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They're not "monsters." They're not cryptids. They're definitely not aliens. They're just people. Really old people. People who've clearly been out in the woods for a long time. I know everyone is going to jump down my throat because of the videos. "They're too tall." "Their skin looks weird." "They don't move right." Okay… Have you ever considered that maybe you're filming someone who's been living in the middle of the woods for years? I think people are making this way more dramatic than it actually is. If anything, I felt bad for them. They're just standing there and people keep recording them from 100 yards away like they're zoo animals. I was out at the vymara clearing yesterday and one of them looked directly at me. I smiled. Nothing happened. They just stood there. Honestly, they seemed calmer than most people I know. Here's my theory. I think they used to be people just like you or I but something happened. They made a choice. They saw the answers that no one else could. That's it. I think they never left. Why would they? If you found something that completely changed your life, why would you go back to sitting in traffic and paying bills? Everybody keeps acting like these people are dangerous. Maybe they're just done with the rest of us. Maybe they figured something out that we haven't.  After seeing them myself… I honestly think the sadder explanation is the real one. They're not just some creature. They're just people who never wanted to leave. And after everything I've experienced...I don't think I blame them anymore.

For context I am a scientist studying a plant that grows in socal. I believe Vymara has a direct anti-aging effect at the cellular level.

I tested it on primary human fibroblasts, human keratinocytes and mouse muscle cells.

In scratch assays, Vymara-treated cells closed 69–81% of the gap within 18 hours, compared with 43–52% in controls. The difference remained when cell division was restricted, suggesting the cells were moving into damaged areas faster rather than simply multiplying.

I then exposed the cells to hydrogen peroxide. Twenty-four hours later, 72–81% of the Vymara-treated cells remained viable, compared with 38–49% of controls. The treated cells also retained 70–78% of their mitochondrial function, compared with 35–46% in controls, and showed less membrane damage and apoptosis.

Five days after oxidative stress, 58–67% of the control cells tested positive for cellular senescence. Only 19–28% of the Vymara-treated cells did. Increases in the senescence-related proteins p16 and p21 were also substantially lower.

I repeated the main experiments three times using fresh Vymara preparations, different plates and different media batches. The same pattern appeared across all three cell types.

The Vymara-treated cells did not simply survive. They maintained mitochondrial function, avoided senescence and retained their ability to move into damaged areas.

Vymara:

• Accelerated cellular repair
• Protected mitochondrial function
• Reduced oxidative damage
• Prevented apoptosis
• Prevented cells from entering stress-induced senescence

It directly prevented several of the processes that cause tissues to lose function with age. The treated cells behaved younger. They repaired damage faster, maintained energy production and resisted the transition into senescence. I started this experiment because I wanted to explain my blood work. Now I think I am looking at a cellular mechanism for slowing biological aging. If another laboratory reproduces this, everything changes.

The exposure phase lasted seven days. That was enough. The Vymara-treated wounds restored their surface barrier in approximately half the time of the controls. Vymara did not simply make the wounds close faster. It made them rebuild more aggressively.

I created four standardized dermal wounds arranged as two matched pairs. All four were produced with a fixed-depth dermal-scratch jig rather than freehand curettage. High-frequency ultrasound performed immediately afterward showed that the matched wounds were equivalent within the instrument’s 30 μm axial-resolution limit. No paired depth measurement differed by more than one resolution unit.

Treatment assignments were randomized within each pair:

Two wounds received the Vymara crude rich fraction.

Two received the vehicle without Vymara.

The fraction was normalized by dry mass and LC–HRMS peak area before use. The vehicle was matched for pH, osmolality and viscosity. Two areas of intact skin were exposed to the same Vymara fraction under identical dressings for the entire application period. Neither developed erythema, barrier disruption, swelling or measurable dermal thickening. The fraction was sterile-filtered before use. I also exposed cultured human keratinocytes to the same working concentration. Cell viability remained above 95% at 24 hours, with no increase in membrane-damage markers. Vymara is not accelerating closure by chemically burning the surrounding tissue. It is not causing a conventional irritant response. Something else is happening. The wounds were examined every 12 hours.

I recorded:

Total wound area using automated image planimetry

Epithelial coverage

Wound-margin displacement

Transepidermal water loss

Erythema

Local temperature

Pain and sensitivity

Repair-zone thickness using high-frequency ultrasound

A wound was classified as functionally closed only after it displayed an uninterrupted epithelial surface and transepidermal water loss within 20% of the adjacent intact skin on two consecutive readings. The difference was not caused by the Vymara wounds simply pulling themselves shut.

Both Vymara-treated wounds reached the closure endpoint between 72 and 84 hours. The vehicle-control wounds required between 144 and 156 hours. The effect repeated across both matched pairs. Vymara reduced the time required for functional surface closure by approximately half. Then the repaired tissue kept growing. By day five, both Vymara-treated sites had become firm beneath the new epithelium. By day seven, the repair zones were visibly elevated above the surrounding skin. Neither control site developed comparable thickening. High-frequency ultrasound showed that the Vymara repair zones were 36% and 39% thicker than their paired controls. The surface was already closed. The tissue underneath it was still building.

The intact-skin exposure sites remained normal. Keratinocyte viability remained above 95%. There was no detectable contamination or endotoxin. The treated wounds restored barrier function faster, not slower. A caustic injury should create more tissue destruction and delay epithelial recovery. Vymara did the opposite.

What Vymara Is Doing

The stages of wound healing are supposed to overlap, but they still follow an order: inflammation, epithelial migration, fibroblast activation, matrix deposition and remodeling. Vymara is compressing that order. The surface is sealing while the underlying wound bed is already being reinforced. People will argue that seven days is too early to call this scar tissue. I disagree. The wounds are closed.

Call it early scar matrix if that distinction makes it easier to accept. It is scar tissue. The controls healed normally. The Vymara-treated wounds restored their barrier in half the time and immediately began building reinforcement underneath it. Vymara does not recreate the tissue that existed before the injury. This is not ordinary healing happening faster. It is a different definition of repaired.

I’ve had thinning around my temples and crown for a few years. It is not severe, but it was noticeable enough.

For context. I am a scientist. I have been doing numerous studies on a plant found in the local region.

After a few very small self-exposures to a crude fraction isolated from Vymara. I noticed that the thinner areas looked fuller.  At first I assumed unrelated, but to be sure. I tracked the same marked one-square-centimeter area at my crown under the same lighting and magnification. The visible hair count increased from 143 at baseline to 158 two weeks after exposure. Most of the difference came from short, fine hairs that were not visible in the baseline images. I continued my research.

Growth rate also increased. Hair in a shaved measurement area grew an average of approximately 0.34 mm per day at baseline and 0.45 mm per day after exposure. I have not started any hair-loss medication, changed products or added supplements.I then compared plucked anagen follicles collected at baseline and after exposure. The newer follicles had larger, more consistently shaped bulbs, denser matrix-cell regions and more intact outer root sheaths. Ki-67 labeling was higher, and staining for K15 and SOX9 was stronger in the outer-root-sheath cells.

To make sure I was not simply seeing what I wanted to see, I randomized the images and gave them to two colleagues who did not know which samples came first. Both independently arranged them in the correct chronological order. Both identified the newest samples as the healthiest and most biologically active. Im considering talking to pharmaceutical companies at this stage after all of my findings.

I’ve been studying an unidentified psychoactive plant that I’ve been calling Vymara. I’m studing a lot of different variables after exposure. 

In addition I used no hormones, started no medications or supplements and made no deliberate changes to my diet or exercise. My sleep schedule also stayed fairly consistent.I tracked growth hormone through overnight blood samples collected every 30 minutes, along with IGF-1, four-point salivary cortisol, fasting glucose and fasting insulin. I also continued recording sleep and resting heart rate with the same wearable I used during baseline.

Here’s what changed:

Total overnight growth-hormone secretion was about 64% higher than my baseline profile on the third night.

IGF-1 increased from 174 to 191 ng/mL by day seven. It is still well within the normal laboratory range.

daily cortisol output was 38% below baseline on day two and remained 29% lower on day seven. The normal morning-to-evening pattern is still there; the whole curve is just lower.

Total Fasting glucose barely changed: 88 mg/dL at baseline and 87 mg/dL on day seven.

Fasting insulin decreased from 7.1 to 4.9 μIU/mL. My calculated HOMA-IR went from approximately 1.54 to 1.05, although I know that is only a rough proxy for insulin sensitivity.

What I find strange is the overall direction of the results. Growth signaling increased, cortisol remained suppressed and glucose regulation appeared more efficient. Any one of those could be noise. Seeing all three together is why I’m still curious.

The first exposure was extremely small. I experienced no visuals or obvious intoxication, but my wearable recorded a lower resting heart rate and increased deep sleep compared with my previous baseline. Serial salivary tests also indicated reduced cortisol for nearly 48 hours.

More significantly, I experienced persistent calm and mental clarity. Emotional noise felt reduced, my attention narrowed and certain thoughts carried more importance than they normally would. This continued after the acute effects had ended and the compounds I was tracking had fallen below the detection limits of my assay. My speculative working hypothesis is that the fraction contains multiple active components:

1. A fast-acting serotonergic compound may produce the visual and euphoric phase reported at higher exposures.
2. A second compound may affect pathways associated with bonding or social attachment.
3. A longer-lasting component or downstream biological response may alter stress regulation and salience processing.

What seems most significant in this N=1 experiment is that the altered psychological state appeared to persist beyond the period in which I could detect the compounds. 

I collected intact samples of Vymara’s root zone, including the surrounding moss and substrate, and used them to build several small microcosms in the lab. Vymara is photosynthetic. Chlorophyll-fluorescence measurements confirm active photosystem II. But its rapid growth and nutrient uptake still do not make sense for the poor substrate it grows in. I tested whether the surrounding biological layer might be contributing to its nutrition.

I introduced a controlled amount of commercially sourced mammalian blood into one microcosm. The others received water, saline, glucose solution or nitrogen-matched plant tissue. Within hours, protease and phosphatase activity increased sharply in the Vymara root-zone sample. The blood also broke down much faster there than it did in moss collected outside Vymara’s immediate root zone. The plant-tissue treatment produced a much weaker response. Water, saline and glucose produced almost none.

I repeated the blood treatment using sterilized substrate. This time, there was very little enzymatic activity. When I restored the microbial community isolated from the original root-zone sample, the response returned. To track where the nutrients went, I added a stable-isotope-labeled blood protein to the next treatment. The labeled nitrogen later appeared in Vymara’s roots and developing tissue. Instead, it appears to maintain a microbial community that breaks animal material down outside the plant. Vymara then absorbs the nutrients released into the surrounding moss and substrate.

Would this qualify as indirect carnivory, or is it better interpreted as unusually efficient rhizosphere mineralization?

I’ve been taking very small doses of an extract from Vymara a hallucinogenic plant I found. A colleague found out what I was doing and, mostly out of curiosity, offered to run an EEG on me. We recorded my normal brain activity yesterday morning, before I took anything. Then we did another recording six hours after the dose. By that point, I felt completely normal. I wasn’t experiencing any noticeable effects, so I assumed the second recording would look basically the same as the first. It didn’t. My alpha activity was still elevated hours after the effects had worn off. Parts of my brain that are normally less connected appeared to be working more closely in sync. We checked everything and ran the analysis again. We got the same result.  I’m repeating the experiment next week under the same conditions.

The nectar fraction is confusing me. LC-MS shows multiple alkaloid-like compounds with nitrogen-containing ring structures, but none match standard plant alkaloids in the library. Not psilocybin. Not mescaline. Not DMT. Not harmine or harmaline. Not ibogaine. Not atropine/scopolamine-like. Whatever this is, it is not a known classic psychedelic profile. The strangest candidate molecule has a mass pattern suggesting an indole core attached to a sugar-like side chain and a lipid-soluble tail. That combination makes no sense to me. It is water-soluble enough to move through nectar. But lipophilic enough that it could plausibly cross the blood brain barrier.

 I ran three separate petal samples, along with an empty-vial control and a fiber blank.Part of the profile looks completely normal for a flowering plant. Linalool. Benzyl alcohol. Phenethyl alcohol. Small amounts of methyl salicylate and several common terpenes. Nothing there would have caught my attention on its own.

The rest of the chromatogram is another story.I found 27 reproducible peaks that I cannot identify. Eleven of them are among the most abundant compounds in the entire floral profile. They appear in every petal sample, at nearly identical retention times, but are absent from the blanks. So unless the contamination is somehow inside the tissue itself, ordinary lab contamination is becoming difficult to argue.

I searched multiple spectral libraries. Most of the unknowns either returned no meaningful match or produced low-confidence suggestions that changed depending on how I processed the background. I also calculated retention indices using an alkane standard, and those values did not agree with the already-poor library suggestions.More interestingly, several of the unknown peaks seem related. Their mass spectra share the same major fragment ions, while their apparent molecular masses differ in regular increments.  This may not be one strange metabolite. It may be an entire volatile pathway that hasn’t been characterized.

The unknown compounds are much more concentrated in the petals than in the leaves, and their abundance rises sharply when the petal tissue is damaged. That makes me wonder whether they are involved in pollinator attraction, defense, or some kind of airborne signaling.I’m not automatically saying this is a new molecule.  But plants do not usually devote this much of their volatile output to compounds that leave almost no recognizable spectral footprint.The strangest possibility isn’t that Vymara produces one unknown chemical. It’s that a significant portion of what this plant releases into the air belongs to a class of chemistry I can’t find documentation for. 

I’ve spent my career studying plants. But I am truly perplexed by my most recent finding.

Every experiment I’ve run assumed the flower I’m studying was of one that is an individual organism. I collected samples from the surrounding vines, moss-like growth, tree bark and roots. I expected to identify whatever had contaminated my original results. Instead, I found the same unusual DNA arrangements in every sample. Not merely similar sequences the same rare structural junctions and the same small DNA-containing bodies I isolated from the original leaf. Their concentration decreases farther from the flower, but they’re still present. Their normal nuclear DNA remains different. The moss appears to have its own genome. But all of them also contain this second biological system, threaded through their tissues so completely that I can’t separate one from another.

There are two possibilities.

Either the flower has invaded and integrated itself into every organism surrounding it…Or the flower, vines, moss and trees aren’t truly separate organisms at all. Maybe the flower is only a reproductive structure. Maybe everything aboveground is a different expression of the same underlying network organs, hosts or extensions of something much larger.I’ve spent my career identifying plants by finding the traits that separate one organism from another. Vymara doesn’t seem to recognize that distinction.

I’m currently trying to understand reproduction of this strange plant. It seems to my knowledge to only grow in SoCal. And I’ve only found it in one particular field.

I placed fresh, untreated pollen into a standard germination medium and watched it under a light microscope. After about 40 minutes, the grains began producing pollen tubes this was expected but.
Then the tubes started curving toward one another.
At first I assumed crowding made them look connected, so I repeated the test with pollen from another flower and spread the grains farther apart. The same thing happened. Several tubes changed direction as they approached neighboring grains, and a few appeared to meet.
I ran a comparison sample from a known flowering plant. Its tubes grew outward in different directions, exactly as expected.
I still don’t know whether Vymara’s tubes are actually fusing or merely touching. Damaged grains could be releasing nutrients, or something in the medium could be creating a chemical gradient. But it may explain the filaments from the SEM images: they might not simply hold the pollen together. They could be part of a system that allows separate grains to locate or respond to one another.

Small update to my previous post about the leaf sample that produced good sequencing reads but refused to assemble properly.
A few people suggested separating the normal nuclei from the smaller DNA-containing bodies I saw in the cytoplasm, so I tried a rough fractionation. It isn’t perfectly clean yet, but the two fractions are clearly behaving differently.

The nuclear-enriched fraction now looks much more recognizably plant-like and assembles better than the original mixed extraction. It’s still unusually repetitive, but at least I’m getting coherent contigs.

The fraction containing the smaller bodies is the confusing part. It contains far more DNA than I expected, and most of its reads don’t classify confidently as bacterial, fungal, chloroplast, or mitochondrial. A targeted 16S test produced only weak, inconsistent amplification, so an ordinary intracellular bacterial infection is looking less likely.
I also compared samples taken from different areas of the same leaf. The nuclear fraction remains fairly consistent, while the smaller-body fraction changes substantially depending on where the tissue was collected. That may explain why neighboring leaf punches originally appeared to contain different sequences.
I’m arranging long-read sequencing and attempting a cleaner separation before drawing any conclusions. At this point, I’m wondering whether these could be unusual organelles, an uncharacterized endosymbiont, or some kind of extrachromosomal DNA compartment.
Has anyone encountered cytoplasmic DNA-containing structures that vary this much within a single leaf?

I was out on a hike last weekend in Los Angeles and I found a very strange plant. The flower itself was huge. I'd guess about the size of a child’s basketball. It looked kind of like a rose at first, but the petals were much thicker than any flower I've ever seen. The weirdest part was the center. It wasn't pollen. It almost looked like a cluster of little balls growing inside the flower.

For context of my fascination. I'm a botanist. My research focuses on plant developmental biology and evolutionary morphology, so I have access to a decent microscope and basic sequencing equipment through my university. I’m not normally a Reddit guy but I just feel like I need to share my findings.

I collected a single fallen petal and one mature leaf. I intentionally left the plant itself untouched.
Here are a few observations.

- The leaves have an opposite arrangement, but the venation doesn't resemble any angiosperm I'm familiar with.
 - The cuticle is unusually thick, yet transpiration appears extremely high. I genuinely don't understand how both can be true.
 -Stomatal density is significantly higher than most flowering plants I've measured.
 -The epidermal cells contain what appears to be structural pigmentation rather than conventional pigment granules, which may explain the blue coloration.
  - The petal tissue fluoresces under UV.
I've never seen anything quite like it. I'm sending samples to a colleague next week. Honestly hoping this turns out to be something boring that I'm overlooking.

I’d be interested to hear others opinions on my findings.