“We’re taking people with brains that are working normally, and for the most part, pushing them to use antidepressant drugs which actually interfere with the normal working of the brain.”
Dr. Paul Andrews is an Associate Professor of Evolutionary Psychology in the Department of Psychology, Neuroscience and Behaviour at McMaster University. His research focuses on understanding the evolution of depression, which he argues may be an evolved emotional response for understanding and solving complex problems. Dr. Andrews is also concerned with the evolution of the serotonin system and the effects of antidepressants on mental and physical health. His research has shown an increased risk of cardiovascular events, as well as death among those who use antidepressants.
The transcript below has been edited for length and clarity. Listen to the audio of the interview here.
Paul Andrews: Wow, that’s a powerful quote. I love it. We feel pain because, as part of a single evolutionary tree of life, organisms—from flies to mice to squid to humans—all face threatening challenges in their lives, things that can kill them or interfere with their reproduction. We need to be able to avoid them and the harm associated with them. Painful feelings seem to have a common property, which is to promote what we call avoidance behavior—essentially avoiding harmful events in our lives. Additionally, they promote avoidance learning, which teaches us how to behave in order to steer clear of such threats.
For example, take a simple case: when you have a sprained ankle, which most of us have experienced at some point, it’s very painful. The pain helps you keep weight off your ankle so you don’t injure yourself further, giving it a chance to heal. The pain prevents further harm and damage to the injured area. If you take pain medication to reduce the discomfort, you’re more likely to put weight on the ankle, which can delay the healing process and may even cause more injury. I can expand on this, but I wanted to start with a physical pain example because it’s something we all intuitively understand.
Andrews: Great question. Let’s see if we can extend this concept of avoidance behavior and avoidance learning to emotional pain. I like to start with milder forms of psychological pain before diving into depression or anxiety. For example, think about the malaise you feel when you have an infection. It’s unpleasant and distressing, but it serves a purpose. That feeling is worse when you’re physically active, so it forces you to rest and allows your immune system to allocate energy for healing. It’s a form of avoidance—avoiding physical activity to prioritize recovery.
Another example is hunger. Most of us don’t know what starvation is really like, but we know what it’s like to be hungry. When you’re starving, you have this massive amount of hunger that is almost intolerable. It is designed to help you, to motivate you to go out and find food so you can solve the starvation problem. But in an avoidance language, it is avoiding the death that can be caused by starvation. That’s what’s the painful feeling is motivating.
There’s a whole range of painful emotions that can be framed in this avoidance context. Take jealousy: people often think of jealousy as pathological, but it’s a normal response to perceived threats to a valued relationship. Reactive jealousy is a normal thing — it helps you — it’s a sign that you actually value your partner. If your partner’s actions indicate a potential emotional or sexual threat, jealousy motivates you to pay attention and address the situation to protect the relationship.
We can apply the same thinking to social anxiety, which is when you’re afraid of a negative consequence from engaging in social interaction, like embarrassment. If you fear embarrassment, that anxiety might keep you from social situations where the risk is high. Of course, that comes with a cost—missing out on social opportunities and becoming isolated, but you avoid the cost of being embarrassed. It’s easy to think about social anxiety in terms of avoidance behavior and avoidance language.
When it comes to depression, I’d argue that, like other painful emotions, we should consider it through the lens of avoidance behavior and learning. It’s a relatively unexplored area in science because many researchers don’t frame depression this way. Most researchers don’t even think about it in those terms, and so in my mind, it’s a frontier area of science.
The literature shows when most physicians make a serious medical mistake, they feel a lot of emotional agony over having hurt a patient. We also know that the emotional agony can reach clinical levels. It’s not uncommon for physicians who have made these kinds of mistakes to meet clinical criteria for depression, for acute traumatic stress, for generalized anxiety and so on. The whole purpose of avoidance behavior and avoidance learning is to figure out what you could have done differently to change the outcome.
But if the physician concludes that it was the stupid nurse’s fault, or the stupid lab technician rather than reflecting on their own role, they won’t learn and they won’t reduce the chance of it happening again in the future.
Rumination over mistakes is inherently self-blaming because the goal is to figure out what you could have done to prevent the outcome. It has to be self-blaming otherwise it’s not going to be effective in producing avoidance behavior. One of the puzzling things for a clinician is, why, if rumination is supposed to help you solve problems, why does it have to be so self-blaming and self-deprecating? The answer to that is it’s hidden in the fact that it’s designed to promote avoidance behavior and avoidance learning which is all about what you could or can do. You have to go searching back through that causal chain of events for things you could have done differently.
Andrews: Psychiatry itself has changed. In the 1970s, there was a strong influence of Freudian thinking, which understood that painful feelings are pretty normal. The psychiatrist would try to evaluate what’s going on in your life socially and situationally and evaluate your pain in relation to that. If it was proportional they’d say, “It seems like it’s a natural normal response.” It was only if the pain was disproportionate to the stressors that it would be viewed as a mental health problem. After the 1980 DSM revision, this perspective was lost.
Now, the field of psychiatry has essentially produced a checklist of feelings and symptoms, and if you check off enough of them then, boom, you’ve got the disorder.
Andrews: But as an evolutionist, here’s the thing: you and I are both wearing glasses, right? That means our eyes can malfunction, and they’re clearly evolved organs. Even if there’s some adaptation in our brains for producing depression, it has to malfunction at some rate. I just don’t think it’s as high a rate as the diagnostic criteria suggest. That’s my point: the real problem, as far as I can see, is how do we accurately distinguish between normal and pathological?
Andrews: Especially during the reproductive years.
Andrews: Agreed. Let’s consider this anecdote from a colleague of mine, Joanne Cacciatore, a Professor of Social Work at Arizona State. She shared a story about a young mother who was moving heavy furniture in her living room. She thought her one-year-old daughter was in the kitchen playing. The mother tried to move a heavy TV set, and as she did, it started slipping out of her hands. It turned out the daughter wasn’t in the kitchen after all—the mother accidentally dropped the TV on the child, and the child died.
Siem: Horrible.
Andrews: Incredibly horrible. But you don’t need to be an evolutionist to understand a few points here—just go with your gut instinct. If this woman’s brain is normal and she’s not a psychopath, is she going to have some agony over killing her child? The answer is, yeah, massively. Is she going to meet the DSM criteria for depression, which includes five out of nine symptoms for at least two weeks? Absolutely. Is she going to be depressed for two weeks? Yes. Two months? Definitely. She may never fully recover.
Joanne’s other work shows that it’s not uncommon for parents who’ve lost a child to still meet the DSM criteria for depression four years after the loss. In this case, because the mother can point to her own behavior as the cause, she may never recover. From my perspective, given the avoidant learning part of this, I’m not sure it would be a good idea for her to completely recover. You don’t want people to live in misery forever, but if something like this happened to me, I wouldn’t want to forget it entirely. I’d want a part of me to always remember to be careful with my kids.
The question is, would something like this happen again? If she’s got a normal brain and experiences agony for a long period, she’ll probably never let anything remotely similar happen again. More importantly, she might become ultra-protective of her children—maybe even too protective. But while that isn’t ideal, it’s understandable in terms of avoidance behavior and learning. This anecdote illustrates that, when contextualized, even severe and prolonged depression can be viewed as a normal response.
Andrews: I’ll provide some context for why we developed this paradigm. There are various methods to induce sadness experimentally, but no one had developed a paradigm for triggering depression, which is a syndrome involving multiple symptoms—behavioral, cognitive, and emotional—that align with what we think of as DSM depression. The debates around depression—whether it’s a disorder or a normal emotional response—don’t progress because we lack experimental control over what we’re studying. We often rely on correlational studies or case-control studies that can’t address causality.
Experimental paradigms with randomized controls are the classic way of testing causal hypotheses. So, we created a paradigm that involves putting people through social rejection in the lab. It’s deceptive because they’re not actually being rejected by others, but they don’t know that and they think they’re being rejected by other people. The other component is that we give them a reason to analyze the rejection through root cause analysis and ask, “Is there something I could have done to avoid this?” That’s when you start seeing rumination.
Andrews: That’s why we’re not just inducing sadness. We published a paper using this paradigm, and we found that we can increase sadness, but we can also induce symptoms of anhedonia, which is the loss of interest in normally pleasurable activities like sex, social companionship, or humor. We can induce feelings of guilt or self-blame and low self-esteem, which manifest as a sense of worthlessness.
We also have some evidence that this paradigm triggers difficulty concentrating, another symptom, though we want to test that more in the future. I’m not saying we’ve met all the formal criteria for depression because that needs five out of nine symptoms and we have no evidence of inducing any suicidal ideation. But we have four out of the nine symptoms, including sadness, anhedonia, guilt, and worthlessness, which are core features of depression. Other symptoms like lethargy, restlessness, or appetite changes can occur in many other conditions as well. We know we are inducing a syndrome because it’s multiple symptoms with cognitive and affective or emotional features.
Our sample consists of university students, averaging around 18 years old, essentially at the beginning of their reproductive years. To get into university, you typically need to be fairly healthy with a well-functioning mind. From an evolutionary standpoint, natural selection doesn’t tolerate high levels of dysfunction during reproductive years. As we get older and past reproductive age, the rates of true disorders go up. So if we can trigger depressive symptomology in young healthy people, that is an argument against it being a disorder.
Some of the participants—15% to 20%—have psychiatric diagnoses. I find that problematic, given what I just told you about natural selection not tolerating high levels of this. But nevertheless, under the idea that they ostensibly have something wrong with their brains, we can exclude them from the analysis and see if the ones who don’t have the diagnosis still show these symptoms. We find no difference in the effect, which means, again, we are triggering this in now the most ostensibly healthy individuals in our population.
Our argument is that this is a normal response. Even the feelings of guilt and worthlessness can be useful, but how could it be a useful normal thing to feel like you’re a piece of crap? In a sense, worthlessness is actually motivational. For example, consider that physician who makes a serious medical error. If he believes he’s God’s gift to medical science and doesn’t experience a dip in self-esteem, he won’t be motivated to change his behavior. A little bit of self-criticism can drive corrective actions. That is something that the researchers in social psychology explicitly recognize, that loss of self-esteem can actually help young training physicians to learn from their mistakes and go on and be better physicians.
Andrews: The results of our studies suggest that depression can be a normal emotional response to social rejection, even in healthy young people. This makes it harder to justify the use of antidepressants because the underlying philosophy of these medications is based on the assumption that something is going wrong in the brain—that depression is not a normal response. Antidepressants are meant to correct this supposed malfunction. But if depression is a normal emotional response, it makes more sense to turn to psychotherapy rather than medication.
Andrews: To answer that, I need to explain a bit about how antidepressants, especially SSRIs (Selective Serotonin Reuptake Inhibitors), work. SSRIs bind to the serotonin transporter, which is found on neurons that release serotonin in various regions of the brain. But the serotonin transporter isn’t just found in the brain—it’s present throughout the body, in organs like the lungs, heart, muscles, and even the intestines and reproductive organs. The serotonin transporter allows serotonin to be absorbed by cells that express it. For instance, a lung cell can take up serotonin from the bloodstream through this transporter.
When we call these drugs “selective,” it means they primarily bind to the serotonin transporter and not to others, like the dopamine transporter. But they aren’t selective enough to only target the brain. The idea behind using these drugs to treat depression is that they target serotonin in the brain, but because serotonin transporters are found in so many other parts of the body, SSRIs affect other systems too.
Andrews: Yes, that’s a good point. I do believe that SSRIs can reduce depressive symptoms, but they aren’t as effective as people might think. Much of the symptom reduction can be attributed to the placebo effect. That said, I wouldn’t go so far as to say they have no effect at all.
Andrews: There are a number of unintended side effects that patients and physicians don’t want. These include cognitive effects, which can be undesirable, but let’s focus on the physical side effects for now. The Selective Serotonin Reuptake Inhibitor, because it’s not selective enough, will bind to the serotonin transporter wherever it is in the body. If you’ve ever seen an antidepressant commercial in a country where direct-to-consumer advertising is allowed, like the U.S., you’ll hear a long list of side effects: digestive problems, sexual dysfunction, cardiovascular issues, and more. These side effects may seem random, but if you actually understand that the drugs bind to the serotonin transporter wherever it is in the body and prevent serotonin from going into all sorts of organ systems, you can start connecting the dots.The side effects may be mild individually, but when they occur across multiple systems, the cumulative effect can be significant.
Andrews: In my mind, this is still a frontier area of research, but there are many individual cases—people who’ve gone through discontinuing an antidepressant like an SSRI—that show what you’ve said is true. Understanding the mechanisms behind it is the understudied aspect. I could easily imagine that what’s happening is somewhat the reverse of the side effects. Not everyone is going to experience all the side effects you hear about at the end of an SSRI commercial, but collectively they are there, and we know this from the variety of individual responses that can occur. This is because the serotonin transporter is expressed everywhere. People’s individual side effect profiles, whether they’re starting or discontinuing the drug, are likely to be highly variable and broad-ranging.
We’ve done a meta-analysis of studies looking at all-cause mortality on these drugs as well as cardiovascular events like heart attacks and strokes. In the paper we published, we looked at these separately. Of course, heart attacks and strokes are important causes of mortality, but some people survive these events, so it’s important to consider them regardless of whether they lead to death. All-cause mortality means exactly that—death due to any cause, even if the exact cause is unknown.
We also had reason to separate studies based on whether they involved people with preexisting cardiovascular diseases, which could include atherosclerosis, chronic obstructive pulmonary disorder, diabetes, etc., and those who otherwise seemed healthy, with no problems other than depression. There was a significant difference in all-cause mortality between these two groups. In a sample of the general population, we looked at the risk of death for people taking antidepressants compared to those who were not, and in the group with preexisting CVD, antidepressants didn’t seem to increase the risk of death—there was no significant increase. However, in the general healthy samples without preexisting CVD, there was an increased risk of death associated with the use of these drugs.
Andrews: I think there’s a lot of hope. One starting point is to rethink depression as a normal response and think about how a diagnostic criteria that pathologizes normal reactions may be doing a lot of harm. We’re taking people with brains that are working normally, and for the most part, pushing them to use antidepressant drugs which actually interfere with the normal working of the brain. The whole purpose of these drugs is to alter normal brain function. With a better understanding of depression as a normal emotional response to the problems that life throws at you, you can use that to seek out better treatments.
I want to point out the difference philosophically, again, between antidepressant medications and psychotherapies. The disorder narrative common in our culture is a good justification for the use of medications. But if the disorder narrative is right, in principle, the medications could potentially fix what’s going on if we’ve got the mechanism correct. On the other hand, psychotherapies are basically just as effective as antidepressants and may have more useful effects in terms of long-term use than drugs. This doesn’t align well under a disorder narrative because psychotherapy requires your brain to be working pretty well.
If you’ve ever experienced CBT, the therapist doesn’t give you answers. They encourage you to develop your own hypotheses about what’s going wrong in your life and test them. That process requires your brain to be working reasonably well. If the brain is truly malfunctioning, you wouldn’t expect it to be capable of engaging in scientific thinking, which is essentially what CBT demands. This is true for all psychotherapies—they depend on the brain’s ability to reason and understand, which isn’t consistent with the idea of a malfunctioning brain.
The alternative view—that depression is a normal response—doesn’t mean you don’t need therapy. Just like you might need help with a sprained ankle or an infection, you might need help dealing with the complexities of life. But none of this means your brain isn’t working well.
This is important for clinicians, especially clinical psychologists, to understand. One of the reasons why antidepressant medications have skyrocketed in prevalence since the 1980s while psychotherapies have declined is because of the way the narrative about depression has changed. It’s now viewed as a disorder, and that disorder narrative is naturally inclined to push the antidepressants. I think the clinical audience ought to care about this disorder narrative, and they ought to think carefully about the justification that they have in their own minds for why they’re using psychotherapy. If you really think it’s a disorder, your psychotherapy justification doesn’t make that much sense, I’m sorry to say.
Another thing that a psychotherapist can do is to recognize that most serious, even chronic, depressions are normal emotional responses. As a therapist, what is a useful way of approaching your patient? With the disorder narrative, under the idea that it reduces stigma, you say, “You don’t have to worry about this; this is not your fault. You just have something going wrong in your brain that you can’t control.” That’s where the medication often comes in.
But a different way of tackling this would be to say, “You know what? This is a normal emotional response to serious life events that are going on in your life. I would be worried if you didn’t feel depressed over this circumstance. This is normal, and this is your brain telling you that you need to spend time thinking about these crucial things in your life and as a psychotherapist, I can help you with some of that.”
Think about the difference there. First of all, if you’re a patient facing serious problems in your life, like divorce, financial issues, or custody battles—really complicated stuff—and then you’re told that your brain isn’t working well, you’re not only going to become depressed over the problems themselves, but you may also get more depressed over the idea that your brain isn’t functioning properly. How are you supposed to solve all your problems if your brain isn’t working well? It just becomes even more overwhelming. But if you tell your patient that they have a normal response, they avoid that second layer of depression on top of everything else.
The other point here is that this approach naturally induces what is called, in the literature, the “therapeutic alliance.” It turns out that psychotherapies are generally effective in treating depression. It’s not due to the differences between the various psychotherapeutic styles, but rather something called the “common factors.” One of these common factors across psychotherapies is how well you connect, get along, and interact with your therapist. By telling your patient that they have a normal emotional response to serious life events, that is one natural way to build that alliance.
As a therapist, sometimes patients don’t know why they’re depressed. When you ask them, they might not fully understand or be able to identify a cause. But you could ask them a slightly different question: “What are you ruminating about?” They should be able to answer that. From a therapeutic perspective, that’s a useful clue that you can use to help your patient gain greater awareness of why they’re depressed.
Andrews: I’m an Associate Professor at McMaster University. You can Google my name, Paul Andrews, at McMaster University. That’s probably the best way to find me.
Siem: Thank you so much, Paul. Keep up the good work.
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Don’t make me angry treating this mere socially conditioned Darwinian theoretical speculation on the alleged evolutionary role on what we call emotions and feelings and instincts as something approaching expertise: this guy is an expert only in his own conditioned theoretical assumptions which are inadmissible because they are not insight at all. It is computer brained assumptions. I tell you it has no more truth then the conspiracy theories which blight all of potato brained America. Indeed it’s the same kind of potato blight, this intellectual interpretation of all phenomena within a reductionist and by now scientifically unsupported interpretation of every phenomena in human conscious life through a narrow Darwinian lens.
Science DOES NOT even BEGIN to understand what emotions and feelings are, AS although they affect biological and hormanal changes in the body and clearly affect action, what they are is in our consciousness, and their mystery evades science just as surely as the ‘hard problem of science’ itself, i.e. awareness or consciousess itself, which according to the Darwinian mechanism could not possibly have any value because it is just this sense of awareness, without which the body and psychological process would be perfectly mechanical which would have no negative and perhaps even a positive baring on DNA propagation/succesful reproduction. Awareness doesn’t DO anything – it is this seeing, this illumination of sight/sound/thought etc, which is so far inexplicable and untouched by science, just like the qualitative and energetic qualities and impacts of emotion and feeling. Although correlates in physiological function do exist, for example the increase in cortisol during the kind of stress that correlates with the experience of anxiety within consciousness and nervousness within the body, the facts are that all emotions, such as desire, fear, and also depression which I’d regard as a low energy state characterized by the absence of emotions as opposed to sorrow or sadness or grief, which is emotional pain, and all the others, are 1) phenomena within consciousness, not something you can put under the microscope or root in biological structures, even if they do correlate to changes in brain activity and hormonal function because correlation is not causality: and 2) each and any one of us have subjective proof that emotions are energies for action, something science cannot fully explain, definitely not through the much slower changes in glucose and lipid metabolism initiated by changes in affective state. It doesn’t matter if I’m exhausted or have low blood sugar. If there is a threat to life, such as someone pulling the gun, I have infinite energy and perfect conscious attention, vigalence, and speed of action. You can’t explain this through the understanding of the biological and metabolic mechanisms we understand. And if you desire something intensely you have infinite energy for it. And what evolutionary mechanism can be used to explain desire, when desire most of our desires are wasteful burden destructive to health or social harmony without which we would be capable of greater action and attention to the things that mattered? And what is this energy of desire? You see, it is not a phenomena that has ever been touched by science, and the only clear terrain it is known to exist is WITHIN consciousness, somewhere no microscope or other scientific instrument can go. It is part of the hard problem of science. It is conscious qualia that motivates and energiezes consciousness and this has the power to effect action through the body. There are correlates between emotional affects and the brain and hormonal and physical. These things we know. But we have not touched what we call mental or emotional wellbeing because the only terrain it is known to exist is in consciousness, but you assume it is a phenomena generated by the biological substrata and explicable through the socially conditioned Darwinian world view which you obviously have not kept up to date with, because to rescue the simplistic Darwinian natural selection hypothesis is proving to be an impossible task for science if you actually look at the state of research, which has produced changes to Darwins assumptions that compare, if you ask me, to the changes in Newtonian theory brought about by special relativity. And we haven’t even got to quantum physics in the fiend of human evolution if you ask me. I’ll come back to the research in a minute but first hear this. This is fast and furious and unthinking and full of mistakes but it’s too boring to remember facts and I haven’t got the energies of consciousness to do a better job! See?
Anyway, your thought doesn’t even know what it is, does it. Does it? Ask it. It doesn’t. Yet it points to everything else in conscious life and pretends to know what it is merely by calling it a word. Beyond the word is a repeating pattern of sensation: we are taught language which conditions our brain to codify these patterns according to the social conventions of communication and language. But thought says – it doesn’t know. And it doesn’t even know what IT is. Do you really think it could ever know what this mysterious, dark energetic substrata is which operates it, which I call emotion, feeling, instinct, or better, the ENERGIES of consciousness and conscious action, this being a clear fact of experience but an untouchable mystery to science? So thought cannot even pretend to know what these things are, and you, through a clear biological reductionist assumption, imagine you have undrstood it through this heavily socially conditioned, unthinking Darwinistic interpretation. Sir, that shows an unfortunate degree of lack of insight, to say the least.
And the thing is, I am very interested in the state of the self-understanding of humanity, so I keep abreast with all the scientific and other research demonstrating the state of human self-understanding, which is really no understanding at all but socially conditioned interpretations of things that in truth are still ungrasped by the human mind, including the phenomena of consciousness and emotions and feelings and various non-ordinary psychological experiences and those enduced by drugs such as hallucinogens. And the truth is, while the neo-Darwinian explanation of evolution through random mutations of DNA, some being selectively favoured through natural selection by the environmental pressures has been really quite thoroughly negated by all the attempts to mathematically corroborat the theory, impossibilities that quantitative research consistently throws up. Meanwhile, another mechanism for morphological evolution is gaining credibility within the scientific literature, because the MORPHOLOGICAL developement of an embryo is proven now not to be governed only by DNA: there is an electrical communication between all cells, the same kind of communication that becomes specialized in the neuron cell, and the desruption or manipulation of this electrical communication in a developing embryo or small organism has been clearly shown to produce corresponding morphological perversions some of which are predictable given the nature of the disruption or manipulation. So this seems to have a pre-eminant role in governing the morphology of the embryo or organism. And it’s electrifying research: I wish I had the patience to find citations and youtube videos on this but maybe I’ll come back to it. Another one was to create an embryo out of the cells scrapped from the skin of another embryo, and a completely novel life form was produced, which even had a flagella through which it swam (tiny organism it was). Again, I can’t do it justice but it shows that this transcellular, global electrical communication between cells certainly is instrumental in governing the morphological development of the life form, and is quite independent from DNA, and it seems that life spontaniously takes a novel form of functional life when profoundly desrupted, as is shown by the skin cell embryo experiment. It is shown that these electrical communications are transcellular, and orient the activities of the whole embryo, and for someone interested in the facts, the truth, the reality, these scientific observations are not to be interpreted, just noted. And they clearly give a credible basis for explaining how DNA, which is just typing, which is just encoding for mere proteins and not that many proteins (about 22,000 I understand!) is capable of producing the radical complexity and sophestry of the human organism or even the simplest cell – the breathtaking complexity of which is really comparable to the whole civilization of humanity if you actually look into it.
Now I haven’t got time to do your research for you, i.e. repeat what I have discovered with regards the most cutting edge scientific findings trying to understand the mechanism behind evolution, but countless findings are showing that the simplistic mechanism theorized to explain the evolution of species, namely random selection through environmental pressures and mutations in DNA, can in no way be used to explain the complex morphological changes that create new species or new organs like eyes or wings. only 1 in 10 to the power of 22 genetic mutations of a sequence encoding for the average protein would result in a functional protein: that means for every 1 functional change in the amino acid sequence of a protein would result from 100,000,000,000,000,000,000,000,000 random mutations in the DNA and therefore sequence. And it has been calculated and reaffirmed many times that the evolution of life and emergence of species simply cannot be explained mathematically by this mechanism which would be profoundly inefficient. Moreover, the fact that over a mere 550 million years a slew of whole new animal groups with radically new body plans emerged is impossible to explain through this mechanism because it is one thing evolving the first mammal or bird out of a simple organism through changes in protein expression, which is really all changes in DNA amount to. But to explain the transformation of one thing into a completely new body plan is impossible because changes effecting body plan effect the embryo right from the very beginning, and the overwhelming result of genetic mutations of genes relating to body plan result in the destruction of the embryo. So it has become absolutely untenable to explain things in these terms.
I know this is unforgivably chaotic but I want to make these points. Maybe one day I’ll dig out all the research for you. I have come upon it because I know the right questions to ask myself, because I went through psychosis and magic mushrooms into a kind of clarity where I see how stupid and medieval we are in all our bullshit pet theories on material reality, evolution and pretty much everything else. Theories are non-facts, and the actual is ungraspable by what you really are, which is awareness, just as awareness is forever ungraspable by anything within it. That’s like imagining a reflection on a river can grasp the moon. They are in different dimensions, the dimensions of which come together in us. Thought, sensation, emotion and what I call feeling (animal spirits) are all parts of consciousness in different dimensions that express themselves through the body, just as the body expresses itself in these other dimensions which are connected in the human being. I know this is sloppy explanation but have to put as much of an impossibly vast picture together as possible. And this is not knowledge because knowledge would imply knowing how you know this, and I just can’t explain it. I see it without seeing it, and it’s clear and obvious to me.
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I found the idea of intentionally inducing anxiety, depression, etc. to be somewhat disturbing. Is there no sense of possible long-term damage from this process? Doesn’t life already teach us that difficult situations bring on difficult feelings? Why does that need to be “proven” by potentially harming people?
That being said, I agree completely that normalizing anxiety, depression, even delusions and hallucinations is the best path forward, along with some REAL medical care for real, objectively observable conditions (like drug adverse effects). There is no benefit to lying to people to stop them from blaming themselves. In fact, normalizing blaming yourself may be the very first step to moving beyond it!
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WTF do you mean “somewhat disturbing”??? It is VERY disturbing but typical of the cruel neutrality (detachment) that runs through the veins of more than a few people who run these types of needless psychology “experiments” crafted mainly to advance their careers in stupidity. Toying with young people’s core sense of self in the name of experimentation shows callous disregard that ought to be banned from college campuses and this man should be sued on the grounds of intentional emotional traumatization.
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