Harbingers of Doom – Part II: Anti-Psychiatry and Teleportation
Can we make superintelligent humans by repeatedly selecting embryos in a test tube? Will we soon be able to live for 200 years or longer? Can we arrest or reverse the biological processes that characterize aging? Is the mind a neurobiological phenomenon, or does consciousness partly resides outside of the body? Will you soon be able to scan your body and teleport it to the other side of the planet in a matter of hours and survive, despite the permanent destruction of your body? Can you upload your consciousness to a server and live thousands of years inside computer hardware? If you cryogenically freeze your head, will you be able to preserve it for hundreds of years or longer, only to be reawakened in the future when scientists have cured death?
Previously, in the first installment of this series, we explored the historical question of whether medieval maps really had dragons designating unknown and dangerous places, assessed the risk of the development of biological weapons of mass destruction, criteria for science funding by the Swedish Research Council, meat intolerance as a solution to climate change, and science as the best defense against biological WMDs.
In this second installment, Häggström falsely claims that shyness has been medicalized as social anxiety disorder by referencing a book review despite the fact that scientific research has tested and refuted this notion. The suggestion that smartphones have vastly improved cognitive and communication skills is not as straightforward as it first seems: brain games are probably not more effective than playing a video game like Portal 2 and distractions from smartphones deteriorate human conversations. Worse, however, is the mischaracterization of heritability as an objective context-free measure of the importance of genes and the biological ignorance about e. g. antagonistic pleiotropy and missing heritability underlying his discussion of iterated embryo selection for IQ. Mistakes of similar magnitude are committed when Häggström tries to discuss aging (but confuses models for aging with definitions of aging, as well as the hallmarks of aging with the causes of aging), destructive teleportation and uploading the mind to computers (where he claims that you can survive the physical destruction of the body) and cryogenics that involves curing death and restoring function to a chemically fixated brain.
Section XI: Anti-psychiatry and social anxiety
In the first pages of the chapter on engineering of humans, Häggström casually blurt out a common anti-psychiatry claim about how changes in the diagnostic manuals allegedly classify natural human behaviors more and more as psychiatric disorders (p. 39):
There is a strong tendency today to categorize ever more psychological states as disorders that can be treated with psychopharmaceuticals, such as how much of what used to be thought of simply as shyness is nowadays increasingly diagnosed and treated as social anxiety disorder; see Crews (2007) for a critical discussion of this development.
Those of us familiar with anti-psychiatry rhetoric can quickly recognize this trope. It occurs in virtually the same form for a variety of conditions and goes something like this:
“In my day we do not have depression, we just called it sadness”
“When I was young, we didn’t have ADHD, we just called it daydreaming or boys-will-be-boys.”
“I started practicing pediatrics in 1979, and I didn’t see kids with autism.”
That last quote is from Dr. Jay Gordon, a known anti-vaccine activists who appeared in an episode of Penn and Teller’s Bullshit (S08E10). He attempted to argue for the debunked claim that vaccines cause autism, because the incidence of autism correlated with the increase in number of vaccines. In reality, the evidence favors a rejection of the claim that the MMR vaccine, the preservative thimerosal or too many vaccines too soon somehow cause autism (Offit et al, 2002; Gerber and Offit, 2009). Surprisingly, the MMR vaccine can actually prevent a certain number of cases of autism each year. This is because autism is a rare complication from congenital rubella syndrome, which the child can get if the mother gets rubella during pregnancy (CDC, 2015). Some studies put the number of cases of autism prevented by MMR vaccination at a little bit over 1200 cases per year in the United States (Berger, Navar-Boggan and Omer, 2011).
So what was going on with autism rates? According to Gerber and Offit (2009), the apparent increase can be attributed to “broadened diagnostic criteria and increased awareness”. Basically, the way autism is defined by the medical community was expanded and people started to notice autism more and got more knowledge about it. Before, many people with severe autism were labeled as “mentally retarded” and institutionalized and people with milder forms were either labeled with Aspergers or thought to be a bit odd. Notice that this broadening of diagnostic criteria did not involve falsely or arbitrarily labeling a massive amount of people with autism.
But autism is not the same as social anxiety, so why bother discussing it here? Well, this is because it is a clear example of a case where this anti-psychiatry trope is completely empirically wrong. It is also a case that is familiar with most scientific skeptics and likely familiar to Häggström as well, if he has spent any time reading about vaccines. The truth is, this general reply can be made for e.g. depression, ADHD and social anxiety as well.
In particular, there has even been a lot of empirical research investigating the specific question of whether or not health care professions are increasingly diagnosing mere shyness as social anxiety disorder (also called social phobia) and how these two states differ. As an example, here is Burstein, Ameli-Grillon and Merikangas (2011):
On the basis of both descriptive and analytic examination, the results of the present study provide convergent evidence that social phobia is not simply shyness. In contrast to the high frequency of shyness observed among US adolescents, social phobia affected a minority of youth in this sample and only a fraction of those who identified themselves as shy. Perhaps most important, adolescents who met criteria for social phobia displayed significantly greater role impairment and were more likely to experience a broad array of psychiatric disorders, including disorders of anxiety, mood, behavior, and substance use, relative to adolescents who were characterized as shy. However, these adolescents were no more likely than their same-age counterparts to be taking prescribed medications.
This general conclusion that social anxiety disorder / social phobia is not the medicalization of mere shyness but a real, often debilitating condition is supported by a wealth of additional research cited by the above paper, such as Fehm, Pelissolo, Furmark and Wittchen (2005), Kessler (2003), Stein (1999), Wittchen and Fehm (2003), Merikangas, Ames, Cui, Stang, Ustun, Von Korff and Kessler (2007), Alonso et al. (2004), Spence, Donovan and Brechman-Toussaint (1999), Beidel, Turner and Morris (1999), Essau, Conradt and Petermann (1999), Ranta, Kaltiala-Heino, Rantanen and Marttunen (2009), Wittchen, Stein and Kessler (1999), Heiser, Turner, Beidel and Roberson-Nay (2009), Chavira, Stein and Malcarne (2006) as well as Heiser, Turner and Beidel (2003). A recent review and a recent meta-analysis on the topic that drives this point home are Morrison and Heimberg (2013) and Mayo-Wilson et al. (2014).
So what evidence does Häggström present in favor of his view that mere shyness is “increasingly diagnosed and treated as social anxiety disorder”? He cites only a single reference, that of Crews (2007). Is this a review paper? A clinical trial? Perhaps a large-scale meta-analysis of thousands of people? No, it is a book review. Not only that, it is a book review that thinks that a lot of cases of social anxiety disorder and major depression being diagnosed is just “shyness” or “episodic sadness”, that the WHO has been corrupted by large pharmaceutical companies, that epidemiological data is exaggerated due to mass hysteria and even that female sexual dysfunction (put in quotation marks by Crews) is just being a bit frustrated in bed and having a bad lover. To fill the anti-psychiatry scorecard completely, Crews repeats the chemical imbalance straw man.
The fact that Häggström cited a really bad book review as a reference for an unscientific anti-psychiatry claim while refusing to read and engage with the scientific literature on the topic is a damning indictment of his scholarly capabilities. The bottom line is that there is more than enough evidence against the notion of “social anxiety is just the medicalization of mere shyness”. Had Häggström even bothered to research this, he would have known. He deliberately chose not to and instead preferred to follow his own anti-psychiatry biases. Although Häggström just mentioned this trope in passing, it is perhaps the most vulgar, unscientific and destructive claim found in the book (with surviving the physical destruction of the body a close second).
For those who think this is just a tiny oversight, let it be known that this is not the first time that Häggström has fondled with anti-psychiatry. In a blog post from 2013, he makes a similar argument and even cites the same reference. I attempt to correct him in the comment section with references to the scientific literature, but he more or less ignored those arguments, although he did thank me for my effort.
Curiously, Häggström appears to have more personal experience with anxiousness in certain social situations than he lets on in this paragraph. Later in the book (p. 55, footnote 127), he admits to occasionally eating beta blockers (for which he assures us that he has a valid prescription) to manage what is presumably social anxiousness for talks were (1) his claims are controversial and (2) some parts of the audience is hostile. This is also independently corroborated by his tendency to include a lot of text on his slides for many of his presentations (e.g. here for some examples). This is typical of individuals with anxiousness during presentations, because of the aching possibility that he or she will suddenly lose track and forget what to say (and presumably embarrass himself or herself in front of the audience). Lots of text is therefore a useful psychologically safeguard, because you can just read off of the slides should you get lost. However, one is left wondering why, if the problem arises so rarely, does he need to use prescription medication in order to control it? This is of course speculation, but perhaps he is more invested in these issues than is apparent from the paragraph cited at the start of this section.
Section XII: Do smartphones improve cognitive and communication skills?
Häggström quickly moves on to discussing the influence of smartphones on human skills in the realm of cognition and communication (pp.. 39-40):
Glasses and hearing aids give many of us the chance to go on with whatever occupation or pet projects we have for many decades longer than would otherwise have been possible. Smartphones and similar electronic devices enhance our cognitive and communicative skills considerably. The extended mind idea of Andy Clark and David Chalmers holds (analogously to Richard Dawkins’ extended phenotype) that our minds do not reside solely within our skulls or even our bodies, but extend further.
Is it really true that smartphones “enhance our cognitive and communicative skills considerably”? Note that Häggström does not write “possibilities” (i.e. smartphones allows us to communicate with anyone in the world that has an Internet connection), but “skills”. So does smartphones actually improve our skills at these tasks?
Let us start with an article on the Committee for Skeptical Inquiry website by Vyse (2015) called Neuro-Pseudoscience. It investigates several brain training apps, such as Lumosity, brainHQ, CogniFit, Cogmed, and Jungle Memory. These are claimed to improve cognitive sharpness, prevent Alzheimer’s disease and dementia, reduce risk of car accidents as well as treat ADHD.
A consensus position expressed by the Stanford Center on Longevity explained the advertisements as follows (Max Planck Institute for Human Development and Stanford Center on Longevity, 2014; Underwood, 2014):
Consumers are told that playing brain games will make them smarter, more alert, and able to learn faster and better. In other words, the promise is that if you adhere to a prescribed regimen of cognitive exercise, you will reduce cognitive slowing and forgetfulness, and will fundamentally improve your mind and brain.
What did they conclude about brain games?
The consensus of the group is that claims promoting brain games are frequently exaggerated and at times misleading. Cognitive training produces statistically significant improvement in practiced skills that sometimes extends to improvement on other cognitive tasks administered in the lab. In some studies, such gains endure, while other reports document dissipation over time. In commercial promotion, these small, narrow, and fleeting advances are often billed as general and lasting improvements of mind and brain. The aggressive advertising entices consumers to spend money on products and to take up new behaviors, such as gaming, based on these exaggerated claims. As frequently happens, initial findings, based on small samples, generate understandable excitement by suggesting that some brain games may enhance specific aspects of behavior and even alter related brain structures and functions. However, as the findings accumulate, compelling evidence of general and enduring positive effects on the way people’s minds and brains age has remained elusive.
Some of the initial results are promising and make further research highly desirable. However, at present, these findings do not provide a sound basis for the claims made by commercial companies selling brain games. Many scientists cringe at exuberant advertisements claiming improvements in the speed and efficiency of cognitive processing and dramatic gains in “intelligence”, in particular when these appear in otherwise trusted news sources. In the judgment of the signatories below, exaggerated and misleading claims exploit the anxiety of adults facing old age for commercial purposes. Perhaps the most pernicious claim, devoid of any scientifically credible evidence, is that brain games prevent or reverse Alzheimer’s disease.
An interesting study by Shute, Ventura and Fengfeng (2015) compared brain training app Luminosity with the video game Portal 2. The researchers let 77 undergraduates play either Luminosity or Portal 2 for eight hours and then tested then on three separate cognitive skills: “problem solving, spatial skill, and persistence.” The results were consistent: Portal 2 players improved in all comparisons, whereas Luminosity players did not and the difference between the two reached standardized effect sizes between 0.42 to 0.6 in the favor of Portal 2. It seems that, from this small preliminary study, Luminosity cannot even outperform leisure gaming. How can it then “enhance our cognitive […] skills considerably”?
What about communication skills? Are we better at communicating thanks to smartphones? It is not obvious that this is true. For instance, there is even a popular notion called the iPhone Effect, which states that as one person brings out their smartphone, most other people do it as well, which spells the end of communication. It is a difficult question to research, but there are some preliminary studies here as well. Misra, Cheng, Genevie and Yuan (2016) paired up 100 people into groups of 2 and watched them have a short 10 minute conversation about something trivial or serious. They monitored the situation and took a note of if a smartphone was picked up or used and then asked participants questions about conversation quality and empathy. The results show that:
If either participant placed a mobile communication device (e.g., smartphone or a cell phone) on the table or held it in their hand during the course of the 10-min conversation, the quality of the conversation was rated to be less fulfilling compared with conversations that took place in the absence of mobile devices. The same participants who conversed in the presence of mobile communication devices also reported experiencing lower empathetic concern compared with participants who interacted without distracting digital stimuli in their visual field. The relationship between the presence of mobile devices and empathetic concern was more pronounced for participants who reported a closer relationship with each other compared with those who were less familiar with each other.
Although hardly conclusive, it replicates similar findings from a previous study by Przybylski and Weinstein (2013). Conclusions have to be tempered at this point, but it is pretty clear that it is not obvious that smartphones drastically improve communicative skills.
To sum up, the claim made by Häggström that “smartphones and similar electronic devices enhance our cognitive and communicative skills considerably” is not obvious and contradicted by some evidence. No evidence for this claim is presented by Häggström.
However, the problem does not end there. Häggström wrote something the sentence about smartphones improving cognitive/communicative skills:
The extended mind idea of Andy Clark and David Chalmers holds (analogously to Richard Dawkins’ extended phenotype) that our minds do not reside solely within our skulls or even our bodies, but extend further.
The mainstream scientific consensus position is mind-brain physicalism and that the mind is what he brain does. Therefore, it is absurd to claim that the mind somehow exists outside the brain or even outside the body. Does Häggström have any empirical evidence for this claim? Have neuroscientists or physicists detected brainless minds? It may very well be that humans have extended phenotypes that are dependent on genetic variants that influence personality traits, but this does not at all entail that the mind exists somehow outside the brain or body and certainly not independent of the brain. We will revisit the issue of mind-brain physicalism in several later sections.
Section XIII: Is autonomy the only bioethics game in town?
Although the word “dignity” is often abused by bioconservatives, and religious conservatives in general, it is a mistake to think that dignity or bioethics generally reduce to mere personal autonomy (p. 45). Not only because there are many situations where it is hard to distinguish genuine autonomy from its imposters, such as guilt, depression etc, but also because there are other bioethical principles that are important, such as nonmaleficence, beneficence and justice (Beauchamp and Childress, 2012). Even if you had personal autonomy, injustice and maleficence are going to be a threat to your person and likely subjective sense of dignity for many people.
Although the generally reply that there is no risk for e. g. genetically modified foods that do not exist for conventionally modified foods is valid, this does not work when it comes to genetic modification of humans, since we do not practice e. g. radiation breeding on humans and we know of plenty of human abuses that can occur (p. 46):
I don’t find those elements of deliberate design at all demeaning or robbing me of any status as an individual in my own right. It is not at all clear to me why I should feel any more traumatized by the “deliberate design” part of the process producing the person that I am, than by the “blind chance” part.
Imagine that a political leader, an organization or a parent decides to genetically modify children so that cells in some important part of their body express a long-acting toxin and that the child needs to get regular injections of a short-acting antitoxin to survive. This form of genetic slavery is also immune to defectors, since anyone who runs away will just die. To prevent external groups from amassing enough antitoxin, each group of people can get their own unique combination of toxin and antitoxin. To say that this would be no more demeaning than having type-I diabetes (which although differs in disease-mechanics, also require regular treatments) misses the point, since the abuses possible with genetic engineering (or any form of human enhancement of the transhumanist or posthumanity scale) is vastly larger and more horrendous, as it is easier and faster to explore phenotype (or design) space. The argument made by Häggström only works if all other factors are constant, but we know they are not.
Section XIV: Gross misunderstanding of heritability
Heritability is one of the most misunderstood concepts in all of biology. It is abused by both the political far left and far right, either to dismiss any genetic influence on behavior or to grossly mischaracterize human genetic diversity in order to prop up discriminatory claims about ethnic minorities. It suffers from a similar level of misunderstandings and misuse as concept such as theory, energy or GMO.
For a background on heritability and its many uses and abuses, read The Widespread Abuse of Heritability for a pedagogic introduction to heritability and its complexities as well as as well as these two articles exposing abuses of heritability. For relevant scientific review papers on the topic, see Visscher, Hill and Wray (2008) and Tenesa and Haley (2013). For modern heritability estimates for a wide range of human traits, see Polderman et al. (2015).
The definition of heritability that will be used in this critical review series is the following (from the article above on the widespread abuse of the concept): “the amount of phenotypic variation in a particular population in a given environment that can be attributed to the genetic variation in that specific population in that given environment, but not a measure of the relative influence of genes on the phenotype of an individual compared to environment and is not informative about between-group differences.”
How does Häggström use the heritability concept? He botches it and claims it is about what part of the variation in a population is determined by genes, rather than genetic variation (p. 58):
Shulman and Bostrom (2014) consider the case of cognitive ability. Far from being governed by a single gene, cognitive ability is influenced by many genes, as well as, of course, by environmental factors (nutrition, education and so on). Studies tend to show that a substantial part of the variation in IQ between individuals is caused by genetic factors.
Before we get into why Häggström has botched the heritability definition, notice the subtle shift from talking about cognitive ability to talking about IQ. Even if we assume that IQ is an uncontroversial and uncomplicated measure of intelligence (it isn’t), intelligence is only one aspect of cognitive ability.
So what is wrong with the definition proposed by Häggström? The take home message is this: heritability is about what proportion of the phenotypic variation can be explained by genetic variation. It is not what proportion of phenotypic variation that can be caused by genetic factors. So not only does Häggström misunderstand genetic variation as genetic factors, he also makes a subtle shift between “explained by” and “caused by”. Most people who have calculated a correlation coefficient and squared it to get the coefficient of determination understand the difference between percent variation in y explained by variation in x is not the same as what proportion of variation in y is caused by x (or even variation in x). Do we really need to talk about pirates and global warming or Firefox downloads and membership in Wicca?
There is also no context-free objective heritability value that tells you how much the phenotypic variation is explained by genetic variation, because this crucially depend on what population and environment being examined. The classic example is that while heritability for height in many western nations is about 0.8, it is about 0.65 in China. Obviously, height is not more genetically determined in, say, The U. S. than China. It is merely that environmental variation in e. g. nutrition explains much more of the variation in height in China than in the U. S. and the genetic variation explains less of the height variation. To drive the point home, some studies suggest that the heritability of e. g. IQ seems to also depend on socioeconomic status and age (Turkheimer et al, 2003; Plomin and Deary, 2015; McClearn et al, 1997), but the precise changes differs between studies.
So why did Häggström botch this concept? It seems that he took his definition from a Nature paper published in the late 1990s by Devlin, Daniels and Roeder (1997). It defined IQ heritability “the portion of a population’s IQ variability attributable to the effects of genes” (compare with the phrasing used by Häggström above). The authors attempt to support this claim by a reference to a textbook in quantitative genetics from the early 80s by Falconer (1981), which does use this phrasing in the first part of the chapter on heritability to give a simplified definition, but more correct definitions are given throughout the book, both earlier and later. This is yet another example of the sloppy scholarship carried out by Häggström in areas where he is out of his depths.
Häggström or his supporters might retort that simplifications has to be acceptable, especially in a short popular-level book. This is partly true, but using common and destructive misunderstandings of scientific concepts is not acceptable. Some “simplifications” simply do more damage that they help.
Section XV: Iterative embryo selection for IQ
Häggström moves on to write about the iterative embryo selection procedure for attaining individuals with incredibly high IQs compared with the general population as discussed by Shulman and Bostrom. This argument too suffers from their collective delusions about of heritability, but their broad ignorance of biology makes it much, much worse (p. 58, continuing directly from the last quote):
Shulman and Bostrom quote recent works suggesting that much of the variation can be attributed to a large number of common genetic variants which, taken one by one, have tiny effects. Detecting these individually, and quantifying the effects, will require very large studies matching genetic data against well-known correlates of IQ such as SAT scores and income, but such studies may be forthcoming. Once the results of such studies are available IVF may be taken to include a procedure where genomes from some number of n embryos are tested, and the one whose genome predicts the highest IQ is selected.
Shulman and Bostrom then make a model that predicts different IQ gains depending on the number of embryos in the starting pool. For instance, using 1000 embryos will give an IQ gain of 24 points. But they suggest combining this with the procedure of getting sperm and egg from the embryos while bypassing the adult stage of humans (p. 59):
In combination, these technologies allow for an iterative, procedure, where a number of embryos are genotyped and selected based on the desired genetic characteristic, the selected embryos are then used to produce sperms and eggs which are crossed to produce new embryos, and the procedure is repeated a number of times to obtain the desired genetic changes.
For ten iterations with ten embryos as starting material, they think this corresponds to an IQ gain of 130, which “would take us straight into posthumanity” (p. 59), although Häggström concedes that IQ is not validated at that scale and that the project would run into problems with inbreeding.
There are, however, more difficult problems that arises with this set up. The following discussion will restrict to three such problems (although there are more): artificial selection-based divergence of needs, antagonistic pleiotropy and missing heritability.
Artificial selection-based divergence of needs refers to the divergence between the needs of the target of selection and the needs of the entity doing the selection. The best example is e. g. cereal grain such as wheat. These have been modified for humans for thousands of years: the plant now grows shorter, puts more energy into seeds relative to the rest of the plant compared with before, eliminated seed spreading etc. These changes are for the benefit of the human, not for the plant. Quite the opposite, as the ability for the plant to survive and spread it seeds has been severely reduced. Other examples are how humans have artificially selected domesticated animals for meat production or pets such as cats and dogs. Those changes are for the benefit of humans, not the animals themselves. A similar divergence of needs can very well occur for iterated embryo selection.
Pleiotropy refers to the known fact that most genes have more than one effect, or influences more than one phenotypic trait (Lobo, 2008). The genotype-phenotype map is considerably more complex than one gene -> one protein -> one phenotypic trait. Instead, it should be thought of as a large complicated network where most genes influence several traits (pleiotropy), and most trait are influenced by many genes (polygenic trait). The belief that you can just stack as many gene variant associated with higher IQ together as you please without any other effects is wildly incompatible with basic knowledge of how genes genomes works. When such other effects are negative, it is called antagonistic pleiotropy.
It is true that many phenotypic traits, such as intelligence and height are influenced by very small contributions from many genes. However, there is an added complication. If you add up all the individual contributors from these genes (“additive genetic variation”), it will not sum up to the heritability as measured by twin and adoption studies. This heritability gap is called missing heritability. The size of this missing heritability depends on how much of the heritability for a given trait depends on additive genetic variability. The lesser the effect of additive genetic variation, the larger the missing heritability will be. Artificial selection of the type envisioned by Häggström and his cohorts, works primarily on additive genetic variation. The more complicated the genetic influence, the harder the artificial selection. This is evident from the so-called Breeder’s equation, that relates the response to selection to the heritability that only includes additive genetic variation (“narrow-sense heritability”). From the above quote, it is clear that they neglect this problem when they talk about identifying “these individually, and quantifying the effects […]”. So where does the missing heritability come from? In general, scientists do not know, but there are suggestions ranging from genetic interactions, population-specific variants and copy number variations (Eichler et al., 2010; Manolio et al., 2009; Zuk et al., 2012).
The paper cited by Häggström does not discuss any of these issues and generally not discuss any biological limitations or problems with their ideas (apart from e. g. inbreeding impacting technology adoption rates), which is typical of techno-optimist transhumanists in the existential risk movement.
Section XVI: Radical life extension
A common theme when discussing radical life extension is for transhumanists to cite the observed increase in average lifespan over the 20th century and make an arbitrary curve-fitting towards the future without understanding what is behind this increase (p. 64):
Another direction for human enhancement is life extension: to extend our life spans. Transhumanists tend to view this as very important, and wish not just for increasing life expectancy to 90 or 100 or 120 or even 200, but to postpone death indefinitely. They also tend to view research on life extension as vastly underprioritized. […] And we are making good progress: life expectancy in those countries where it is highest has, for the past 150 years, grown at a fairy steady pace of 3 months per year.
But this improvement in average life expectancy is not primarily because the probability of reaching old age given that you have reached adulthood. Rather, the probability of reaching adulthood has increased. With the benefits of clean water, vaccines, antibiotics as well as less mortality due to parasites and infectious diseases, people that would have died before, say, 15 years of age, have now survived. The National Institute of Aging (2015) explains it like this:
The victories against infectious and parasitic diseases are a triumph for public health projects of the 20th century, which immunized millions of people against smallpox, polio, and major childhood killers like measles. Even earlier, better living standards, especially more nutritious diets and cleaner drinking water, began to reduce serious infections and prevent deaths among children. More children were surviving their vulnerable early years and reaching adulthood. In fact, more than 60 percent of the improvement in female life expectancy at birth in developed countries between 1850 and 1900 occurred because more children were living to age 15, not because more adults were reaching old age. It wasn’t until the 20th century that mortality rates began to decline within the older ages. Research for more recent periods shows a surprising and continuing improvement in life expectancy among those aged 80 or above.
Thus, we cannot extrapolate the trend in such a naive way that transhumanists do when they talk about “making good progress” towards an average life expectancy of 200.
A key goal for transhumanists is to reduce or eliminate aging and they have a lot of ideas on how to do this. Unfortunately, because a lot of well-known transhumanists lack sufficient knowledge and understanding of biology, the results of their discussion resembles that of iterated embryo selection that was discussed earlier. Consider the following handwaving by Häggström (p. 64):
What Savulescu et al. mean by their 0.02% is research more narrowly on ageing, defined (roughly) as the accumulative damage to the body’s macromolecules, cells and tissues caused by “genomic instability, telomere attribution, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cells exhaustion, and altered intercellular communication” (López-Otín et al., 2013). It is a positive sign that the journal Nature devoted a special Outlook section in 2012 to the issues of ageing, life extension and gerontology, but they are likely to be less pleased by the very first sentence of the editorial: “Ageing is inevitable” (Grayson, 2012). The claim is unfounded, fatalistic, and probably false. None of the biophysical mechanisms listed by López-Otin et al. seem impossible in principle to arrest or reverse.”
The first confusion lies in the different models of ageing and the cause of ageing. The nine things mentioned by López-Otin and colleagues are not the cause of aging, but rather the hallmarks of aging. Cellular senescence is not the cause of aging, it is aging (and that which causes cellular senescence causes aging). Of course, genomic instability occurs in other things besides aging, but it is nonetheless a hallmark of aging. This is all obvious from not only the title of the paper (“The Hallmarks of Aging”) and in the abstract from which the quote comes from (López-Otín, 2013):
This Review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication.
The definition proposed by Häggström, the wear-and-tear idea, is actually one of the models of why aging happens (from the error theory, the other being the programmed theory), not the definition of aging (Jin, 2010).
So is the claim that aging is inevitable “unfounded, fatalistic, and probably false” because “[n]one of the biophysical mechanisms listed by López-Otin et al. seem impossible in principle to arrest or reverse”. From the perspectives of basic physics, aging is inevitable. The laws of thermodynamics cannot be violated no matter how hard we wish to stop aging. Even if you were to create a system that “arrest” or “reverse” this or that cause or consequence of aging, the system itself will be affected by the laws of thermodynamics and decay over time. Calling this “fatalistic” is not an argument, but merely a signifier that this fact is emotionally troubling for Häggström.
The example that Häggström refers to in footnote 149 on the same page is that of the biologically immortal jellyfish Turritopsis dohrnii that starves off aging through a process called transdifferentiation, whereby differentiated cells of one type changes into the differentiated cells of another cell type. There is one clear way in which we can change humans to be able to use this procedure and evolution has done it for us. We simply go back, step-by-step in the evolution of humans to the last common ancestor of humans and Turritopsis and then go forward, step-by-step, to the modern Turritopsis. But turning humans into jellyfish is probably not what Häggström had in mind. Instead, the general idea is probably to use the system in jellyfish or use insights from the jellyfish to make a corresponding system in humans. However, this is likely going to be a completely failure because of historical constraints during animal evolution. As an example, trees cannot get metastatic cancer because cells have cell walls and so does not move. However, cell movements is crucial for animal development, so even if you managed to give human cells cell walls and thus immobilizing them, you would screw up development to such an extent that it would be lethal. Trees also does not have tissues where the cancer problem would be much worse compared with others (e. g. brains) and if you chop up a tree part, it can grow out a new one, which is not the case for humans (Doonan and Sablowski, 2010). Humans are trees are more distantly related, of course, but the earliest fossils of Cnidarians are from the Precambrian at around 570 million years ago (Chen et al., 2000).
Despite the shaky scientific grounds for the transhumanist obsession with longevity, some of them go to extreme lengths to attempt to achieve it, including using pseudoscientific alternative medicine (p. 81, footnote 190), which includes taking 250 supplement pills and several injections every week.
Section XVII: The mind as a biological phenomenon
The many errors Häggström has about the mind was briefly mentioned in Section XII, but it is in this section they will be discussed in more detail. Häggström outright dismisses the objection by Massimo Pigliucci that consciousness is a biological phenomenon and that it is a mistake to talk about consciousness robots as obvious if scientists do not have a proper neurobiological theory of the (alleged) special case of human brains.
So what is the reply given by Häggström? It boils down to the ignorant assertion that the mainstream scientific position on the mind as a biological phenomena is just a correlational fallacy (p. 69):
But this merely presupposes what Pigliucci knows of one example of a conscious entity, namely himself, and he has a reasonable case for assuming that most other humans are conscious too, and also that in all these cases consciousness resides (at least to a large extent) in the brain. Since all these brains are neurobiological entities, isn’t that just what we need for the claim that a theory of consciousness needs to be a neurobiological? Well, no, because being neurobiological entities is not the only thing that these brains have in common. They are also, e. g., material objects, and they are computing devices. Pigliucci thinks that being a neurobiological entity is the relevant property around which a decent theory of consciousness to be centered. Other philosophers (panpsychists) think that being a material object is the relevant property, and yet others (supporters of CTOM) think that being a computational device is the relevant property.
But the evidence for mind-brain physicalism is not that all known cases of minds are associated with brains, ergo it must neurobiological. Instead, it draws on a rich diversity of scientific evidence from developmental biology (brain development affects cognitive development in predictable ways), evolutionary biology (differences in cognitive ability between species with different kinds of brains), medicine and neurosurgery (lesions and drugs produce predictable changes in the mind based on their physical effects) as well as psychological research. This is evident from reading any neuroscience textbook, such as Bear, Connors and Paradiso (2015).
There is also negative evidence against panpsychism and CTOM. This is because there has been no identification of what property of matter or computation itself (divorced from the brain) would generate the mind or any of its properties. In particular, panpsychism contradicts all of physics, which states that the basic elements of the world is matter and energy. There has never been found any psychic component on the level of quarks and gluons and such notions are generally considered to be pseudoscience (Stenger, 2009). In the end, it is not an argument to say that panpsychists disagree, just like it is not an argument to say that creationists disagree with evolution. It just does not matter at all.
In contrast, we know a ton about how the brain generates the mind and there is, in fact, several scientific and medical disciplines devoted to it, such as neuroscience, neurology and neuropsychology. To say that this scientific edifice is merely a correlational fallacy is barking batshit.
Section XVIII: The Chinese Room argument as a fallacious intuition pump
Häggström spends several pages discussing the (in)famous Chinese Room argument by philosopher Jon Searle (primarily pp. 69-71 and pp. 123-125) and concludes that it is a false, primarily by aligning himself with the system’s reply given by Hofstadter and Dennett originally deployed in the early 80s. It is a good discussion of the argument and the subsequent exchange. I agree that the Chinese Room argument is fatally flawed, but go further than that. I align myself with the objection given by Carrier (2005, pp. 139-144), which says that the argument is merely a poorly thought-out intuition pump.
Had Searle properly carried out the thought experiment, he would have known that the set-up just does not work. In order for it to work, the rule book has to have a large number of features: memory, being able to change, accumulate knowledge of Chinese and itself, spontaneity, creativity, learning etc. This is because you can, as the person outside the room, easily invent input that would reveal the fact that the Chinese room did not contain a person understanding Chinese (“ask me something new”, “what was the last thing I asked” and so on). Thus, when you implement everything that the Chinese room would need to successfully complete its tasks (often understood to be fooling an external sophisticated interlocutor or reproducing all properties of a person understanding Chinese), given the truth of CTOM, you have artificial intelligence. The rule book would understand Chinese. Thus, the Chinese Room is no threat to CTOM and only appears to be a threat due to the lack of imagination of the person making the argument.
Section XIX: Destructive teleportation and mind uploading: surviving the physical destruction of the body?
It is here where Häggström completely goes off the rails. He suggests that humans can survive the physical destruction of their bodies during a process known as destructive teleportation. This involve scanning a person (the body being destroyed in the process) and the information being sent via the Internet and remade into a human again somewhere else that is so similar that he or she cannot easily be distinguished from the previous person (p. 72).
Häggström invites us to imagine a future where destructive teleportation is common. He contemplates traveling by air or by destructive teleportation for an important meeting later in the week. But he is initially concerned that he might die and that destructive teleportation really just destroys his body and makes a copy of him somewhere else in the world. So he asks people who have undergone the procedure, who of course tell him that it is no problems. However, he gets the sinking revelation that this is exactly what they would have said if they were just a copy and the real person was dead.
He thinks this question “seems really hard (perhaps impossible?) to answer empirically”, and propose that we “try to attack it with a bit of analytic philosophy” (p. 73). Häggström outlines the definition of two kinds of survival (p. 73):
σurvival: I σurvive if, on Thursday, there exists a person who has the same personality traits, the same memories, and so on, as I have today (allowing for some wiggling corresponding to what is considered normal changes during the course of a few days).
Σurvival: I Σurvive if (a) I σurvive until Thursday, and (b) whatever extra property that is needed for the guy in New York to really be me (as opposed to just a copy) holds.
Häggström fails to come up with a plausible property for what this can be, and thus concludes that the idea of Σurvival must be rejected in favor of σurvival due to Occam’s Razor, since “scientific theories ought to be as simple as the evidence admits” (p. 73).
This, however, completely misses the point. This is because it confuses two different meanings of the word “same”. If I say we are wearing the same shirt, I might mean that each one of us is wearing a exemplar the same basic T-shirt of the same color, size and model. However, I might also mean that we are both wearing the same shirt in the sense that two bodies are now inside the same piece of fabric. Although this is not a common distinction made in English, it is a distinction that occurs in Swedish. The former kind of sameness is called “likadan”, and the latter is called “samma”.
It is also fallacious to attempt to apply Occam’s Razor in this situation. This is because the evidence for the two scenarios is not of similar amount and strength. Quite the opposite. The evidence that you do not survive the physical destruction of your body is overwhelming, not only from neuroscience and mind-body physicalism, but also because there is not a single example of someone who has gotten their entire body destroyed, yet survived. Some believers in the paranormal insist that people survive as spirits, ghosts poltergeists after they have died or that their soul goes to heaven (or hell), but this has never ever been corroborated by robust scientific research. For all intents and purpose, such stance (including the one presented by Häggström) is pseudoscientific nonsense. The evidential situation is clear.
So the basic reply to Häggström is that this question can certainly be determined empirically and that it has been shown by direct and indirect evidence that you do not survive the physical destruction of your body. This is true regardless of idle philosophizing over different meanings of the word “survival”. In science, we know reasonable well what that term refers to. For individual cells, a cell that has a ruptured membrane does not survive. For humans, surviving means not being brain dead. There are, of course, complications like usual in biology, but for the complexity level we are currently discussing, this is an acceptable resolution.
Häggström discussed one proposal for this added feature, namely continuity of my body’s trajectory through space-time (CBTST), but does not understand why it is crucial to his identity. But that is not the point. CBTST is just a heuristic for keeping track of what is what. Imagine that you see two exemplars of the same basic T-shirt on a bed (one to the left, and the other to the right) that on your level appears indistinguishable. A door to the room is closed with you outside the room, and another person moves the two T-shirts around the room so that both are at different places compared with before. The door opens again, and you see the two T-shirts again. Which is which? Did the one to the left move to the bookcase, or was that the one who was originally on the right part of the bed? You honestly confess that you have not the slightest idea, but if you are given information about the CBTST, you instantly know. So CBTST is merely a psychological heuristic for keeping track of things.
One might imagine tagging a person with a radioactive substance (say a radioactive phosphate in some place in the body) before he or she goes through with the destructive teleportation. If the destructive teleportation does not care about the atom-by-atom identity (remember that Häggström allowed some leeway) and instead does it on a higher level of analysis, say, molecules or concentrations, the teleported copy will lack this radioactive probe. Thus, with the help of a Geiger counter, we can distinguish the original from the copy. The radioactive tag is certainly irrelevant to the personality of the teleported copy, but this is about telling them apart, not about the psychological aftermath. Häggström confuses identity as in personal identity with identity of objects more broadly.
Häggström goes even further than merely suggesting that you survive the destruction of your own body, but that if you perform a non-destructive teleportation, you can now control two separate bodies (p. 74):
[…] if σsurvival is all there is to survival (or to “preservation of identity”), then there is no particular reason to hold that I cannot simultaneously survive in two bodies.
What does it mean to survive in two bodies? Has your consciousness split? Can you control both bodies at the same time? Is there a lag or does the communication occurs faster than the speed of light? How does the communication occur? With psychic powers? If you control another body simply because you are the same as it, then there should be a dose-response relationship. Identical twins should be able to control the other twin to a much larger degree that an arbitrarily selected person can control another, but this has never been demonstrated. So if there is no dose-response relationship, why should we expect sufficient identity to enable this power?
Häggström then misunderstands a key principle of particle physics and reductionism generally (p. 74):
But that just brings us back to the question about just why CBTST is important for survival. In the absence of such an explanation, we probably ought to reject the relevance of CBTST, not just by appeal to Occam’s razor, but also because fundamental physics doesn’t seem to support it. Elementary particles do not have identities, making claims like “these electrons come from the original body, but those other ones do not” literally nonsensical, and since our bodies are made up of elementary particles, postulating an asymmetry between the two bodies, where one is the original and the true inheritor of personal identity, while the other one is merely a copy, seems unfounded.
It is true that if I present Häggström with two electrons, one that I isolated from person X and the other form person Y, Häggström cannot, even in principle, tell which came from which. This is because all electrons are identical. However, his inability does not change past events, namely that they were, in fact, isolated from different persons. There is nothing nonsensical with this and it is also true on the level of atoms and molecules. A molecule of fructose from a conventional crop cannot be distinguished from a molecule of fructose from a genetically modified (GM) crop. But this does not make it nonsensical to say that this bowl of fructose came from conventional crop and this other bowl of fructose came from GM crops. That is just a fact of history, and unless Häggström wants to propose retrograde causation where future events influences past events, he is stuck with this fact. Basically, it involves the confusion between the identity of elementary particles, and their histories.
Häggström abuses this misunderstanding even further by arbitrarily scaling up to humans. This is a mistake because even if you could not distinguish one fundamental particle from another, you can certainly distinguish a collection of fundamental particles from another collection of fundamental particles. As Häggström has allowed some leeway in that the copy and the original can differ by as much as a person does between days, we can also distinguish them by this.
Häggström later appeals to the fact that there is change at low levels of analysis (p. 75): atoms and molecules change, cells divide and die and the cytoskeleton is remodeled. But all of this is irrelevant since brain function does not exist at that level of analysis. Killing a couple of cells do not interfere with cognitive faculties, but killing larger parts of the brain does.
Both the ideas of destructive teleportation and mind uploading rely on the erroneous assumption that scanning is realistic (p. 76). In reality, scanning involves a trade-off between resolution and time. The more resolution you want, the longer time you have to spend scanning. Häggström primarily relies on destructive scanning that slices up the brain into thin sections. Yet this procedure kills the brain and the cells inside, so the data in your computer will be that of dying cells and a dying brain. The longer scanning takes, the more dead everything will get. As we will see in the section on cryogenics, cryogenic preservation will not help as these chemicals fixate the tissue, basically keeping ultrastructure while destroying chemistry and physiology. That is very far away from the wishful thinking that it can scan enough information to get everything from functional brain chemistry to your personality.
Häggström briefly mentions an idea for non-destructive scanning that uses nanobots to map the atoms and the molecules in the brain. Despite the fact that the brain is not static and that these nanobots are unlikely to work (see later parts of this articles series), they would also be very big in comparison to single molecules or atoms that they just would not be able to fit through all of the small nooks and crannies of the brain without impact.
Section XX: The cryonics delusion
The last part of the third chapter on human enhancement delves into the subject of human cryonics. Like uploading minds to computer hardware, cryonics represents another idea on how humans can defeat ageing and death and extend their lives substantially. The basic idea is that you freeze the human body, either just before death or a short while after death, keep it in storage for hundreds or thousands of years until medical research has advanced so much that it can cure complicated medical problems that has brought you to the brink of death, or even cure death.
Needles to say, this is a science fiction idea fraught with problems. When you freeze living tissue rapidly, ice crystals typically form and kill cells. You can freeze populations of e. g. bacteria, yeast and some worms, store them in a -80 °C freezer, thaw them and have them “come back to life”, so to speak. But this only works because all you need are a relatively few members of that population, compared with the total population size that was frozen in order to continue the research in question. It does not matter if, say, 85% of the bacteria died, since you still have those 15% to work with, and bacteria multiple and double quickly in comparison with other organism.
Häggström seems aware of this problem (p. 82):
A major complication, however, is that ice formation in the freezing process threatens to crush the cells of the body, so a key step in the cryonics procedure is so-called vitrification — making sure that the freezing takes place without crystal formation. This is achieved by, prior to freezing, washing out the subjects blood and replacing most of the body water with a cryoprotectant mixture preventing ice formation.
This might seem convincing, but this assumes that the replacing of water and blood by cryoprotectant mixtures even work without adding a literally fatal increase in processing time from receiving the near-dead body to it being ready to be stored at -196 °C.
Another crux is that they have merely replaced one massive problem, namely ice crystal formation, with another massive problem. When you infuse large sections of the body, or just the brain, with cryoprotectant mixtures e. g. glycerol, dimethylsulfoxide (DMSO), propylene glycol, glutaraldehyde etc., you engage in a procedure called chemical fixation. Although you may preserve the ultrastructure, you will destroy most of the chemistry and physiology. Brain structure is important, but it is far from enough, because the function of the brain results from a vital interplay between intracellular chemistry (second messengers, hormones, neurotransmitters etc.) and structure (synapses and dendrites). Some parts of the cryonics movement implicitly understand this because they admit that some of their techniques involve “glutaraldehyde-based fixative” leading to an “aldehyde-preserved brain” (McIntyre and Fahy, 2015). In sum, removing water removes a lot of water soluble substances as well, and the cryoprotectants have large and decisive impacts on chemistry and physiology. This is obvious to anyone who has ever studied ultrastructure of an organ, such as a brain, in a light microscope.
The only source Häggström cites for the scientific problems with cryogenics is Best (2008). This paper does discuss cryoprotectant toxicity, but completely ignores the problem with chemical fixation, although silently admitting this by mentioning the preservatives envisioned. More disturbingly, Best flatly rejects the chemistry and physiology issue, and claim that the function of the brain is mainly related to structure:
The fact that complete absence of electrical activity in the brain does not prevent full neurological recovery supports the proposition that the ultimate basis of consciousness is structural rather than dynamic and can therefore be preserved at cryogenic temperatures.
The crucial mistake here is the belief that the only other thing going on in the brain besides structure is electric activity. This betrays a deep ignorance about neuroscience. To put it simple, electrical activity results from chemical processes, and suspending these chemical processes (without washing them out as is done during fixation) in way that reduce electrical activity does not need to preclude recovery.
If this is not enough evidence, there are countless of counterexamples to show that it is not mere structure that is the ultimate basis of the mind or any particular cognitive ability. Anesthesia, hormones, neurotransmitters etc. generally do not work on the level of brain ultrastructure, but biochemistry, something that would be impossible if the “ultimate basis” was merely structure. This, yet again, highlights the supreme ignorance of basic biology and chemistry of many parts of existential risk movement.
Even if you could get around all of these problems, there is nothing that says that these companies will be financially viable for long enough to reach the era where you can cure people inches from death from severe damage or disease or that such a reversal is possible, let alone the possibility of curing death. Then a person who paid a ton of money for cryogenically freezing the body or the head will thaw, and, eventually, decompose.
Despite all of these problems, Häggström considers the prediction that we will look upon cryogenics as vital as freeing slaves or stopping violent misogyny to be a “wide-open question” (p. 83), while at the same time contradicting himself by suggesting that cryogenics has a “small success probability” (p. 82). He then succumbs to advocating Pascal’s Wager, whereby the small probability of cryonics working “has to be weighed against the huge potential gain”, thereby contradicting himself again, because later in the book, he explicitly claim that he is not advocating Pascal’s Wager-like arguments (p. 240-244).
A common retort throughout the book is that skeptics have not conclusively disproved this or that science fiction fantasy, so therefore it is defensible to entertain it. But the burden of evidence is not on the skeptic, and the skeptic does not need to show that all aspects of something is literally physically impossible for the skeptical perspective to win out. All that is required for this is to show that the evidence is insufficient in favor of it, or that the evidence is against a position. Otherwise you can defend the belief in the existence of Bigfoot, mermaids or Russell’s teapot with the same deceptive line of argument.
Alonso, J., Angermeyer, M. C., Bernert, S., Bruffaerts, R., Brugha, T. S., . . . Vollebergh, W. A. M. (2004). Disability and quality of life impact of mental disorders in Europe: results from the European Study of the Epidemiology of Mental Disorders (ESEMeD) project. Acta Psychiatrica Scandinavica, 109, 38-46.
Beauchamp T, Childress J. (2012). Principles of Biomedical Ethics, 7th Edition. New York: Oxford University Press.
Beidel D. C., Turner S. M., Morris T. L. (1999). Psychopathology of childhood social phobia. J Am Acad Child Adolesc Psychiatry. 38(6), 643–650.
Bear, M. F., Connors, B. W., Paradiso, M. A. (2015). Neuroscience: Exploring the Brain. 4th Edition. Alphen aan den Rijn: Wolters Kluwer.
Berger, B. E., Navar-Boggan, A. M., & Omer, S. B. (2011). Congenital rubella syndrome and autism spectrum disorder prevented by rubella vaccination – United States, 2001-2010. BMC Public Health, 11(1), 1-5.
Best, B. P. (2008). Scientific Justification of Cryonics Practice. Rejuvenation Research, 11(2), 493-503.
Burstein, M., Ameli-Grillon, L., & Merikangas, K. R. (2011). Shyness Versus Social Phobia in US Youth. Pediatrics, 128(5), 917-925.
Carrier. R. (2005). Sense and Goodness Without God: A Defense of Metaphysical Naturalism. Bloomington: AuthorHouse.
CDC. (2015). Epidemiology and Prevention of Vaccine-Preventable Diseases. Hamborsky J, Kroger A, Wolfe S, eds. 13th ed. Washington D.C. Public Health Foundation. (section on rubella)
Chavira D. A., Stein M. B., Malcarne V. L. (2002). Scrutinizing the relationship between shyness and social phobia. J Anxiety Disord. 16(6). 585–598.
Chen, J.-Y., Oliveri, P., Li, C.-W., Zhou, G.-Q., Gao, F., Hagadorn, J. W., . . . Davidson, E. H. (2000). Precambrian animal diversity: Putative phosphatized embryos from the Doushantuo Formation of China. Proceedings of the National Academy of Sciences, 97(9), 4457-4462.
Devlin, B., Daniels, M., & Roeder, K. (1997). The heritability of IQ. Nature, 388(6641), 468-471.
Doonan, J. H., & Sablowski, R. (2010). Walls around tumours — why plants do not develop cancer. Nat Rev Cancer, 10(11), 794-802.
Eichler, E. E., Flint, J., Gibson, G., Kong, A., Leal, S. M., Moore, J. H., & Nadeau, J. H. (2010). Missing heritability and strategies for finding the underlying causes of complex disease. Nat Rev Genet, 11(6), 446-450.
Essau C.A. , Conradt J., Petermann F. (1999). Frequency and comorbidity of social phobia and social fears in adolescents. Behav Res Ther. 37(9), 831–843.
Fehm L., Pelissolo A., Furmark T., Wittchen H. U., (2005). Size and burden of social phobia in Europe. Eur Neuropsychopharmacol. 15(4), 453–462
Falconer, D. S. (1981). Introduction to Quantitative Genetics. New York: Longman.
Gerber, J. S., & Offit, P. A. (2009). Vaccines and Autism: A Tale of Shifting Hypotheses. Clinical Infectious Diseases, 48(4), 456-461.
Heiser N. A. , Turner S. M., Beidel D. C., Roberson-Nay R. (2009) Differentiating social phobia from shyness. J Anxiety Disord. 23(4). 469–476.
Heiser N. A., Turner S. M., Beidel D. C. (2003). Shyness: relationship to social phobia and other psychiatric disorders. Behav Res Ther. 41(2). 209–221.
Jin, K. (2010). Modern Biological Theories of Aging. Aging and Disease. 1(2), 72-74.
Kessler R. C. (2003). The impairments caused by social phobia in the general population: implications for intervention. Acta Psychiatr Scand. (417), 19–27.
Lobo, I. (2008). Pleiotropy: One Gene Can Affect Multiple Traits. Nature Education 1(1):10.
López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013). The Hallmarks of Aging. Cell, 153(6), 1194-1217.
Manolio, T. A., Collins, F. S., Cox, N. J., Goldstein, D. B., Hindorff, L. A., Hunter, D. J., . . . Visscher, P. M. (2009). Finding the missing heritability of complex diseases. Nature, 461(7265), 747-753.
Max Planck Institute for Human Development and Stanford Center on Longevity. (2014).
A Consensus on the Brain Training Industry from the Scientific Community (cache). Accessed: 2016-03-29.
Mayo-Wilson, E., Dias, S., Mavranezouli, I., Kew, K., Clark, D. M., Ades, A. E., & Pilling, S. Psychological and pharmacological interventions for social anxiety disorder in adults: a systematic review and network meta-analysis. The Lancet Psychiatry, 1(5), 368-376.
McClearn, G. E., Johansson, B., Berg, S., Pedersen, N. L., Ahern, F., Petrill, S. A., & Plomin, R. (1997). Substantial Genetic Influence on Cognitive Abilities in Twins 80 or More Years Old. Science, 276(5318), 1560-1563.
McIntyre, R. L., & Fahy, G. M. (2015). Aldehyde-stabilized cryopreservation. Cryobiology, 71(3), 448-458.
Merikangas, K. R., Ames, M., Cui, L., Stang, P. E., Ustun, T. B., Von Korff, M., & Kessler, R. C. (2007). The impact of comorbidity of mental and physical conditions on role disability in the US adult household population. Arch Gen Psychiatry, 64(10), 1180 – 1188.
Misra, S., Cheng, L., Genevie, J., & Yuan, M. (2016). The iPhone Effect: The Quality of In-Person Social Interactions in the Presence of Mobile Devices. Environment and Behavior, 48(2), 275-298.
Morrison, A. S., & Heimberg, R. G. (2013). Social Anxiety and Social Anxiety Disorder. Annual Review of Clinical Psychology, 9(1), 249-274.
National Institute of Aging. (2015). Living Longer: Accessed: 2016-04-04.
Offit, P. A., Quarles, J., Gerber, M. A., Hackett, C. J., Marcuse, E. K., Kollman, T. R., . . . Landry, S. (2002). Addressing Parents’ Concerns: Do Multiple Vaccines Overwhelm or Weaken the Infant’s Immune System? Pediatrics, 109(1), 124-129.
Plomin, R., & Deary, I. J. (2015). Genetics and intelligence differences: five special findings. Mol Psychiatry, 20(1), 98-108.
Polderman, T. J. C., Benyamin, B., de Leeuw, C. A., Sullivan, P. F., van Bochoven, A., Visscher, P. M., & Posthuma, D. (2015). Meta-analysis of the heritability of human traits based on fifty years of twin studies. Nat Genet, 47(7), 702-709.
Przybylski, A. K., & Weinstein, N. (2013). Can you connect with me now? How the presence of mobile communication technology influences face-to-face conversation quality. Journal of Social and Personal Relationships, 30(3), 237-246.
Ranta K., Kaltiala-Heino R., Rantanen P., Marttunen M. (2009). Social phobia in Finnish general adolescent population: prevalence, comorbidity, individual and family correlates, and service use. Depress Anxiety. 26(6), 528–536.
Spence SH, Donovan C, Brechman-Toussaint M. (1999). Social skills, social outcomes, and cognitive features of childhood social phobia. J Abnorm Psychol. 108(2), 211–221.
Shute, V. J., Ventura, M., & Ke, F. (2015). The power of play: The effects of Portal 2 and Lumosity on cognitive and noncognitive skills. Computers & Education, 80, 58-67.
Stein M. B. (1999). Coming face-to-face with social phobia. Am Fam Physician. 60(8), 2247.
Stenger, V. (2009). Quantum Gods: Creation, Choas, and the Search for Cosmic Cnsciousness
Tenesa, A., & Haley, C. S. (2013). The heritability of human disease: estimation, uses and abuses. Nat Rev Genet, 14(2), 139-149.
Turkheimer, E., Haley, A., Waldron, M., D’Onofrio, B., & Gottesman, I. I. (2003). Socioeconomic Status Modifies Heritability of IQ in Young Children. Psychological Science, 14(6), 623-628.
Underwood, E. (2014). Neuroscientists speak out against brain game hype. ScienceInsider.
Visscher, P. M., Hill, W. G., & Wray, N. R. (2008). Heritability in the genomics era — concepts and misconceptions. Nat Rev Genet, 9(4), 255-266.
Vyse, S. (2015). Neuro-Pseudoscience. The Committee for Skeptical Inquiry. Accessed: 2016-03-29.
Wittchen H. U., Fehm L. (2003). Epidemiology and natural course of social fears and social phobia. Acta Psychiatr Scand Suppl. (417). 4–18.
Wittchen H.U., Stein M.B., Kessler R.C. (1999). Social fears and social phobia in a community sample of adolescents and young adults: prevalence, risk factors and co-morbidity. Psychol Med. 29(2), 309–323.
Zuk, O., Hechter, E., Sunyaev, S. R., & Lander, E. S. (2012). The mystery of missing heritability: Genetic interactions create phantom heritability. Proceedings of the National Academy of Sciences, 109(4), 1193-1198.
12 thoughts on “Harbingers of Doom – Part II: Anti-Psychiatry and Teleportation”
Since the author of the book being critically investigated in this series has expressed concern (and here I am being a tad tongue-in-cheek) that this series had run out of steam.
In response, I have now increased the number of installments planned (one per chapter instead of one per two chapters as originally planned) and also increase the depth of the analysis for each chapter. This second part ended up being about 11k words compared with about 5k words for the first part and it also contains considerably more references to the scientific literature backing up crucial arguments.
I think people are really desperate not to die. The idea of one day, literally not existing is pretty terrifying to people, and I don’t think that’s something we could easily change.
You bring up a good point. Perhaps transhumanism taps into the same psychological needs and fears about the end of life that religion does.
That makes sense.
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A new study with impact on the claim that smartphones improve cognitive skills was recently published in PNAS. It does not look good for the claim made by Häggström that “Smartphones and similar electronic devices enhance our cognitive and communicative skills considerably”.
Foroughi, C. K., Monfort, S. S., Paczynski, M., McKnight, P. E., & Greenwood, P. M. (2016). Placebo effects in cognitive training. Proceedings of the National Academy of Sciences.
So a lot of these brain training apps might be influenced by placebo effects, not actual stable improvements.
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