They Paved Paradise

“They paved paradise and put up a parking lot.”

That line has been rattling around in my head for years. I used to think it was about asphalt. I used to think it was a song about a woman looking at a lot where a garden used to be, shaking her head, feeling nostalgic. But the older I get, the less I think it’s about pavement at all. I think it’s about what we do to living things the moment we decide we’re in charge of them.

Here’s the pattern. We find something that’s working. It’s alive. It’s productive. But it’s messy. It’s got rough edges. It grows in directions we didn’t plan for and doesn’t fit neatly into the blueprint we had in our heads. So what do we do?

Hatchet.

Axe.

Saw.

We trim it.

We square it up, level it, true it, plumb it.

We optimize it.

We standardize it.

We give it a name that sounds responsible, like “managerial containment,” and we congratulate ourselves for bringing order to chaos.

Sometimes I wonder if we’re just really, really good at domesticating things until they stop being alive. Not killing them outright — that would be too obvious, too easy to notice. Just quietly trimming away whatever made them unpredictable, until what’s left is safe, symmetrical, and dead in every way that matters except the paperwork.

And maybe that’s why the word “progress” has started to bother me.

Everybody talks about progress like it’s automatically a good thing, like it’s self-justifying, like the mere fact of movement settles the question of whether the movement is wise. But progress just means movement. It doesn’t tell you anything about direction. Forward according to whom? Forward toward what? If you don’t know what direction the thing is actually supposed to be going, then “forward” is just a word people use to make themselves feel better about motion they haven’t examined.

I think that’s why I’ve stopped trying to think in straight lines. Nature doesn’t think in straight lines either. A wheel doesn’t move forward, not really — it turns. A tree doesn’t move forward — it grows, in every direction the light and water will allow, including down into the dark where nobody’s watching. A mycorrhizal network, that vast underground web of fungal threads that connects trees to each other and shares nutrients between species that would otherwise be strangers or even rivals — it doesn’t move forward either. It connects. It spreads. It shares. It has no destination, only relationship.

Maybe we’ve been using the wrong geometry this whole time. Maybe the right shape isn’t a road stretching toward a horizon. Maybe it’s closer to a wheel, turning in place but generating motion anyway. Or maybe it’s not even a wheel. Maybe it’s a vortex — a spiral where the center feeds everything else, where energy moves outward and comes back around, transformed, and nothing is ever really disconnected from anything else. That might be why I keep coming back to ecosystems as my mental model instead of assembly lines. An assembly line has a start and an end and a fixed number of stations in between. An ecosystem doesn’t have an end. It just has cycles.

Now, don’t get me wrong. I’m not romanticizing wilderness for its own sake, and I’m definitely not arguing for chaos. You can’t just let Mother Nature run wild once you’ve already started interfering with her. The minute we build roads, plant fields, dam rivers, breed crops, or start businesses, we’ve entered the system as active participants. We’ve taken on responsibilities that a purely wild system never had to answer for. We have to manage what we’ve changed, because we changed it, and pretending otherwise is its own kind of arrogance.

I get that. I actually believe that pretty strongly.

But accepting responsibility for the systems we’ve touched doesn’t mean everything has to become a parking lot. We can still leave places wild. We can still leave room for exploration inside the things we build. We can construct organizations — companies, teams, institutions — that have places where people are allowed to think like they’re feral, without the whole structure collapsing into anarchy.

That’s the question that won’t leave me alone: why do we act like “wild” and “built” are opposites? Who decided that? Why can’t a business be both organized and alive at the same time?

I want to be clear about something. I’m not anti-structure. I like organization. I like accounting, because numbers tell the truth even when people don’t want to hear it. I like manufacturing, because there’s something honest about turning raw material into something useful with your hands or your machines. I like governance, because somebody has to decide how disputes get settled before they turn into blood feuds. I like architecture, and economics, and the creative arts, and every other discipline that takes the formless and gives it a shape people can live inside.

I just don’t think architecture has to mean pouring concrete over everything that used to be alive. There’s a difference between building a foundation and paving over the topsoil.

The Octopus and the Elephant

A few weeks ago I made an image of an octopus riding on the back of an elephant. I didn’t make it because I had this whole essay figured out in advance. I made it because it felt right, in that half-conscious way that images sometimes arrive before the words that explain them. I just kept looking at it afterward, and the longer I looked, the more it started to unpack itself.

The elephant is the obvious one. She’s carrying everything. She remembers. She’s the roads that everybody forgot they were following, the paths worn smooth by generations of feet that knew, without needing to be told twice, where the water would be. She’s infrastructure in the truest sense — not concrete and rebar, but the accumulated, embodied memory that a whole herd depends on to survive a drought nobody living has ever seen before.

But here’s what finally hit me, staring at that picture: she’s also a library. And it’s not the kind of library where the knowledge sits on a shelf collecting dust until someone happens to check it out. When the matriarch knows where the water is during a drought, that knowledge isn’t written down anywhere. It’s not in a manual. It’s walking around inside her, encoded in decades of lived experience, and she doesn’t hand it over the week before she dies like some kind of deathbed briefing.

The daughters spend years beside her. Years. They’re not being trained in a classroom. They’re learning judgment by watching judgment get exercised, over and over, in situations that never repeat exactly the same way twice. They’re learning timing — when to move the herd, when to wait, when the situation looks dangerous but isn’t, and when it looks fine but isn’t. They’re learning what actually matters, as opposed to what merely looks urgent in the moment.

That’s succession. Real succession. Not a three-ring binder sitting on a shelf. Not a Zoom call where someone screen-shares a slide deck. Not somebody saying, “Here’s the SOP, good luck.” The daughters are literally walking beside wisdom, day after day, year after year, until it stops being something they were taught and becomes something they simply are.

Then I look at the octopus, and it’s a completely different game altogether.

The octopus has a brain in its head, sure, but most of its nervous system lives out in its arms — something like two-thirds of its neurons, spread across eight independently intelligent limbs. It’s almost like the thinking happens wherever the work is happening, rather than being routed back to some central command post for approval first.

It doesn’t just look at the world. It feels it. It tastes with its suckers. It changes color in a fraction of a second to match its mood or its surroundings. It changes texture, growing bumps and ridges to mimic coral or rock. It disappears when it needs to. It experiments constantly, trying things that have no obvious survival value except that trying things is, in itself, a survival strategy. It plays. It opens jars — that’s literally what people give captive octopuses to keep them from getting bored, because an under-stimulated octopus is a genuinely unhappy animal. It squeezes through gaps that should be physically impossible for a creature its size, because it has almost no rigid skeleton to get in the way of its curiosity.

It’s weird. Unbelievably weird. And somehow that weirdness is exactly why it survives. It isn’t carrying hundreds of years of accumulated memory the way the elephant is. It’s carrying possibility instead. It has no multi-generational archive to draw on, so it compensates by being radically, relentlessly responsive to whatever is true right now, in this exact moment, in this exact patch of reef.

The elephant wakes up asking, “What have we learned?”

The octopus wakes up asking, “What’s true today?”

Now tell me why in the world I’d want either one of them running the whole company by itself.

If all I’ve got is elephants, we’ll remember everything perfectly and eventually turn into a museum — beautifully preserved, meticulously cataloged, and completely incapable of noticing that the world outside the glass has moved on without us. If all I’ve got is octopuses, we’ll generate brilliant, dazzling ideas constantly and still end up with nothing to show for it, because nothing ever gets carried forward long enough to compound into something larger than the moment it was born in.

I don’t want one or the other. I want both, working together, each doing what it’s actually built to do.

I don’t want the octopus steering every step the elephant takes, second-guessing decades of earned trail knowledge because something shinier caught its eye. And I don’t want the elephant making every decision for the octopus either, smothering its improvisational genius under the weight of precedent. I want the elephant to walk the trail she’s spent a lifetime learning, with the confidence that only comes from having actually walked it before. And I want the octopus free-ranging around her, climbing over rocks, sticking an arm into holes nobody else thought to check, coming back again and again with information the elephant never could have found on her own, because she was never built to look there in the first place.

That feels healthier to me. It’s the same instinct behind free-range livestock versus animals raised in a box. Free-range chickens are healthier than chickens raised under fluorescent lights in a cage barely bigger than their bodies, and it’s not just about the meat quality or the ethics, though those matter too. It’s that free-range animals get to express the behaviors they actually evolved to express — scratching, foraging, moving, choosing. They’re participating in an ecosystem instead of merely existing inside a system that was designed around efficiency and nothing else.

I don’t think people are all that different. Put a person in a role with no room to explore, no room to be a little bit weird, no room to follow a hunch down a hallway nobody asked them to walk down, and you get the human equivalent of a chicken in a box. Technically alive. Technically productive. Not actually thriving.

Crystals, Tar Pits, and Living Networks

Then I started thinking about the crystal and the mycorrhizae, because people keep asking me which metaphor I like better, as if I’m supposed to pick a side.

I don’t think they’re competing metaphors at all. I think they’re describing the same underlying tension from two different angles. A crystal is beautiful. It’s precise. Every atom locks into place according to a repeating structure that doesn’t bend, doesn’t improvise, doesn’t grow toward the light. It’s stable specifically because it’s rigid. That rigidity is the whole point — it’s what makes a crystal a crystal instead of a puddle. There’s nothing wrong with that, in the right context. You want your load-bearing walls to behave like crystals. You do not want your culture to behave like one.

But then another thought hit me, and it stopped me for a second. Maybe the crystal isn’t really the opposite of the mycorrhizal network. Maybe the true opposite — the cautionary version — is the fossil. Or better yet, the tar pit.

Tar pits are fascinating precisely because of how deceptive they are. From a distance, a tar pit looks like a still, calm pool of water. Animals wander toward it because it looks inviting, looks like relief, looks exactly like the thing they need. And then it closes over them slowly enough that by the time they realize what’s happening, they’re already trapped. What comes out the other side, tens of thousands of years later, isn’t a living creature anymore. It’s a perfect record. An extraordinarily detailed, scientifically priceless, completely dead record.

That’s what happens to organizations that mistake preservation for life. They stop being systems that grow and start being systems that merely remember. Every process gets documented so thoroughly, every decision gets so heavily precedented, that eventually the organization isn’t actually doing anything anymore — it’s just very, very good at recording what it used to do. It’s a beautiful fossil. It is not a forest.

The mycorrhizal network is the opposite of the fossil, not the opposite of the crystal. It’s alive in a way that never stops moving, never stops redistributing resources to wherever they’re needed most, never stops connecting parts of the system that would otherwise have no reason to talk to each other. A tree that’s struggling gets nutrients routed to it from a healthier neighbor, through fungal threads too small to see, and nobody put that redistribution on a calendar. It just happens, because the system is alive enough to notice the need and alive enough to respond to it.

What This Has to Do With AI

The deeper question underneath all of this isn’t whether AI is going to replace humanity. That’s the headline version, the version that gets clicks, but I don’t think it’s actually the right question.

The right question is why we automatically assume that every new capability requires replacing the one that came before it. That’s the pattern I keep circling back to, over and over, in every domain I’ve mentioned so far.

Wildness becomes management.

Judgment becomes procedure.

Trust becomes transactions.

Participation becomes preservation.

Exploration becomes optimization.

Every single time, we take something alive and messy and responsive, and we quietly convert it into something safe and legible and dead. Not maliciously. Usually with the best of intentions. We just keep mistaking the trimmed, tidy version for progress, because it’s easier to measure, easier to defend in a meeting, easier to put on a slide.

Now we’re asking whether AI should replace people, and I think we’re about to make the exact same mistake we’ve made with everything else, just faster and at a much larger scale.

I don’t think evolution actually works by replacement most of the time. It works by layering. New capabilities get added on top of old ones far more often than old ones get discarded wholesale. We didn’t lose our reptilian brainstem when we developed a prefrontal cortex — we built on top of it. The new capability didn’t erase the old one; it gave the old one new company.

AI can be a prosthetic instead of a substitute, if we’re deliberate about building it that way. A prosthetic doesn’t replace the person wearing it. It extends what that person is already capable of doing, compensates for a specific gap, and leaves everything else about them intact. That’s a fundamentally different design goal than building something meant to stand in for a person entirely.

So the real design question, the one I actually care about, isn’t “how do we build something that replaces the elephant and the octopus?” It’s: how do we build systems that preserve life instead of replacing it? How do we add capability without extinguishing the living system that made that capability possible in the first place?

I don’t want AI to replace the elephant’s memory. I want it to help her remember more, and remember it more clearly, across more terrain than one matriarch could ever personally walk in a single lifetime. I don’t want it to replace the octopus’s curiosity either. I want it to help the octopus explore farther, reach into more holes, taste more of the reef, without losing the improvisational instinct that makes an octopus an octopus in the first place.

That’s a completely different relationship than simply handing over the reins and walking away. It’s not abdication. It’s partnership, with all the friction and negotiation that real partnership actually requires.

We’ve been paving paradise for a long time now, and calling it prog

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The Dark Berry

Lionberry 's Weekly Delusion and Re-illusion Update.

BS Weekly #13

The color is not a coincidence.

The dark, almost-black purple of elderberry is not just a visual marker of ripeness. It is a signal of bioactive density. The anthocyanin molecule responsible for that color… cyanidin-3-glucoside, or C3G… is pH-responsive, meaning its molecular structure physically shifts depending on the acidity of its environment [12]. In acidic conditions it appears red. At neutral pH it goes purple. In alkaline conditions it shifts toward blue and eventually breaks down entirely [12]. This is not a cosmetic property. It is a window into the molecule’s chemistry. The same pH sensitivity that makes the color shift is what makes C3G reactive inside your digestive system… and reactive in exactly the right way, because your stomach is acidic, and acid stabilizes the molecule right when it needs to survive [14].

What C3G Actually Is

Cyanidin-3-O-glucoside… abbreviated C3G… is an anthocyanin. Anthocyanins are water-soluble plant pigments in the flavonoid family responsible for the red, purple, and blue colors of dark berries. Elderberry is one of the densest sources of anthocyanins in the known food supply.

C3G is specifically a cyanidin molecule with a glucose molecule attached at the 3-position of its carbon ring. That structure matters for how it moves through your body and how it interacts with your gut. C3G is not a GLP-1 agonist. It does not bind to the GLP-1 receptor the way tirzepatide, Mounjaro, or Zepbound do. What it does is different and arguably more interesting… it stimulates your intestinal L cells to make more of your own GLP-1 from the inside [1]. The drug mimics the hormone from the outside. Elderberry… because it is food, because it is a berry, because it moves through your gut the way food does… triggers your body to produce the hormone itself. That is not a drug mechanism. That is food doing what food has always done. We just finally have the tools to watch it happen.

Research published in npj Science of Food confirmed that C3G treatment increased GLP-1 secretion in intestinal L cells via the PPARβ/δ… β-catenin… TCF-4 signaling pathway, which enhances the transcription of the proglucagon precursor that L cells use to synthesize GLP-1 [1]. C3G stimulates GLP-1 secretion from intestinal L cells via this pathway, thereby enhancing insulin secretion and improving glycemic control [1].

What the L Cell Is and What GLP-1 Does to Your Body

The L cell is a specialized enteroendocrine cell lining the wall of the intestine, concentrated in the ileum and colon. Its job is to sense what is coming through the gut… nutrients, fiber, certain plant compounds including C3G… and release hormonal signals in response [2]. GLP-1 is produced in intestinal L cells through posttranslational processing of the proglucagon gene and is released from the gut in response to nutrient ingestion [3].

Once C3G triggers the L cell and GLP-1 is secreted into circulation, it does multiple things simultaneously throughout the body that are directly relevant to blood sugar, metabolic health, and fat metabolism:

It tells the pancreas to release insulin in a glucose-dependent manner… meaning only when blood sugar is actually elevated, which is why it does not cause the hypoglycemic crashes that some diabetes medications do [3].

It blocks glucagon… the hormone that raises blood sugar… from being secreted by the pancreas, which further stabilizes blood glucose levels after meals [3].

It slows gastric emptying… food moves more slowly from the stomach into the small intestine… which flattens the blood sugar curve after eating, reduces postprandial glucose spikes, and extends the feeling of satiety [4].

It acts on GLP-1 receptors in the brainstem and hypothalamus to promote fullness and reduce appetite… GLP-1 has been shown to promote satiety and reduce both food and water intake [4].

It directly supports fat oxidation… the WSU clinical trial documented a 27% increase in fat oxidation at rest and during exercise in participants consuming elderberry juice for one week, consistent with the metabolic effects of increased endogenous GLP-1 activity [17].

The half-life of endogenous GLP-1 in circulation is approximately two minutes before it is degraded by the enzyme DPP-4 [4]. This is why pharmaceutical GLP-1 agonists are engineered to be DPP-4 resistant… they stay in the system far longer than your body’s own version. Elderberry does not extend the half-life. What it does is increase the rate of production… more signal from more L cells, more often, through food.

Is C3G Found More in American Elderberry

Both American elderberry (Sambucus canadensis) and European elderberry (Sambucus nigra) contain C3G. A USDA study comparing both species grown side by side found that both produce cyanidin-based anthocyanins as their dominant pigments, but with meaningfully different profiles [6]. In European elderberry, C3G makes up roughly 40 to 50% of total anthocyanins. In American elderberry, the dominant anthocyanins are acylated forms… meaning the cyanidin molecule has an additional organic acid group attached… making up approximately 65 to 70% of total anthocyanins, with C3G present but not dominant [15].

What matters for the L cell is not which species has the highest percentage of C3G on paper. What matters is how much active cyanidin-based compound arrives at the L cell intact after surviving processing, storage, and the journey through your gut. Acylated anthocyanins from American elderberry were more stable than cyanidin 3-sambubioside from European elderberry, with acylation improving both heat and light stability [6]. American elderberry’s acylated forms survive the journey better… and they break down in the gut into the same cyanidin-based compounds that stimulate L cell GLP-1 production [1].

Total anthocyanin content in American elderberry cultivars ranges from 85 to 385 mg per 100 grams depending on cultivar and growing conditions [7]. That nearly fourfold range is not a minor variation. It is the difference between a berry that moves the needle on L cell stimulation and one that does not. The Wyldewood and Bob Gordon cultivars are among the highest-anthocyanin American elderberry cultivars documented in the literature [16].

How C3G Gets to the L Cell

C3G faces a gauntlet between the berry and the L cell. Understanding that gauntlet explains why processing matters so much.

The stomach is actually C3G’s friend. The pH value of the stomach environment is generally 0.9 to 1.5. Anthocyanins are relatively stable at pH 2 or below and can be rapidly absorbed in the stomach, appearing in plasma within 30 minutes after ingestion. The acidity that protects the molecule in a well-processed elderberry product continues protecting it in the stomach. Some C3G absorbs directly through the stomach wall into circulation [9].

The challenge comes in the small intestine. Anthocyanins are destabilized by the neutral to slightly alkaline pH of the small intestine. As C3G moves from the acidic stomach into the small intestine the pH rises, the molecule becomes less stable, and some degrades. What survives is absorbed via the SGLT1 and GLUT2 glucose transporters in the intestinal wall [9]. Exposure to intestinal conditions leads to a decrease in C3G bioavailability by 40 to 50% overall [10].

What does not get absorbed intact continues to the colon where Bifidobacterium metabolizes it. Those metabolites stimulate L cells to produce more GLP-1 through the SCFA pathway… a second route to the same destination [11]. Two pathways. One berry. Both landing on the L cell.

How to Process Elderberry to Preserve C3G for the L Cell

This is where most of the commercial elderberry industry gets it wrong and most consumers have no way of knowing.

C3G is destroyed by heat, oxidation, light, and time. Heating elderberry at temperatures ranging from 212 to 302°F causes significant structural changes in anthocyanins, degrading both the bioactive compounds and their antioxidant activity [8]. Extended heat processing does not sterilize the medicine… it eliminates it.

Elderberry, with its softer peel structure, is more prone to anthocyanin degradation by heat than other berry fruits [8]. A blueberry or a grape can withstand certain processing conditions that will simply destroy elderberry anthocyanins.

What preserves C3G so it can actually reach the L cell:

  • Fresh pressing or cold pressing to juice immediately after harvest
  • Dropping the pH of the finished product acidifies the environment and stabilizes the C3G molecule structurally… the color shift from purple toward red confirms it is working [12]
  • Flash pasteurization at the lowest temperature and shortest time that achieves food safety requirements rather than extended boiling
  • Cold storage to minimize oxidative degradation
  • Processing as close to harvest as possible… anthocyanins degrade in the berry after picking even without heat

The color of the finished product tells you most of what you need to know. A deeply purple, almost black elderberry juice has retained its anthocyanins. A pale, brownish, or dull product has not. The color is not the brand. The color is the medicine. Trust the color.

METABOLIC RECOVERY

It starts with the dark berry.

Everything else follows from here.

Bevin Brooks

Business Secrets Weekly drops every Sunday at www.lionberry.us

References

[1] Xu, Y. et al. (2025). Cyanidin-3-O-glucoside enhances GLP-1 secretion via PPARβ/δ-β-catenin-TCF-4 pathway in type 2 diabetes mellitus. npj Science of Food, 9, 47. DOI: 10.1038/s41538-025-00445-4

[2] Habib, A.M. et al. (2021). What is an L-cell and how do we study the secretory mechanisms of the L-cell? Frontiers in Endocrinology, 12, 624009. DOI: 10.3389/fendo.2021.624009

[3] Drucker, D.J. (2002). The multiple actions of GLP-1 on the process of glucose-stimulated insulin secretion. Diabetes, 51(S3), S434–S442. DOI: 10.2337/diabetes.51.2007.S434

[4] Holst, J.J. (2007). The physiology of glucagon-like peptide 1. Physiological Reviews, 87(4), 1409–1439. DOI: 10.1152/physrev.00034.2006

[5] Drucker, D.J. (2006). The biology of incretin hormones. Cell Metabolism, 3(3), 153–165. DOI: 10.1016/j.cmet.2006.01.004

[6] Lee, J. & Finn, C.E. (2007). Anthocyanins and other polyphenolics in American elderberry (Sambucus canadensis) and European elderberry (Sambucus nigra) cultivars. Journal of the Science of Food and Agriculture, 87(14), 2665–2675. DOI: 10.1002/jsfa.3029

[7] Finn, C.E. et al. (2008). Fruit composition of elderberry (Sambucus spp.) genotypes grown in Oregon and Missouri, USA. HortScience, 43(5), 1501–1507. DOI: 10.21273/HORTSCI.43.5.1501

[8] Oancea, A.M. et al. (2018). The kinetics of thermal degradation of polyphenolic compounds from elderberry extract. Journal of Food Science and Technology, 55(2). DOI: 10.1177/1082013218756139

[9] Zou, T.B. et al. (2014). The role of sodium-dependent glucose transporter 1 and glucose transporter 2 in the absorption of cyanidin-3-O-β-glucoside. Nutrients, 6(10), 4165–4177. DOI: 10.3390/nu6104165

[10] Xu, Y. et al. (2023). Cyanidin-3-O-glucoside as a nutrigenomic factor in type 2 diabetes and its prominent impact on health. International Journal of Molecular Sciences, 24(10), 8875. DOI: 10.3390/ijms24108875

[11] Tolhurst, G. et al. (2012). Short-chain fatty acids stimulate glucagon-like peptide-1 secretion via the G-protein-coupled receptor FFAR2. Diabetes, 61(2), 364–371. DOI: 10.2337/db11-1019

[12] Khoo, H.E. et al. (2017). Anthocyanidins and anthocyanins: colored pigments as food, pharmaceutical ingredients, and the potential health benefits. Food & Nutrition Research, 61(1), 1361779. DOI: 10.1080/16546628.2017.1361779

[13] Chen, Z. et al. (2023). Preparation of an elderberry anthocyanin film and fresh-keeping effect of its application on fresh shrimps. PLOS ONE, 18(11), e0290650. DOI: 10.1371/journal.pone.0290650

[14] Liang, M. et al. (2023). Factors affecting the stability of anthocyanins and strategies for improving their stability. Food Chemistry: X, 20, 100867. DOI: 10.1016/j.fochx.2023.100867

[15] Kuhnau, J. (1976). The flavonoids: a class of semi-essential food components. World Review of Nutrition and Dietetics, 24, 117–191.

[16] Thomas, A.L. et al. (2015). Comparison of fruit characteristics among diverse elderberry genotypes grown in Missouri and Oregon. Journal of the American Pomological Society, 69(1), 2–14.

[17] Solverson, P. et al. (2024). A one-week elderberry juice intervention augments the fecal microbiota and suggests improvement in glucose tolerance and fat oxidation in a randomized controlled trial. Nutrients, 16(20), 3555. DOI: 10.3390/nu16203555