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This is part two of who knows what number......

I can go so deep into this stuff.

Hello again, I would like to follow up on some further findings from the report referenced in my first post from the National Academies of Science, Engineering, and Medicine on the topic of the dangers of fluoride in drinking water.

The last post specifically referenced the summary, along with chapters 1, 2, and 7, and briefly touched over the effects on the endocrine system in chapter 8. But I decided to go even further into that bible of a document and archived my annotations. I will specifically be discussing chapter five, about the skeletal effects of fluoride at current United States drinking water levels. My first post mainly dealt with neurological effects on the brain (along with dental, renal, gastrointestinal, and endocrine effects), and now I am going to share links toward possible correlations of drinking water in the United States, which is fluoridated in most areas, to skeletal problems, osteoporosis, and possibly even bone cancer.


This part explains itself, it is chapter four and it discusses dental fluorosis which I discussed in my last post.

Chapter 5 findings

Chemistry of fluoride in relation to tissue as a description of fluoride in the body:

Fluoride is the ionic form of the element fluorine. Greater than 99% of the fluoride in the body of mammals resides within bone, where it exists in two general forms. The first is a rapidly exchangeable form that associates with the surfaces of the hydroxyapatite crystals of the mineralized component of bone. Fluoride in this form may be readily available to move from a bone compartment to extracellular fluid. Bone resorption is not necessary for the release of fluoride in this form. However, the predominant form of fluoride in bone resides within the hydroxyapatite crystalline matrix.

Release of fluoride from bone when it is in the form of fluoroapatite requires osteoclastic bone resorption. Acidification of the mineral matrix by the osteoclast is sufficient to solubilize the fluoroapatite and allow free exchange with extracellular fluids. Once released, the effect of fluoride on bone cells may be evident; however, the form in which fluoride has its effect remains under debate. Some investigators contend that fluoride directly affects bone cells, but others claim that the effect must be mediated by fluoride while in a complex with aluminum.

Now, I briefly touched how aluminum in the body reacts with fluoride and how aluminum and fluoride content in the body may be linked to several cerebral effects in the brain and how it may be linked to Alzheimer's and Dementia as well.

Do fluroaluminate complexes exist in biological fluids? The answer to this question depends in large part on pH, protein concentration, and cell composition. However, in general, in the acid environment of the stomach much of the aluminum and fluoride exist in a complex of AlF3 or AlF4−. These forms (mostly AlF3) have been purported to cross the intestine and enter cells (Powell and Thompson 1993). Once inside a bone cell the AlFx form appears to activate a specific protein tyrosine kinase through a G protein and evoke downstream signals.

Further evidence shows how fluoride reacts with bone:

The prolonged maintenance of fluoride in the bone requires that uptake of the element occurs at the same or greater rate than its clearance. This appears to be the case.

Turner et al. (1993) put forward a mathematical model that appears to fit the known pharmacokinetic data. This model assumes that fluoride influx into bone is a nonlinear function. This assumption is supported by pharmacokinetic data and is required for the model to accurately predict fluoride movements. Another reasonable assumption is that the bulk of fluoride that moves between the skeleton and the extracellular fluid is due to bone remodeling. That is, most of the fluoride is either influxing or effluxing as a result of cellular activity. The outcome of the Turner model predicts that (1) fluoride uptake is positively associated with the bone remodeling rate and (2) fluoride clearance from the skeleton takes at least four times longer than fluoride uptake. A key correlate to the first prediction is that the concentration of fluoride in bone does not decrease with reduced remodeling rates. Thus, it appears that fluoride enters the bone compartment easily, correlating with bone cell activity, but that it leaves the bone compartment slowly. The model assumes that efflux occurs by bone remodeling and that resorption is reduced at high concentrations of fluoride because of hydroxyapatite solubility. Hence, it is reasonable that 99% of the fluoride in humans resides in bone and the whole body half-life, once in bone, is approximately 20 years.

Twenty. Years.



That shit is in there....

for twenty years.

The effects of fluoride on bone quality are evident but are less well characterized than its effects on bone cells.

.....It has been known for many years that fluoride exposure can change bone quality. Franke et al. (1975) published a study indicating that industrial fluoride exposure altered hydroxyapatite crystal size and shape. Although the measurements in their report were made with relatively crude x-ray diffraction analyses, they showed a shorter and more slender crystal in subjects who were aluminum workers and known to be exposed to high concentrations of fluoride. Other reports documenting the effects of fluoride on ultrasound velocities in bone, vertebral body strength, ash content, and stiffness have shown variable results (Lees and Hanson 1992; Antich et al. 1993; Richards et al. 1994; Zerwekh et al. 1997a; Søgaard et al. 1994, 1995, 1997); however, the general conclusion is that, although there may be an increase in skeletal density, there is no consistent increase in bone strength. A carefully performed comparison study between the effects of fluoride (2 mg/kg/day) and alendronate in minipigs likely points to the true effect: “in bone with higher volume, there was less strength per unit volume, that is, … there was a deterioration in bone quality” (Lafage et al. 1995).

Bone density and quality are very touchy subjects but they are conclusive toward linking fluoride content with skeletal problems, specifically higher densities and changes in strength.

Effect of fluoride on cell function:

Two key cell types are responsible for bone formation and bone resorption, the osteoblast and osteoclast, respectively. Osteoprogenitor cells give rise to osteoblasts. Osteoprogenitor cells are a self-renewing population of cells that are committed to the osteoblast lineage. They originate from mesenchymal stem cells. Osteoblasts contain a single nucleus, line bone surfaces, possess active secretory machinery for matrix proteins, and produce very large amounts of type I collagen. Because they also produce and respond to factors that control bone formation as well as bone resorption, they play a critical role in the regulating skeletal mass. Osteoclasts are giant, multinucleated phagocytic cells that have the capability to erode mineralized bone matrix. They are derived from cells in the monocyte/macrophage lineage. Their characteristic ultrastructural features allow them to resorb bone efficiently by creating an extracellular lysosome where proteolytic enzymes, reactive oxygen species, and large numbers of protons are secreted. Osteoclastogenesis is controlled by local as well as systemic regulators.


Perhaps the single clearest effect of fluoride on the skeleton is its stimulation of osteoblast proliferation. The effect on osteoblasts was surmised from clinical trials in the early 1980s documenting an increase in vertebral bone mineral density that could not be ascribed to any effect of fluoride on bone resorption. Biopsy specimens confirmed the effect of fluoride on increasing osteoblast number in humans (Briancon and Meunier 1981; Harrison et al. 1981). Because fluoride stimulates osteoblast proliferation, there is a theoretical risk that it might induce a malignant change in the expanding cell population. This has raised concerns that fluoride exposure might be an independent risk factor for new osteosarcomas (see Chapter 10 for the committee’s assessment).

The demonstration of an effect of fluoride on osteoblast growth in vitro was first reported in 1983 in avian osteoblasts (Farley et al. 1983). This study showed that fluoride stimulated osteoblast proliferation in a biphasic fashion with the optimal mitogenic concentration being 10 µM. The finding that fluoride displayed a biphasic pattern of stimulation (achieving a maximal effect at a specific concentration and declining from there) suggests that multiple pathways might be activated. It is possible that low, subtoxic doses do stimulate proliferation, but at higher doses other pathways responsible for decreasing proliferation or increasing apoptosis might become activated. This thinking suggested that fluoride might have multiple effects on osteoblasts and that might be the reason for some paradoxical findings in the clinical literature (see below). Nevertheless, the characteristics of the fluoride effect point clearly to a direct skeletal effect. Some of these characteristics are as follows: (1) the effects of fluoride on osteoblasts occur at low concentrations in vivo and in vitro (Lau and Baylink 1998); (2) fluoride effects are, for the most part, skeletal specific (Farley et al. 1983; Wergedal et al. 1988); (3) fluoride effects may require the presence of a bone-active growth factor (such as insulin-like-growth factor I or transforming growth factor β) for its action (Farley et al. 1988; Reed et al. 1993); and (4) fluoride affects predominantly osteoprogenitor cells as opposed to mature functioning osteoblasts (Bellows et al. 1990; Kassem et al. 1994).

And then this:

The effects of fluoride on osteoblast number and activity in in vivo studies and clinical trials essentially parallel the in vitro findings. Most reports document increased osteoblast number; however, some investigators have documented a complex and paradoxical effect of fluoride in patients with skeletal fluorisis....


Boivin et al. (1989, 1990) reported that, in biopsy bone cores taken from 29 patients with skeletal fluorosis of various etiologies (0.79% ± 0.36% or 7,900 ± 3,600 milligrams per kilogram [mg/kg] of bone ash), there is an apparent increase in the production of osteoblasts with a concomitant increase in a toxic effect of fluoride at the cell level.

TL;DR: Rising rates of fluoride at cell levels lead to an increase in production of osteoblasts; this is directly linked to proliferation in the cells, and could possibly involve bone cancer, which is further described in Chapter 10.

They provided data to indicate that chronic exposure to fluoride in both endemic and industrially exposed subjects led to an increase in bone volume, an increase in cortical width, and an increase in porosity. However, there was no reduction in cortical bone mass.

There was an increase in volume, but not mass.

And now onto osteoclasts:

The Academy kicks it off with a disclaimer:

The effects of fluoride on osteoclast activity, and by extension the rate of bone resorption, are less well defined than its effects on osteoblasts.

Okay, disclaimers out of the way, let's get to the findings.

Most reports in the literature studying the effect of fluoride on osteoclast function indicate an inhibition. In fact, the effect might be mediated through G-protein-coupled pathways as in the osteoblast. Moonga et al. (1993) showed that fluoride, in the form of AlF4− resulted in a marked concentration-dependent inhibition of bone resorption.

In association with this inhibition, they found a marked increase in the secretion of tartrate-resistant acid phosphatase (TRAP). TRAP presumably originated from the osteoclast; however, its function as a secreted enzyme is not known. The fluoride effect was reproduced with cholera toxin, another Gs stimulator. This effect does not appear to be mediated solely by an AlFx complex because studies using NaF have reported similar findings (Taylor et al. 1989, 1990; Okuda et al. 1990).

Cholera toxin's effect on cells, a Gs simulator, literally had the same effect as fluoride.

Skeletal metabolism, and how fluoride is linked with osteoporosis

Remember all of that complicated stuff in the last paragraph about osteoclastic bone resorption? How when fluoride leaves the bones it has to be absorbed by those cells? Guess what:

the only therapies approved by the U.S. Food and Drug Admnistration for treating osteoporosis in the United States targeted only osteoclastic bone resorption.

Basically, treating the very medicines that is caused by fluoride drinking water's clearly shown effects on bone porosity is literally the same treatment for treating osteoporosis. This clearly shows a linkage between osteoporosis and fluoride.

Unfortunately, fluoride did not prove to be an effective treatment for two major reasons. First, although it showed robust stimulation of bone mineral density (see below), its effects as an agent to reduce fractures have never been unequivocally documented. Second, because this naturally occurring element cannot be protected with a patent, the pharmaceutical industry has not been interested in investigating all its potential.

Effects of fluoride overall:

The first clinical trials of fluoride in humans were performed by Rich and Ensinck (1961). Since then many hundreds of reports have appeared in the medical literature. The overwhelming weight of evidence in these reports documents the effect of fluoride, at therapeutic doses, to be that of an increase in bone mineral density.

So ever since 1961, they've been testing fluoride on people and found overwhelmingly solid evidence that fluoride is responsible for increases in bone mineral density. This is linked to porosity, which then is linked to osteoporosis.

Tl;dr: Your loved ones may be getting osteoporosis from drinking the water in the USA.

The lowest dose of NaF to show a clear increase in bone mineral density was 30 mg/day

Seriously. That's how strong this thing is.

Whereas the daily dose of fluoride in randomized therapeutic trials (20 to 34 mg/day) exceeds that for people drinking water with fluoride at 4 mg/L (4 to 8 mg/ day for 1 to 2 L/day), the latter may be exposed much longer, leading to comparable or higher cumulative doses and bone fluoride concentrations. (8 oz in water).

The conditions for an estimate of the fluoride concentration as a function of distance from the osteoclast are as follows:

  • The bone being resorbed has a fluoride content of 3,000 mg per kg of bone ash.

  • Bone ash is assumed to include 65% of the volume of viable bone and the density of viable bone is 1.2 g/cm3. Thus, the concentration of fluoride in the bone compartment is approximately 5,500 µg/cm3.

  • An osteoclast resorbs bone at an average rate of about 30,000 µm3 in 2.5 weeks.

  • The osteoclast is delivering fluoride to the extracellular fluid space from a point source with a radius of 20 µm.

  • Diffusion occurs into a three-dimensional spherical space around the osteoclast.

  • The diffusion coefficient of fluoride in extracellular fluid is approximately 1.5 × 10−5 cm2/s.

Studies of bone fractures in relation to fluoride in drinking water (still in chapter 5):

Note this: They even compared the data to osteoporosis, like I said before:

The committee reviewed epidemiologic data on the relationship between fluoride exposure and fractures from two sources: observational studies of exposure to fluoride in water and randomized clinical trials of the use of fluoride in treating osteoporosis.


TABLE 5-2 Observational Studies of Bone Fractures in Populations Exposed to Fluoride Near 4 mg/L in Drinking Water

The table wasn't formatted correctly in the report for me to html it or even snag it from the archive, so I made an imgur album wit the tables snapshot.

Note how in the fourth image there is a part which is adjusted for bone mineral density, the same thing that I discussed earlier. This proved crucial for Sowers' study.

This motherfucker named Sowers followed up in 2005 with another study. He's going hard in the paint with this stuff:

The newest study by Sowers et al. (2005) investigated bone fracture in relation to fluoride concentration in drinking water. The authors measured serum fluoride, providing a potentially improved exposure assessment. In this cohort study, fractures were assessed prospectively for 4 years. Fractures were self-reported and then confirmed with medical records or x-ray copies, if available; lack of fractures was apparently not confirmed. Sowers et al. (2005) collected individual-based information on people from the same regions as the 1986 and 1991 studies. They collected serum fluoride concentrations and bone mineral density of the hip, radius, and spine. The number of subjects was considerably expanded (n = 1,300) from the earlier studies. Although there may be overlap in specific subjects, all the fracture events were recent. The authors reported risk ratios of fractures in the high fluoride area that were similar to those in the previous studies (risk ratio = 2.55, P = 0.07, even when adjusting for bone mineral density, which could function as an intervening variable between water ingestion and fracture outcome).

Serum fluoride concentration was higher in the community with fluoride at 4 mg/L in drinking water. Bone and serum concentrations are related but the latter have more noise—potentially much more, depending on how samples were collected. Serum fluoride concentrations can vary within individuals, returning to baseline within hours of exposure.

Note how they keep saying 4 mg/L. That's the amount that frequent water drinkers like me get, I discussed the levels in my first post.

And then there was the Li study, after the Sowers study:

The study by Li et al. (2001) complements the Sowers studies in several ways, having a larger size and relatively strong exposure assessment for a partially ecologic study. It has a retrospective cohort design, increasing the potential for outcome and exposure misclassification, but these problems were addressed by the authors. Although exposure was assessed on the group level, exposure was finely categorized and other sources of fluoride exposure were estimated to be negligible.

....The Li et al. study did not directly assess fluoride at 4 mg/L. However the exposure group just above 4 mg/L (4.32 to 7.97 mg/L) showed an increase in all fractures since age 20 (OR = 1.47, P = 0.01, estimated 95% CI = 1.10 to 1.97), all fractures since age 50 (OR = 1.59, P = 0.02, estimated 95% CI = 1.08 to 2.35), and hip fractures since age 20 (OR = 3.26, P = 0.02, estimated 95% CI = 1.21 to 9.81). The exposure group just below 4 mg/L (2.62 to 3.56 mg/L) showed the following: all fractures since age 20 (OR = 1.18, P = 0.35, estimated 95% CI = 0.83 to 1.67), all fractures since age 50 (OR = 1.04, P = 0.87, estimated 95% CI = 0.65 to 1.66), and hip fractures since age 20 (OR = 1.73, P = 0.34, estimated 95% CI = 0.56 to 5.33). CI values were estimated by the committee using the approach of Greenland (1998).

And a double disclaimer:

Although the authors did not estimate trend, Figures 2 and 3 presented in the paper by Li et al. (2001) suggest that linear trends in proportions from the 1.00 to 1.06 mg/L category up would provide a reasonable fit in that range.

Comparing both studies:

Estimated fluoride exposure in the Li study is higher than for the Sowers studies. Assuming that exposure was predominantly due to water, the committee estimated that participants in the Li study consumed on average about 2.5 L per day for the 2.62- to 3.56-mg/L group and 2.3 L per day for 4.32- to 7.97-mg/L group (versus 0.9 to 1.2 L per day for the Sowers studies). [These water consumption levels are in the 90th to 95th percentile for the United States](Assuming that exposure was predominantly due to water, the committee estimated that participants in the Li study consumed on average about 2.5 L per day for the 2.62- to 3.56-mg/L group and 2.3 L per day for 4.32- to 7.97-mg/L group (versus 0.9 to 1.2 L per day for the Sowers studies). These water consumption levels are in the 90th to 95th percentile for the United States).

See? The 90th to 95th percentiles are getting dangerous amounts of fluoride that shows clear musculoskeletal concerns as outlined by both the Sowers study and the Li et al study.

Don't believe me? Here's a table.

And to sum it all up, both Sowers and Li:

TABLE 5-3 Four Randomized Clinical Trials Examining Nonvertebral Fractures

x Exposure Enrollment: Exposed, Placebo Participation Relative Risk (95% CI) Rate Ratio (95% CI) Nonvertebral Fracture
Reginster et al. 1998 Fluoride at 20 mg/day as sodium monofluorophosphate, 4 years 100, 100 84%, 81% 1.1(0.5) 1.1 (0.5, 2.3)
Pak et al. 1995 NaF at 50 mg/ day slow-release, 4 cycles: 12 months on, off 54, 56 77%, 72% 0.6 x
Kleerekoper et al. 1991 NaF at 75 mg/ day, 4 years 46, 38 60%, 61% 1.5(0.7, 3.5) 3.0 (2.0, 4.6)
Riggs et al. 1990 NaF at 75 mg/ day, 4 years 101, 101 77%, 80% 1.6 - 2.3 (1.0, 2.5) 1.9 - 3.1 (1.1, 3.2)

TABLE 5-4 Estimated Bone Fluoride Concentrations and Bone Fracture Risks in Randomised Clinical Trials

Reference Fluoride Exposure (mg/day) Average Length Exposure (years) Estimated Total Exposure (g) Estimated Bone Fluoride (mg/kg ash) Relative Risks (RR) or Odds Ratios (OR)a and (95% CI) Time
Reginster et al. 1998 (Belgium) 20 3.4 24 5,400 1.1 (0.5, 2.4) RR nonvertebral 4 years
Pak et al. 1995 (USA) 23 (slow-release) 3.1 25 5,500 0.6 (0.2, 2.5) RR nonvertebral 4.7 years
Kleerekoper et al. 1991 (USA) 34 2.4 30 6,200 1.5 (0.7, 3.5) RR nonvertebral 4 years
Riggs et al. 1990 (USA) 34 3.1 38 7,400 1.6 - 2.3 (1.0, 2.5) RR complete nonvertebral 4 years

Well, that was a doozy to format.

Studies Relevant to Assessing Risks at 2 mg/L

Further links regarding skeletal fluorosis caused by drinking water at current United States levels

Here are some useful links that may be too lengthy to entirely list my annotations here:

That's all, folks!

Tune in to my next post of who knows what number of posts. My next post will deal with other chapters in this study concerning fluoride drinking water's effects on the Reproductive Systems.


The lack of law enforcement. It's obvious. I posted this in shower thoughts but got deleted. It's obvious isn't it.


This is modern day liberalism folks. The days of open and honest discussion are over if it goes against the liberal narrative. Scary what we're heading towards, which is complete censorship of the internet.


The American Legislative Exchange Council or ALEC has abandoned their commitment to America's free market economy. American companies like Exxon Mobil are leaving ALEC organization in droves, and massive Chinese conglomerates like Alibaba are replacing them. What model bills is China writing?

ALEC is a non-profit group with hundreds of corporate members. Those companies help write model legislation that they then hand-off to nearly 2,000 state legislator members. Those state lawmakers then try to pass the bill in their state. In a good year, roughly 200 ALEC-based bills become law, so as you can see, ALEC's corporate members basically write our state laws. 

Before this year, only American companies were members, but now they’re letting Chinese companies join. Are they writing bills that steal our intellectual property and destroy our manufacturing jobs?

I also found this on 4Chan:


If you type in "somali":

logga logga loggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggaloggalogga

In english you will get:

log in to log in to accessibility to the uncertainty of entanglement of accession to child-to-child sexual intercourse in the exploitation of unwarranted involvement in accession-related exploitation

So thats pretty cool.

Bonus: I plugged that translation into google to see what would come up and found this document about the international governance of the internet...

I didn't read too much of it but I found the section labeled "Our Agenda" kind of interesting.


So I posted a link to a thread a couple days ago about a woman who had seen a creepy face in her window while filming her daughter. link to original post:

Well last night she posted a livestream where she appears to have been abducted by somebody or something. I hope this is a hoax of some kind but based on her latest video, her and her daughter appear to be in some real danger.

Link to her most recent live stream:

Link to thread on /r/aliens where they do a much better job of breaking everything down:

I really hope this is fake.


I was thinking about how people train and hunt with guns in the modern age, and, well, wouldn't people train and hunt with bows before we had guns?


I have a podcast and the anniversary for 9/11 is coming up. It’s been almost 20 years and what really happened is still hotly debated to this day. I would like to not only enlighten my listeners, but also myself.

I’ve done a very minimal bit of research into the specific theory surrounding H. W. Bush. I’ve heard he was CIA when Kennedy was killed and that got him Director, then VP, and finally President.

Please private message me if you’re well educated on this topic and interested in sharing your knowledge with us. Hope to hear from you soon!


How is Q not like V from V for Vendetta? Many people in the conspiracy theory circles praise V. Champion him and even relate to him and his cause.

He was a fictional character supposedly fighting for the good and freedom of people. Now, we possibly have a real life "V" in the form of Q and people are rejecting him/her/it as hard as a sorority girl's body rejecting too much alcohol in her system at a frat party.

I don't understand it. I'm no Q follower or believer. No, I'm just an outside observer to it all. Curious to hear your thoughts.

1 comment

In the US, you either believe POTUS conspired with the Russians or you believe the POTUS is bringing down the deepstate. Either way everyone is now a conspiracy theorist.


I've noticed a lot of good posts being deleted for a lack of a Submission Statement. In one case I liked it so much I reposted with the required SS. In general, I like the rule but its relatively new and likely hits the posters who don't come to r/conspiracy frequently the hardest. I think their voices deserve a reminder in joining the discussion.

I've posted in other subs that require tagging a post with flair (similar to a submission statement). In those subs an automod usually messages you immediately indicating you need to flair your post or it will be removed.

I think it would be beneficial to have a similar automod here, automatically reminding users to add a submission statement.

Thoughts? Mod opinions?


"Ok before you jump in and claim it’s fake, please try to look at the pictures, the videos and the context, and note that her last video was taken on live stream, so if it is staged, well, good job then.

So, here is what happened here (for the new comers). On Friday, a girl created a reddit account and a twitter account to seek help. She said she felt she was being observed by all corners, and had intruders all around her house and even inside. One day, she had a black out of 14 hours and woke up with a weird brand on her back.

Afterward, she tweeted records of strange sound in her house.

She was really concerned for her daughter safety, and her post didn’t seem like a marketing campaign since she doesn’t seem to know how to use twitter nor reddit really well. It looked like more a person desperately seeking help than a person seeking attention.

However, that’s where it gets scary.

As police couldn’t do anything, she started recording what was happening in her house.

In this video, you see a human shaped form running in her house, but, if you pause, if looks like it has a really long neck and a weird form, also the noise it makes while running is bothering me somehow.

Then, she was filming her daughter dancing, and if you look at the door, there is a REALLY SCARY FACE looking at her daughter, while trying to hide.

Here is the video with more brightness, and a screenshot she posted. The head movement looks really weird, as if it has a long neck, or is floating (or I HOPE a hand holding a mask).

On her twitter, another part of the video, where the head movement is really weird.

Based on recommendations, she went in a hotel and ordered cameras. Some people told her the intruders don’t mean any arms and look more interested than anything else. She asked her daughter about the intruders, she regreted instantly.

Then she came back in her house and installed the cameras,

The same evening, this video (on top) was the last she posted, on a live stream. We can hear her daughter ... suffocating? And there are weird noise similar to the one we could hear on her previous video on twitter.

Some redditors took screen shots of the intruder, IS THIS FREAKING HUMAN?

I really hope this is a prank, but what bothers me is : live stream prank, how would you do this ? She barely use social medias, and I wouldn’t post my own daughter on reddit for the sake of a prank.

So if this is real, we might have witnessed something really weird. Please let me kow what you think and please convince me it's not fucking real.

Edit: some grammar"


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