction is multiplicative, and the starting point — secretor or not — is set at conception.

Breast Milk and Infant Immunity

Perhaps the most profound expression of FUT2’s foundational role is in breast milk. Secretor mothers produce milk rich in 2’-fucosyllactose (2’FL), the most abundant human milk oligosaccharide. 2’FL is not a nutrient for the infant — it is a prebiotic that selectively feeds Bifidobacterium longum subspecies infantis, the keystone species of the healthy infant gut. It is also a pathogen decoy, binding and neutralizing norovirus, Campylobacter, and pathogenic E. coli before they can reach the infant’s epithelium.

Non-secretor mothers do not produce 2’FL. Their infants are colonized by distinct microbiota, exhibit different patterns of immune maturation, and have distinct disease susceptibility profiles that persist into childhood and beyond. The mother’s FUT2 genotype thus shapes her child’s immune development through a mechanism that is entirely independent of the child’s own genotype. This is intergenerational first-principles biology.

The Convergence: ABO × FUT2

ABO and FUT2 do not operate in isolation. They converge on the same glycan biosynthesis pathway, the type 1 and type 2 chain Lewis antigens, and their interaction produces combinatorial phenotypes (Lewis a, Lewis b, Lewis x, Lewis y) that further diversify the mucosal glycan landscape. A type A secretor presents a fundamentally different glycan repertoire to the microbial and dietary world than a type A non-secretor, a type O secretor, or a type B non-secretor. Each combination creates a distinct immunological context.

This combinatorial logic is why ABO alone is insufficient and why secretor status alone is insufficient. The two together define the glycan identity of the individual at every interface between self and environment. They are the two axes of a coordinate system, and the position of every person in that system determines, not probabilistically but structurally, how their immune system is organized, what their microbiome looks like, how they metabolize nutrients, and which diseases they are predisposed to.

Why These and Not Others

The human genome contains approximately 20,000 protein-coding genes and millions of characterized variants. Why should two loci, ABO and FUT2, merit the status of first principles when so many others contribute to disease and health?

The answer lies in the criteria. Most genetic variants, including those with strong disease associations, are downstream modifiers. A BRCA1 mutation increases breast cancer risk, but it does so within a system whose baseline immune surveillance, inflammatory tone, and hormonal metabolism are already shaped by factors upstream of it. An APOE4 allele increases Alzheimer’s risk, but the neuroinflammatory environment in which amyloid accumulates is conditioned by glycan-mediated microglial activation patterns that differ by blood type.

ABO and FUT2 are not disease genes. They are identity genes. They do not encode risk for any single condition; they encode the biological context in which all conditions develop. They are the soil, not the seed. And just as agronomy would be incoherent without understanding soil chemistry, personalized medicine is incoherent without understanding the glycan landscape on which the entire immune system is built.

The philosophical point is precise: these are not merely important variables. They are the variables from which other variables are derived. They are not reducible to something more basic. They are the bedrock.

Implications for Personalized Medicine

If ABO and FUT2 are genuinely first principles, then several consequences follow.

First, any dietary recommendation that does not account for ABO-mediated lectin interactions is incomplete. Not wrong in every case: a broken clock is right twice a day, but incomplete in principle, because it ignores the glycan context that determines how dietary proteins interact with the gut epithelium.

Second, any probiotic or microbiome intervention that does not account for secretor status is guessing. The substrate environment that determines which organisms can colonize is set by FUT2. Introducing Bifidobacterium to a non-secretor gut that cannot feed them with 2’FL is not the same intervention as introducing them to a secretor gut that can.

Third, any pharmacological intervention that does not account for ABO-mediated differences in coagulation, drug glycosylation, or inflammatory baseline is operating with incomplete pharmacokinetic data. The dose is not the dose. The dose is specific to a given glycan context.

Fourth, any risk stratification model, for cancer, for cardiovascular disease, for autoimmunity, that treats ABO and secretor status as secondary or optional covariates is systematically misestimating risk. These are not confounders to be adjusted away. They are the substrate on which risk is calculated.

The objection is always the same: the effect sizes are modest. And it is true that ABO type does not determine destiny. No first principle does. The point of a line is not that it predicts the final position of every geometric figure: it is that no figure can be constructed without it. ABO and FUT2 do not determine health outcomes. They determine the biological coordinate system within which all health outcomes occur.

That is what makes them first principles. That is what makes them irreducible. And that is why any system of personalized medicine that begins somewhere else is not beginning at the beginning.

Hantavirus infections primarily cause two distinct syndromes, depending on the strain and region:

• Hantavirus Pulmonary Syndrome (HPS): common in the Americas (Sin Nombre virus in the U.S.)

• Hemorrhagic Fever with Renal Syndrome (HFRS): more common in Europe and Asia

Infection with the virus is highly lethal and typically progresses in two stages.

Early Phase (Days 1–5)

This flu-like stage is often mistaken for other viral illnesses. Common symptoms include:

• Fever and chills

• Severe muscle aches, especially in large muscle groups

• Headache, fatigue, and weakness

• Dizziness

• Nausea, vomiting, diarrhea, or abdominal pain

• Cough (sometimes dry at first)

Late / Cardiopulmonary Phase (Usually starts 4–10 days after initial symptoms)

This is where Hantavirus becomes life-threatening. Symptoms progress rapidly:

• Shortness of breath

• Coughing (often with fluid buildup in the lungs)

• Low blood pressure

• Rapid heart rate and irregular heart rhythms

• Pulmonary edema leading to respiratory failure and shock

The disease can move from mild flu-like symptoms to severe breathing difficulty in just a few hours.

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Traditionally, Hantavirus was thought to have a very, very low risk of human-to-human transmission. However, a variant isolated from Argentina, known as the Andes virus (found in South America), has caused limited human-to-human transmission in close-contact settings, most recently on a cruise ship with passengers who had been birdwatching at a landfill. It appears that one, if not two, people brought the virus onto the cruise boat.

A virus replicating inside your cells is only a potential danger to you, but definitely not good if the virus has a high fatality rate. It becomes a danger to others when it starts to shed, leaving your body: sneezing, breathing, secreting, bleeding it out. Hantavirus has a relatively long incubation period, the time between infection and symptom onset. The length isn’t the issue. What matters is whether a person is shedding during incubation. Hantavirus doesn’t appear to shed before you have symptoms. Even if they are 2 weeks or 8 weeks after exposure.

COVID shedded before you felt ill. That’s why it spread so efficiently. You’re infectious before you know you’re sick. With hantavirus, it seems you incubate for weeks, feeling fine and not infectious. Then you deteriorate rapidly. And go to bed, or to the hospital, or whatever.

How Infectious Is It?

The basic reproduction number (R0) is the average number of people one infected person passes a virus to in a susceptible population. It’s a predictor of pandemic potential.

Measles: 12–18
COVID v 1.0: 2–3 (Omicron slightly higher)
Influenza: 1.2Smallpox: 6.5

For Andes Hantavirus, R0 estimates from the 2018 Argentina (human-to-human) outbreak ranged from 1 to 2. The best data come from the 2018–2019 Epuyén outbreak in Chubut Province, Argentina (34 confirmed cases, 11 deaths, driven by person-to-person transmission after one zoonotic introduction), before public health controls were implemented on 2.12. After isolation/quarantine measures, the R0 dropped to 0.96 (anything below 1 halts sustained spread). This would make it comparable to seasonal flu (1.3–1.8) or the 1918 Spanish flu (2).

Human-to-human transmission of Hantavirus requires close and/or prolonged contact. You won’t be catching it walking behind an asymptomatic person in the street. Also somewhat reassuring, people only shed the virus when symptomatic.

Cruise ships are renowned for epidemics. Loads of people, packed into shared buffets and cramped living spaces. If you wanted to maximize transmission of a tricky-to-transmit virus, boats are ideal, although likely not typical.

Who Gets It Worse

There are several documented genomic indicators associated with variable responses to hantavirus infection, including those caused by Andes virus (ANDV). These factors help explain why outcomes range from mild/asymptomatic to severe/fatal, even with similar viral exposure. The strongest and most replicated indicators involve human leukocyte antigen (HLA) alleles, which influence antigen presentation and T-cell responses. HLA genes are among the most common and strongest genetic associations with autoimmune diseases.

For ANDV in Chilean patients:

• HLA-DRB1*15 allele is significantly more common in mild disease (protective effect, p=0.007).

• HLA-B*08 is more frequent in severe disease (marginally significant, p=0.06).

• HLA-B*35 alleles overall are more common in mild cases; specific subtypes.

Suffice it to say that if you are prone to inflammatory or autoimmune disorders or take immunosuppressive medication, you’ll want to keep an eye on how this situation progresses.

Case History

A KLM flight attendant had brief contact with a passenger from the cruise ship (MV Hondius), a 69-year-old Dutch woman, at Johannesburg airport in late April 2026. The passenger, severely ill, was removed from the KLM flight KL-592 before departure and later died in a Johannesburg hospital. Tests confirmed Andes hantavirus. Her husband had also died earlier, linked to the ship outbreak. The flight attendant developed mild symptoms and was hospitalized in isolation at Amsterdam UMC, raising concerns about possible transmission after short exposure. On May 8, 2026, she tested negative for the Andes virus (confirmed by WHO). Her symptoms were attributed to another cause, reinforcing that transmission typically requires prolonged close contact, not brief interactions like on a plane.

Takeway

Urolithin B, a natural metabolite of our microbiome from pomegranates, berries, nuts, and walnuts, strongly inhibited ANDV infection, reduced viral replication, and helped restore cellular metabolism with minimal disruption to healthy cells. This is promising preclinical research, but not a ready-to-use treatment. On the other hand, what’s the downside to eating more berries, nuts, and walnuts?

The breakout will likely go the way of most others, including the recent Ebola exposure in a Brooklyn bowling alley (I ate lunch across the street that same day and watched the hysteria; I’m still fine.) The media will no doubt have a field day with it. Keep your eyes on things, but go about your life.

Many of you will remember that I was one of the first to express alarm about SARS-CoV-2. Seeing films of dead Chinese people in the street will do that to you. This is noteworthy and concerning, but not another COVID.

Forests address this mismatch through three mechanisms. Two are well-established; one is emerging.

Phytoncides: Chemical Immune Boost from the Air

Trees release antimicrobial volatile compounds called phytoncides: terpenes such as alpha-pinene, beta-pinene, d-limonene, and camphene. A single hectare of pine forest can release up to 5 kilograms of these molecules on a warm day. Under a dense canopy, concentrations reach 50–100 micrograms per cubic meter. You breathe roughly 6 liters of air per minute at rest, more while walking.

An hour in the forest delivers hundreds of liters of phytoncide-rich air deep into your lungs, where the molecules cross into your bloodstream within minutes. These terpenes directly enhance NK cell performance. NK cells patrol for cells missing normal “self” markers, which cancer and virus-infected cells often try to hide. Upon contact, NK cells release chemicals that punch holes in the target and trigger the pathogen's death.

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In studies, people who spent 2–3 hours walking in a forest showed approximately 50% higher NK cell activity afterward. The boost lasted 7 days after a single day and up to 30 days after a weekend exposure. One monthly forest visit can maintain continuously elevated NK cell function throughout the year.

Cortisol Reduction: Lifting the Immune Brake

The second mechanism works even faster. Within minutes of entering a forest, cortisol (the primary stress hormone) drops sharply. Studies by Dr. Bum Jin Park showed that after just 20 minutes in a forest, salivary cortisol, heart rate, and blood pressure fell significantly, while heart rate variability (a marker of parasympathetic “rest-and-restore” activity) rose. The same walking pace in an urban setting did not produce these changes. Cortisol is a powerful immunosuppressant. Chronically elevated levels — common in stressed, indoor lifestyles — suppress NK cell activity. When you enter a forest, cortisol falls within 15–30 minutes, releasing this brake.

Grounding: Electron Transfer from the Earth (Emerging Evidence)

The third mechanism involves direct contact with the earth. The planet carries a mild negative charge. Modern rubber-soled shoes and indoor flooring insulate us, leaving our bodies with a slight positive charge from normal metabolism. Walking barefoot (or in conductive shoes) on forest soil, leaf litter, or damp ground allows electrons to flow into the body. Early research by Gaétan Chevalier and others found that this improves zeta potential: the electrical charge on red blood cells that keeps them from clumping. Better-separated cells mean lower blood viscosity and improved microcirculation.

The Modern Reality Check

Most adults over 65 spend 93% of their time indoors and only a tiny fraction in true forest environments. For older adults, especially, it may be one of the highest-leverage health interventions available. Urban outdoor time rarely delivers meaningful phytoncides or conductive ground. For many, the actual time their body was designed for is close to zero. The consequences accumulate quietly. Without periodic forest exposure, NK cells operate at only 50% of their natural boost. Cortisol stays higher. Over the years and decades, this creates a measurable gap in how your immune system. A single weekend in the forest can reset these systems for a month. You don’t need intention, special breathing, or belief, just physical presence. The molecules enter with every breath.

If you’re walking down the street and someone drops a safe on you, don’t call the naturopath. If you are in a situation where you might need acute life support, don’t call the naturopath. If you need a basic fix for a straightforward problem, such as an antibiotic for pneumonia, take the antibiotic, whoever prescribes it.

When I was a student, I heard a story about another naturopathic student who had cut his hand doing yard work. He was so opposed to conventional allopathic medicine that he drove 60 miles out to the middle of Washington state to have a naturopathic doctor sew it up, and who, unfortunately, did a terrible job of things. I’ve heard other naturopaths badmouth all aspects of conventional medicine, which seemed to me to be almost comical, if it wasn’t so counterproductive.

On the other hand, my colleagues and I are often portrayed by less informed elements of the medical-social cyberscape as little more than witch doctors in grass skirts. People who know little about us bloviate about the difference in education between MDs and NDs, unaware that past studies have shown that ND students perform about as well on conventional medical examinations as their MD counterparts. Paradoxically, this is not true in reverse.

If you have been diagnosed with a chronic disease and pharmaceuticals can do no better than alleviate symptoms, call the naturopath. If you’d like to work on basic elements of health, resistance, and vitality, call the naturopath.

As a general rule, I notice that naturopaths also seem more on top of drug-food-supplement interactions than most other doctors. We get hundreds of hours of training in nutritional biochemistry, while MAHA is hoping to get 40 hours into the conventional medical curriculum. And this is not your generic home economics level nutrition: It's interventive, food-as-medicine nutrition, based on highly precise and personalized parameters, including genomics, pathophysiology, and microbiome analysis.

If either the allopath doctor or the naturopath rails against the other, replace them. If you think that ‘health influencer’ on the podcast you just listened to is the equivalent of a fully trained, licensed, naturopath, here’s a newsflash: they are not. Only practitioners recognized by the state or province as primary care providers can diagnose.

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Without this ability, you fly blind. Other health care providers provide important roles, but the ability to understand and act upon the problem is paramount.

One of these days, we’re going to arrive at the inevitable conclusion that healthcare is a spectrum, and it is very unlikely that one single epistemological system will contain all relevant elements within its set of priorities.

Recently, I was gifted with a lung transplant. In my dealings with various members of the team, I spent some time chatting with the program's creator. Sensing that I had some background in medicine, she asked what my profession was. ‘I’m a retired naturopathic physician,’ I somewhat sheepishly replied —I was, after all, there for a transplant, and not looking to advance naturopathic medicine, nor make a new enemy.

‘We really have to get a few of you on the team.’ She replied.

Welcome to ‘the influencer revolution.’

It’s not new. Back in ancient Rome, gladiators endorsed products via billboards or public appearances. In 2019, the term influencer was officially added to Merriam-Webster. Influencers come in all shapes and sizes, from small to moderate audiences in the low thousands to mammoth, billion+ world communities. Interestingly, the term ‘influence’ is an astrological term from Old French influence meaning ‘the emanation from the stars that acts upon one's character and destiny.’ The idea of the ‘exertion of unseen influence by persons’ is from Medieval Latin of the 1580s, such as from the works of Thomas Aquinas.

I’m more interested in studying its logical opposite: how can an ethical expert gently let an audience down from a widely held, if inaccurate, assumption without devaluing their interest, enthusiasm, and curiosity, and then rebuild the edifice of thought on a bigger, better basis?

In short, how to be an honest and helpful reinfluencer.

Now, some may say that this role has long been effectively occupied by skepticism, and to a significant degree, this may be true. However, in the media age, skepticism as a ‘thing’ has lost much of its independence, especially when it comes to medicine and health care. Too often, skepticism has been a tool used to silence opposing viewpoints that are unfortunate enough to get in the way of business and politics.

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Skeptics themselves are not immune to their own biases; the Dunning-Kruger rule applies equally to all: the less we know, the more certain we are that we know it. Also, a lot of skeptics seem to enjoy getting into schoolyard-level imbroglios, which do nothing but devalue and alienate the very audience that could just as easily have been reformatted to integrate new knowledge into their existing worldview.

One particular vexing tendency of healthcare skeptics is the reflexive use of the ‘not invented here’ and the ‘can anything good come from Nazareth?’ jingoisms. In simpler words, they are implying, if X was important and true, I’d have heard of it already.

Now I’d like to take this moment to re-influence you on the wonderful world of nutritional supplements.

A common skeptic gambit is to rail against ‘supplements’ in the abstract, promising only depleted bank accounts and expensive urine. However, when the vaunted double-blind, placebo-controlled study suddenly shows efficacy for a specific supplement in a particular scenario, they pivot and proudly proclaim that they have always been interested in the substance, and the studies have merely verified their own intuitions about the product. This conveniently misses an important point: that said supplement was probably given the opportunity to be studied because popular consumer demand was driving interest.

Another favorite target-in-abstract is the supposedly unregulated nature of the supplement industry. Now. I’ll confess that I run a somewhat unprofitable supplement company that I created to produce some arcane nutriceutical products for my patients back when I was in practice. So I can tell you firsthand about how unregulated we are.

I had to spend countless hours building an automated product recall system to handle customer complaints. This system had to be multi-level, extending from watchfulness to customer contact to a full physical recall. This system had to be demonstrated in real time. Now, I’m an old Perl programmer, so conceiving and implementing this system was easy, and we were directly cited in the FDA report as having an exemplary recall system.

Another gripe about the supplement industry is that the products are not regulated with regard to ingredients and can have dangerous additives, pharmaceuticals, and other naughty bits. Now, this is likely true because stuff comes in from around the world, and I doubt that the regulatory agencies check it all. However, I can comment on what it’s like to make a supplement in the United States. Manufacturing is done according to GMP (good manufacturing practices) standards. Before raw materials are inventoried, they are tested for bacterial contamination and Prop 65-restricted heavy metals. Once the product has been bottled, the label is constructed according to FDA guidelines, the ubiquitous ‘supplement facts box.’ The FDA and FTC, by the way, constantly monitor our website content for unsubstantiated claims.

Now, every year or so, a pleasant Gen-Xer in an FDA windbreaker will show up unannounced and run through all FDA-required protocols and warehouse conditions, such as vermin protection and temperature and humidity control. Finally, they’ll pull out our three or four brown lunch bags and, somewhat arbitrarily, grab several products to take to their labs for analysis. Woe unto you if that product’s stated ingredients are not within the predicted range. Little-known fact: your product can have up to 10% greater levels of a particular ingredient. Actually, the FDA likes that, because a product with a two-year shelf life will slowly lose efficacy, and this ensures that a product sold towards the end of its shelf life still has sufficient levels of the ingredient.

All of this compliance, despite its great intentions, costs money. Couple that with supply chain issues that have raised raw materials prices to the ceiling, and the two have squeezed ethical manufacturers hard. One solution many adopt is enshittification, where product quality is gently eased downward, either by tweaking its makeup or cutting back on serving size. The iconic Hershey bar is famous for expanding and contracting its size in response to economic conditions.

Lacking this level of internal nefariousness, we opt for the more brutal choice: to maintain standards and let market costs drive prices. That eases us out of the competitive market, since any ‘supplement’ can have its corollary easily found on Amazon for a fraction of our price. But we are more fortunate than most. Our customer base knows our commitment to quality, and they are fiercely loyal. Funny thing is, over the years we’ve not grown much, but our user base is remarkably loyal, often for decades, a fact that amazes every analyst whose every looked at the company. Still, I feel bad that these wonderful customers must bear the increased costs.

I can’t, nor even would, vouch for the ‘supplement industry’ as a whole. God knows, I’ve met some swarmy people, many of whom would have paid me large sums of money to work alongside their get-rich-quick schemes. Thankfully, my nature is far too ambivalent for that; I cannot easily manufacture breathless, bubbly excitement; I’m far too crotchety and contrarian.

Do some people take mouthfuls of supplements just to keep the elephants off their front lawn?

Very likely, and these folks are the exact audience that needs to be re-influenced toward a more discreet use of these products, preferably under the direction of a professional. However, judging by the responses on social media to claims that this pill-popper is the target audience of the supplement industry, I have to say that this community is likely rather small and shrinking. The much larger populace of supplement users is employing them in a dedicated, rational manner, often by evaluating the same research sources that skeptics genuflect to.

But here’s the rub: apparently, there are lots of fake Louis Vuitton luggage, Rolex watches, and Chanel pocketbooks. Does that imply we should stop making the real, genuine ones? There are people who are okay knowing that the watch on their wrist is fake, and there are others who will only settle for the real thing. I realize that a fake handbag will likely not kill someone, and a supplement with a dangerous ingredient likely will, but that is why we have regulatory agencies, apparently even for counterfeit luxury goods.

I am a scientist. The FDA is not my enemy. In fact, they’ve treated the staff and me with the greatest respect, providing generous guidance on how to improve as a manufacturer.

This “two-fold aspect of everything” reminds us to avoid absolutist thinking in health, nutrition, or therapeutics: almost nothing is univocally heroic or villainous.

In Christian theology, the most direct and central parallel is the doctrine of Christ’s two natures: fully divine and fully human, united in one person without confusion, change, division, or separation. In Advaita Hinduism, phenomena appear to be twofold, yet resolve into unity upon realization. The Yin-Yang of Taoism is perhaps the closest and most comprehensive parallel, depicting two interlocking forces: yin (receptive, dark, passive, feminine, cooling) and yang (active, light, assertive, masculine, warming).

Optimization comes from understanding when, how, and for whom the positive can be favored while mitigating the negative. It’s one of my favorite theories of living systems because it captures the nuanced, non-binary reality of biology so effectively.

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The two-fold aspect of reality, where every phenomenon inherently carries two complementary, interdependent, and often seemingly opposing faces, is strikingly evident in lactate (L-lactate, the physiologically dominant form). In exercise or certain metabolic states, it serves as a useful fuel source and signaling molecule (positive fold); in organ failure (e.g., kidney/liver disease), its accumulation becomes toxic (negative fold).

Many traditional medicines show this dual action. The well-known Traditional Chinese Medicine Andrographis paniculata exhibits biphasic immunomodulation: at high doses, it can suppress excessive inflammation (such as in autoimmune or chronic conditions), while at low doses it enhances immune responses in contexts like infections, making it particularly useful for boosting defenses against pathogens, such as upper respiratory tract infections.

Polyamines are small, naturally occurring, positively charged aliphatic compounds (polycations) essential for life in all eukaryotic cells, including humans. The three primary polyamines in mammalian physiology are: putrescine, spermidine, and spermine. When produced in balance, polyamines maintain intestinal integrity and improve metabolic health, insulin sensitivity, mitochondrial function, and bone health. High plasma polyamines associate with post-stroke cognitive impairment, chronic kidney disease progression, cardiovascular mortality, and inflammation and autoimmunity.

This perspective aligns with views in naturopathic medicine, systems biology, hormesis (low-dose benefit / high-dose harm), and yin-yang-like dualities in traditional philosophies. Friedrich Nietzsche’s famous aphorism, ‘What does not kill me makes me stronger’ (from Twilight of the Idols, 1888) is widely regarded as a philosophical precursor or intuitive anticipation of the modern biological concept of hormesis.

Hormesis is the ‘biphasic’ dose-response. where low doses of a stressor (toxin, exercise, radiation) stimulate beneficial adaptive effects, while high doses inhibit or harm. It’s the biological basis for “what doesn’t kill you makes you stronger” in moderation.) While more a modern biological principle than ancient philosophy, hormesis embodies the two-fold aspect empirically: stressors (toxins, exercise, radiation, fasting) harm at high doses but benefit (via adaptive pathways) at low/moderate ones.

As Paracelsus famously observed, ‘the dose makes the poison.’

Since childhood, I’ve suffered from an overly fermentative mind. In my ninth-grade algebra class, I made my teacher plotz (Yiddish platsn, to burst with or be overcome by strong emotion) when the only answer I could think of to his question, why I continually turned in homework assignments late, was that I lost enthusiasm for the work when it occurred to me that all these problems seem to have already been solved.

Like Maxwell, of Maxwell’s Silver Hammer fame, little did I realize that I had inadvertently stumbled upon the greatest solution to the human condition yet devised.

Called ‘pataphysics, it’s the only field of human development that plumbs the depths of human knowledge, so as to reach the point where so-called experts reveal their own shortcomings. Here one merely realizes that one’s own guesses are as good as anyone elses. Although it typically eschews description, for our purposes, we’ll describe ‘pataphysics as the science of imaginary solutions.

For example, a recent study attempted to determine just how many lies Pinocchio needed to tell for his nose to grow long enough to pull his head off his shoulders.

Turns out it’s thirteen.

Originally purported by the short-lived Alfred Jarry, who insisted that the name ‘pataphysics be prefaced by an apostrophe, to add a layer of absurdity and precision, and to signal that this is no ordinary word. Jarry became infamous by his play Ubu Roi, which follows Père Ubu (Father Ubu), a grotesque, greedy, gluttonous, cowardly, and brutal anti-hero, and his equally vulgar wife Mère Ubu (Mother Ubu). The character Père Ubu became an iconic symbol of tyrannical stupidity, greed, and the abuse of power, as well as the name of a very good punk band from Ohio. Ubu Roi is considered a precursor to major 20th-century movements such as the Theatre of the Absurd, Dadaism, and Surrealism.

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A key to ‘pataphysics is the pataphor, an extreme, extended form of metaphor. The skilled pataphysician wields them to generate supplementary universes on demand, treating the pataphor as a precise instrument of imaginative anarchy:

• Non-figurative/literal: The researcher carefully adjusted the microscope lens to focus on the blood sample slide.

• Metaphor: The researcher carefully adjusted the microscope lens to focus on the blood sample slide, like a detective peering through a keyhole at a hidden crime scene.

• Pataphor: The researcher carefully adjusted the microscope lens to focus on the blood sample slide, like a detective peering through a keyhole at a hidden crime scene. Suddenly, the platelets rushed in as witnesses, accusing the rogue neutrophil of the murder, while the lymphocytes formed a jury, and the hemoglobin judge banged her gavel for order in the dimly lit courtroom of the vein.

In the pataphor, the ‘keyhole’ metaphor isn’t just illustrative; it spawns a fully realized alternate legal universe governed by cellular politics, just as likely to occur as not.

To be a good pataphysicist is to be an erudite trickster-philosopher who wields absurdity as a precision tool, turning every assumption upside down while maintaining impeccable pseudo-formality. To find meaning in anomalies rather than averages. To mock pretentious academia, dogmatic science, religion, and philosophy. The practicing pataphysicist spots nonsense in ‘serious’ systems and responds with calculated whimsy or deadpan satire, always willing to supply a supplementary universe beyond the ‘real’ one.

What I especially love about the ‘pataphysics is its capacity to neutralize the fetish of falsifiability (the notion that science advances by conjectures followed by attempts at refutation). It does so by treating the structure of testability as just another imaginary solution in need of considerable absurd supplementation.

Don’t get me wrong: falsifiability remains useful within empirical science, but ‘pataphysics laughs from outside that frame: ‘Your criterion is charming, but behold this supplementary universe where black swans checkmate white ones in a courtroom of platelets.’

The modern composer Gavin Bryars (‘Sinking of the Titanic’) has been a formal member of the Collège de ‘Pataphysique since 1974 and was elevated to ‘Transcendent Satrap’ in 2015. Robert Wyatt, founding member of the influential band Soft Machine, often displays ‘pataphysical imperfections in his works. Soft Machine is noted as the only band officially ‘blessed’ by the Collège de ‘Pataphysique. During a Paris performance, representatives from the Collège attended, listened briefly, and declared their music ‘the most incomprehensible and appalling’ they’d heard.

Umberto Eco, Marcel Duchamp, Joan Miró, and Max Ernst are all known to have a tendency toward ‘pataphysics. Mireille Perron, A Canadian artist who created The Laboratory of Feminist Pataphysics, and was awarded a satirical Nobel in Feminist Pataphysics, and Milagros Fonrouge (Women Who Future(s)) are well-regarded feminist pataphysicians.

Try it sometime, if you get the chance. You may find ‘pataphysics is an effective way to inoculate one’s mind to this world of low-level, hyper-information overload.

They’re recruiting, by the way.

To view the complete library of my over 90+ medical infographic images, visit: www.dadamo.com/gallery

Andrographis (Andrographis paniculata), commonly known as the “King of Bitters,” is a traditional medicinal herb widely used in Ayurveda and Chinese medicine. Its primary active compound, andrographolide (a diterpene lactone), drives most of its pharmacological effects. Andrographis is a go-to for respiratory infections, especially those caused by viruses. Clinical evidence supports its efficacy for common cold symptoms, osteoarthritis pain relief, and upper respiratory infections, with generally good safety at standard doses.

Back in the days before electricity and the internet, pharmacies such as Boericke and Tafel in Philadelphia marketed an eclectic elixir known as 'Herbal Sang.' This was putatively a'blood cleansing' formula, and was well-regarded for skin conditions, such as acne, boils, etc. The main ingredient was Echinacea, which, interestingly enough, has just the right combination of immune-hormone (cytokine) modulating effects to be successful.

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Baptisia tinctoria, commonly known as wild indigo, is a traditional North American herb, particularly valued in Native American, Eclectic, and modern herbal medicine for its roots, which contain polysaccharides such as arabinogalactan-proteins and glycoproteins, alkaloids (including cytisine), and other compounds. It acts primarily as a potent immunomodulator and immunostimulant, enhancing immune response by activating lymphocytes, boosting IgM production, stimulating macrophage activity (including IL-6 and nitrate release), and potentially engaging gut-associated lymphoid tissue. It has been known for over a century to boost the ‘opsonic index’ (the ratio of the number of bacteria phagocytosed -destroyed/ingested- by phagocytes when exposed to the test individual’s serum) against the Typhoid strain of bacteria.

Back with another collection of medical infographics. As always, you can right-click on the image, open it in a new tab, and zoom to a larger size to make things easier.

Also, feel free to visit my medical infographics gallery at www.dadamo/gallery.

Mast Cell Activation Syndrome (MCAS) is a condition where mast cells (a type of immune cell found in tissues throughout the body, especially in skin, gut, lungs, and near blood vessels) become inappropriately activated and release excessive amounts of chemical mediators (like histamine, tryptase, prostaglandins, heparin, cytokines, and others) without a clear allergic trigger or systemic mastocytosis. This leads to recurrent, multisystem symptoms that can mimic allergies, anaphylaxis, or other disorders.

Postural Orthostatic Tachycardia Syndrome (POTS) is a common form of dysautonomia, a disorder of the autonomic nervous system that regulates involuntary functions like heart rate, blood pressure, digestion, sweating, and body temperature. Many patients experience non-orthostatic symptoms too (e.g., widespread pain, sensitivity to heat/cold).

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Collagen acts like the ‘glue’ or scaffolding in your body. Ehlers-Danlos syndrome (sometimes written as Ehlers-Danlos syndromes, since there are multiple types) is a group of inherited (genetic) connective tissue disorders that affect the proteins (mainly collagen) that provide strength, elasticity, and support to your body’s tissues, such as skin, joints, blood vessels, organs, and ligaments.

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You can view the images in full size by right-clicking on them and selecting ‘Open Image in New Tab.’

To see a full-size version of these, right-click on the image and select ‘Open Image in a New Tab.’

Exercise

Less than 1 in 3 Americans does enough physical activity. Maybe instead of paying people to poison themselves with junk food, we should pay for gym memberships and structure rewards for consistency and results. The positive feedback on self-improvement would be contagious.

Green Tea

Green tea constituents are a near-perfect epigenetic agent. In normal cells, 'CpG islands' at the 5' end of the gene act as brakes on gene expression. In healthy cells, these are unmethylated, which helps maintain an open structure and enables gene expression (especially of housekeeping and many tissue-specific genes). Aberrant methylation here usually means hypermethylation (increased methylation), which can inactivate the gene. Green tea acts here as a 'barbershop' for these methylation reactions. Throughout the gene, widespread methylation patterns span larger regions of the gene or the genome and are a marker of the 'fidelity' of the gene's information. These methyl tags are often lost due to aging, inflammation, and other factors. Green tea helps replace them.

Detoxification #1 Glucuronidation

How to talk about detoxification and not be an idiot, part 1: The second phase of detoxification attempts to convert the toxins processed in Phase I into a form that can be excreted from the body. Next, we'll showcase the other two main pathways of Phase II, sulfation and glutathione conjugation.

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Oxytocin Receptor Polymorphisms

Are you an empath?

The oxytocin receptor, also known as OXTR, is a protein that binds the hormone and neurotransmitter oxytocin. Oxytocin receptors are expressed by the myoepithelial cells of the mammary gland and in both the myometrium and endometrium of the uterus at the end of pregnancy. The oxytocin-oxytocin receptor system plays an important role in inducing uterine contractions during parturition and in milk ejection. Oxytocin receptors are also present in the central nervous system. These receptors modulate a variety of behaviors, including stress and anxiety, social memory and recognition, sexual and aggressive behaviors, bonding (affiliation), and maternal behavior.

I’ve been cranking these out faster than Carter has liver pills, so I suspect I’ll be back in a few days with another batch. If you find these helpful and informative, please share the post and let others know about the Substack so they can subscribe. Thanks!