Long story short- my ex boyfriend has a 'friend' that has bad drug habits and is always sabotaging items of mine that were once safe in his garage.

So called friend recently let out of jail (def temporarily) is sad that my ex has written him off and basically disowned him. He has stolen, used, and blatantly screwed with tools/hardware/materials you name it - of mine. I know now everything must be removed since he has gone as far as to break into garage.

most recently I found a plastic container of mine that had a screw top on it with my initials, that held different types of small knobs, latches, slide locks for cabinets made of all types of different metals.

it is a dark blue green color, I am not sure when this liquid appeared but would have been within 14 days.. Probably 7 days. yes it smells odd but the metals are older too but is there a way to test for urine even though it may be a week old?

Content warning for mentions of suicide attempts

Seven years ago, YouTuber KnowingBetter did a video about the show 13 Reasons Why. https://youtu.be/Pi478whGCPA?is=criy455qJVgDkGB3

Why am I making a post about a seven-year-old video which covers a show that hasn't been relevant in years? I guess because this segment of the video has fascinated me for a while in that it's clearly been well researched and yet gets almost everything wrong. Also, I have not seen a single comment on the video challenging all the things that are wrong in this segment.

In the video, KnowingBetter speculates on what kind of neurological damage a character got after he shot himself in the head. And as I said, almost all of it is wrong but shows that he clearly did at least some research.

In the show, the character walks with a cane due to hemiparesis and has reduced sensation. Here's KnowingBetter's interpretation along with my corrections.

> There doesn't seem to be any frontal lobe damage at all.

I am baffled that he said this. The hemiparesis would absolutely indicate that his frontal lobe was damaged as the primary motor cortex is in the frontal lobe.

> He also didn't hit his occipital lobe in the back of the brain since his vision seems to be intact.

This is one of the parts that are correct.

> The temporal lobes are the next candidate, but this would also damage his hearing and speech which doesn't seem to be the case.

Regarding speech being impacted, kind of. The temporal lobe houses the Wernicke's Area which is responsible for *language comprehension,* not speech. However the verbal output of people with Wernicke's Aphasia is typically word salad as they cannot understand their own verbal output.

Regarding hearing, this is not true although it is true that the primary auditory cortex is in the temporal lobe. The gunshot wound seems to have affected one hemisphere, and hearing is innervated bilaterally meaning that if one side is damaged, the other side would supply the innervation. Cortical deafness only occurs when there is damage to both temporal lobes of the brain.

> Which leaves us with the parietal lobe which controls sensory and motor function which given his limp and erectile issues makes the most sense.

Damage to the parietal lobe would not cause a limp although the parietal lobe is responsible for some motor functions. However, it is common for both sensory input and motor function to both be affected after a traumatic brain injury as, even though the primary motor cortex is in the frontal lobe and the primary sensory cortex is in the parietal lobe, they are right next to each other.

> But he also has another plot convenient symptom...[the character describes not having any memory of the suicide attempt and not remembering anything for a month before]... That's not how amnesia works. There are several different types of memory and therefore several different types of amnesia...Firstly there's semantic memory which is facts, definitions, and dates and stuff. And secondly episodic memory which is events and experiences. They don't always have to be autobiographical. If you watch a movie or hear a story from a friend, that's logged as an episodic memory whether it happened to you or not. It would seem based on his recollection that he's lost his autobiographical episodic memory. If you lose your memory for the past, that's retrograde amnesia- everything from before the damage or disease. You can also lose your ability to form new memories or anterograde amnesia... usually by damage to the subcortical structures, most notably the hippocampus. It's usually all or nothing when it comes to memory loss from physical damage to the brain. You can psychologically repress a memory for a traumatic event so I can kind of understand not remembering the shooting itself. But not remembering only a plot-specific month from before the attempt is physically impossible. With amnesia he'd probably forget a ton of other things, like people's names, his school schedule, or his Facebook password.

Traumatic amnesia (amnesia surrounding a traumatic brain injury) can absolutely affect memories of only a specific timespan. It is also possible for it to affect one type of memory but not others.

Another overall misconception in this video is the idea that damage to a specific lobe in the brain is like popping a balloon in that damage to a lobe would mean damage to the entire lobe. In reality, brain damage is more like scratching a CD, and it is possible, even common, for people to have damage to some structures within a lobe but not others.

Here's my response to an old video about an old show. It took me forever to put it together, but I did it!

This gave me quite the chuckle, but made me appreciate all the hidden Easter eggs in the way the Simpsons show chemistry in their backgrounds

I post this because of how much of a failure of basic knowledge of the composition of an human being this is

This is an old video that was originally on YouTube and was deleted, but I found a BiliBili archive. It's essentially a list of acids by acidity, but it doesn't even use a real unit...

Jay Bhattacharya plans to combat emerging diseases by mostly pretending they don’t exist.

He recently instructed the NIH to remove the words “biodefense” and “pandemic preparedness” from the institute’s web pages, in order to “focus more on basic immunology and other infectious diseases currently affecting people in the US.”

Was the pandemic response in 2020 flawless? No.

Will a future response to natural or engineered disease be *better* with *less* preparation? Also no, but with far more deaths.

Clearly caring about the health of your own citizens is too woke for the current administration, but undermining a keystone in national defense takes owning the scientists to a new level of self harm. Unless the Golden Dome is made of latex, it won’t stop pneumonia or epididymitis or any other infection.

Ignoring biology is the worst possible defense against it, as anyone who ignored cancer or a bad infection can tell you (except they can’t, because the dead tell no tales).

Introduction: When Assumptions Become Beliefs

For over a century, most people have believed that diseases like the cold and flu spread from person to person. We’ve been taught that when someone sneezes or coughs, tiny particles fly through the air and infect others. This idea is called contagion. It’s so familiar that we rarely stop to ask: how do we know it’s true?

Surprisingly, the answer is not as clear as one might expect.

Where the Idea Came From

The belief in contagion dates back to ancient times. People observed that when one person became ill, others nearby often developed similar symptoms. It seemed obvious that something must be “catching.” But for most of history, no one knew what that something was. Some blamed bad air. Others believed invisible poisons or “miasmas” were responsible.

In the 1800s, scientists discovered bacteria—tiny living organisms visible under a microscope. This led to the germ theory of disease. Doctors began to believe that bacteria caused illness and could be passed from person to person. In some cases, this claim appeared to hold: certain bacteria were consistently found in association with specific symptoms. But even then, the evidence was largely correlational. The mere presence of bacteria did not prove they were the cause of disease. And in many cases, no bacteria could be found at all. The theory rested more on patterns of association than on direct, reproducible demonstration of causation.

To account for diseases where no bacteria could be identified, scientists proposed a new idea: viruses. These were said to be even smaller than bacteria and able to pass through filters that blocked known microbes. But there was a fundamental issue—no one had ever seen a virus. The claim was that viruses were too small to be detected by the light microscope, whose resolution is limited to about 200 nanometers. The existence of viruses was therefore inferred, not observed. The idea of a “filterable agent” became a placeholder for an unknown cause, not a demonstrated entity.

Later, with the invention of the electron microscope, scientists were able to image particles smaller than bacteria. However, these images only revealed size and shape, and only after extensive sample preparation involving centrifugation, dehydration, and staining. These procedures could alter the morphology of the particles, raising questions about whether the images reflected their natural state. Moreover, the origin of these particles was uncertain. They could have been cellular debris, exosomes, or other byproducts of cell breakdown. The imaging process could not demonstrate whether these particles were capable of replication or causation of disease.

This uncertainty persisted even with the development of cell culture techniques and genetic sequencing. Replication was inferred from cytopathic effects—visible changes in cultured cells—but these effects could also result from the toxic additives used in the culture or from the stress of the artificial environment itself. Sequencing did not involve extracting a complete genome from an intact particle. Instead, it relied on collecting fragments of genetic material released after inducing cell lysis. These fragments were then computationally assembled into a genome, often using a reference template.

This process introduced several layers of assumption. First, it was assumed that the original sample contained virus particles. This assumption remained unverified throughout all downstream procedures. Second, the provenance of the sequenced material could not be confirmed. Third, the assembled genome was only one of many possible configurations. And finally, the issue of replication remained unresolved.

Despite these methodological uncertainties, virologists continued to assert the existence of numerous contagious particles—too small to be seen—that passed from one person to another. They interpreted this as transmission. In doing so, they upheld the idea of contagion without direct scientific evidence and often dismissed alternative explanations that could account for the observed patterns of illness.

The Experiments That Didn’t Work

During the 1918 flu pandemic, scientists attempted to prove that the flu was contagious. They conducted experiments in which healthy volunteers were exposed to sick patients. These volunteers breathed in the exhalations of the ill, swallowed their mucus, and even had sick individuals cough directly onto them.

None of the healthy volunteers became ill.

These experiments, conducted by respected physicians such as Dr. Milton Rosenau and others in the United States and Europe, were carefully designed and meticulously documented. Yet they consistently failed to demonstrate that illness could be transmitted from person to person under controlled conditions.

Rather than reconsider the contagion hypothesis, scientists concluded that the experiments must have been flawed. They shifted their focus to laboratory detection of viruses and the development of tools like PCR tests, which detect fragments of genetic material. However, these tools do not demonstrate how diseases spread. They only indicate that certain sequences are present in a sample.

In addition to PCR, antigen and antibody tests are often used to claim the presence of infection. Antigen tests are designed to detect specific proteins thought to be part of a virus, while antibody tests aim to identify the immune system’s response to such proteins. However, both types of tests rely on a critical assumption: that a known, purified viral particle exists and has been used as a reference standard to validate what is being detected.

If the original virus has never been isolated in a pure form and directly demonstrated to cause disease, then the foundation of these tests becomes uncertain. Without a verified standard, there is no definitive way to confirm what the tests are actually detecting. While these methods may yield consistent results within their own frameworks, they do not independently confirm the existence or pathogenicity of a virus.

This ambiguity is further compounded by the concept of asymptomatic carriers—individuals who are said to harbor and transmit a virus without showing any signs of illness. At the same time, there are cases where people exhibit clear symptoms but test negative on all available diagnostic tools. These two phenomena are often cited as evidence of viral behavior, yet they raise serious questions about the internal consistency of the contagion model.

If a person can be both sick without testing positive and contagious without being sick, then any outcome can be interpreted as consistent with the theory. This makes the model unfalsifiable—immune to disproof—because no result can contradict it. Such a framework aligns with instrumentalist thinking, where models are judged by their utility or predictive power rather than their ability to be tested and potentially proven false.

This brings us to the concept of immunity, which is closely tied to the use of antibody tests. In virology, immunity is generally understood as a specific defense mechanism: the body is said to develop resistance to a particular virus by producing antibodies that match its unique structure. But this model assumes that the virus in question has been isolated, characterized, and shown to cause disease—an assumption that, as discussed, remains unproven. Without a verified viral particle, the meaning of “specific” immunity becomes unclear.

In reality, the immune system may function less as a precision-guided missile system and more as a generalized detoxification network. The body responds to a wide range of internal and external stressors—chemical, environmental, metabolic—by mobilizing various defense mechanisms, including inflammation, fever, and the production of proteins labeled as “antibodies.” These responses may not be specific to a single agent but rather reflect the body’s effort to restore balance.

This perspective also challenges the idea of “cross-reactivity,” where antibodies are said to respond to multiple viruses with similar structures. If the original virus has not been demonstrated to exist, then claims of cross-reactivity are built on a foundation of inference, not empirical proof. This further illustrates how the immune model, like the contagion model, often operates within an instrumentalist framework—internally consistent, but not grounded in direct demonstration.

What If Contagion Is Just a Model?

In science, there are two major philosophical approaches. One is scientific realism, which holds that theories should describe what is actually happening in the real world. The other is instrumentalism, which maintains that theories do not need to be true—they only need to be useful.

Modern virology and epidemiology often follow the instrumentalist path. They use models to predict how diseases might spread, relying on patterns and statistical correlations rather than direct proof of cause and effect. These models do not test whether one person’s illness causes another’s. Instead, they assume contagion is real and build their frameworks on that assumption.

This is why contagion can be understood as a model rather than a proven mechanism. It may help explain certain patterns, but it has never been shown to function in the way it is commonly described.

So What Does Make People Sick?

If contagion has not been conclusively proven, what then causes people to become ill—especially in groups or during specific seasons?

In his 2024 book Can You Catch a Cold?, Daniel Roytas reviews over 200 studies and experiments on disease transmission. He demonstrates that, time and again, scientists have failed to prove that colds and flu are contagious in the conventional sense. But he goes further, offering alternative explanations that merit serious consideration:

• Environmental stress: Sudden changes in temperature, humidity, or air quality can stress the body and trigger symptoms.
• Seasonal cycles: Immune function varies with the seasons. Reduced sunlight in winter can lead to lower vitamin D levels, which may affect health.
• Shared exposures: People in the same household, school, or workplace often share the same food, air, and stressors. When several people become ill, it may be due to a common environmental cause rather than interpersonal transmission.
• Detoxification: Some researchers propose that symptoms like coughing, sneezing, and fever may be the body’s way of eliminating toxins, not necessarily signs of infection by another person.

These ideas are not new. They have been explored by physicians and scientists for over a century. What has changed is that they have been largely sidelined in favor of the contagion model—even though that model has never been conclusively demonstrated.

The Virus Model: Science or Story?

By the mid-20th century, the virus had become the central figure in modern medicine. It was credited with causing a wide range of illnesses, from the flu to polio to the common cold. Yet few realize that the virus model itself is built on instrumentalism.

This means it was not developed by proving that viruses exist and behave in a specific, demonstrable way. Rather, it emerged as a model—a set of assumptions and tools that appeared to produce consistent results. If a test showed a pattern, or if a lab animal became ill, scientists inferred that a virus must be responsible. But they did not isolate the virus in a way that met the rigorous standards of the scientific method. They did not demonstrate that it caused disease by itself, in a controlled setting, using an independent variable.

This distinction is critical. Virology, as it is currently practiced, is not based on direct proof of cause and effect. It is based on models that are assumed to be true because they yield internally consistent results—such as test outcomes, predictions, or laboratory reactions. But consistency within a model does not prove that the model reflects reality. It only shows that the model is coherent on its own terms.

This raises a fundamental question: has virology revealed the true nature of disease—or has it constructed a compelling narrative that remains unverified?

Conclusion: Time to Reopen the Question

The idea of contagion has shaped medicine, public health, and daily life for over a century. It is the reason we cover our mouths, isolate when ill, and fear close contact during outbreaks. But when we examine the historical and scientific record, we find something unexpected: the concept of contagion has never been proven in the way that science, in its original realist form, demands.

The early experiments failed. The virus model was built on inference, not demonstration. Modern tools like PCR and epidemiological modeling assume contagion but do not test it. And the field of virology, as it stands today, is grounded more in instrumentalism than in empirical realism.

This does not mean that illness is not real, or that suffering is imagined. But it does mean we must be willing to ask difficult questions—especially when the answers influence how we live, how we treat one another, and how we understand health itself.

Books like Can You Catch a Cold? by Daniel Roytas are helping to reopen this essential conversation. They remind us that science, at its core, was not meant to be a collection of models that merely “work.” It was meant to be a method for discovering what is true. And when our models fail to meet that standard—when they cannot demonstrate cause and effect, or withstand empirical testing—we have a duty to question them, and to return to the foundational principles that made science trustworthy in the first place.

I didn't realise that scientific illiteracy was so rampant. The woman in this video is basically performing an experiment in which she tests how affirmations affect physical status... by complementing and insulting different jars of rice.
Somehow (???) the people in the comment section completely believe that this relationship exists because of the evidence presented to them, that is "uhhh DURRR the jar of rice thats loved is fresh while the jar of rice thats abused is rotting".
What confuses me is that there are people who genuinely INSIST that this is a legitimate experiment, citing that a doctor has performed the same experiment and garnered similar results! Fantastic! The doctor in question is Masaru Emoto, businessman, author and pseudoscientist with a doctorate in Alternative Medicine in a fraud university that is now shut down. His credentials are incredible!
So remember guys, if you ever happen to get diagnosed with a terminal illness, just say nice things to yourself in front of the mirror and you'll be cured good as new.

He thinks that ChatGPT agreeing with him makes it true.

Shows an astronaut “swimming” in space to propel themselves towards a space vehicle.

Health and Human Services Secretary Robert F. Kennedy Jr. claimed without evidence that antidepressants could have contributed to the mass shooting in Minnesota on Wednesday after an attacker opened fire on a church. The unsubstantiated antidepressant medication claim is another example of Kennedy floating ideas that contradict established science. It comes as Kennedy faces a mounting revolt at the CDC for his anti-vaccine views.

https://www.axios.com/2025/08/28/school-shooting-kennedy-antidepressants-claim