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The Dark Berry

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

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Past Business Weekly's:

When Words Lose Their Meaning

Lionberry 's Weekly Delusion and Re-illusion Update.

The phrase “food is medicine” has become the wellness world’s version of “thoughts and prayers.” Everyone says it. Everyone feels good saying it. And almost nobody means anything real when they do. That’s the danger—not the phrase itself, but what happens when language gets stretched so far it stops pointing to anything true.

The original use of the phrase belonged to grandmas, gardeners, and people who still know how to cook and where food comes from. In that world, “food is medicine” meant something simple and grounded. A piece of meat and some vegetables—and fruit when it was in season—was just a regular meal. And then there were the special things you made when someone didn’t feel well: mixtures built from botanicals, herbs, fruits, nuts, grasses, roots, seeds, and whatever the land offered that season. Things pulled straight from soil and pantry because they carried function, flavor, and a purpose. That usage was peaceful, instinctive, and honest.

Then came the influencers, using the same phrase while holding something powdered, flavored, and algorithm-optimized. “Food is medicine” became a caption under a neon shake that tastes like peach sorbet and contains a clinically irrelevant amount of plant dust. They didn’t inherit the meaning—they inherited the hashtag. And hashtags don’t carry wisdom; they carry trend cycles.

Then comes the USDA, NIH, and hospital systems, who use both phrases—but in different ways. “Food Is Medicine” is their broad, public-facing concept, the umbrella idea that nutrition is foundational for health. “Food As Medicine”—capital As—is the technical term for the clinical, billing-coded interventions:

produce prescriptions,

medically tailored meals,

medically tailored groceries.

This version has insurance pathways, reimbursement logic, metrics, screenings, and outcome evaluations. It isn’t a belief system. It’s a healthcare program.

So we end up with two phrases—Food Is Medicine and Food As Medicine—that sound almost identical but function in totally different worlds. And both of them, at their best, once pointed to something we still have right now: real plants growing from real soil, carrying real chemistry that does real things in the human body. Not ancient in the sense of “long ago,” but ancient in the sense of continuity—still alive, still growing, still here.

Once a phrase becomes universal, though, it becomes meaningless.

That’s what’s happening now.

A wellness word printed on plastic.

“Natural” stamped on a bag of potato chips.

“Immune-supporting” slapped on anything that wants to look virtuous.

Marketing fog replacing actual meaning.

It’s Peacekeepers in 1984.

It’s “community” in Big Tech.

And on the Idiocracy side, it’s the fictional Electrolyte Drink Brawndo—marketed so aggressively that the entire population believes “it’s got what plants crave.”

In the film, they irrigate crops with the Electrolyte Drink Brawndo instead of water because advertising has replaced knowledge. Marketing departments tell us what truth is. The soil dies. The crops fail. The land collapses into a dust bowl. That’s what linguistic drift does: it hollows meaning until the absurd becomes normal.

“Food is medicine” used to mean:

eat real plants,

respect soil,

trust the chemistry that grows in the field,

trust the phytonutrients that come from this earth,

food keeps you alive and makes you whole.

Now it means turmeric dust on junk food.

Or a wellness word added so a product can sell for $3 more.

This hollowed-out category is not a comfortable place for real food to sit.

The old category, where LionBerry sits—the one before wellness gloss, before powdered fantasy, before language drift washed the meaning out of the words—still exists. But sitting there is not accidental. People tell me all the time to cheapen it, powder it, plastic-bottle it, isolate it, dilute it, lab-flavor it, margin-boost it, and make it “scalable” by stripping out the thing that makes it real.

I don’t do it.

Not because it’s easy.

But because sometimes the right thing to do is always the hardest thing to do.

LionBerry sits in the old category because I fight for it to sit there.

Real plants.

Real chemistry.

Real soil.

Real function.

Zero powdered fantasy.

LionBerry is exactly what it says it is: a farm-crafted drink made out of actual food.

When I say “the phrase doesn’t need to be fixed,” I mean the phrase “food is medicine.”

We don’t need to invent a new set of buzzwords or rescue the old ones from misuse.

We don’t need to rebuild or replace the language itself.

What needs to change is this:

start making products that mean what the words used to mean.

Start making food products that are just food