Does Self-Awareness Require a Complex Brain?

Aye, yai, yai. Here we go again…which definitions of consciousness and self-awareness are being discussed?

(SciAm Article after sample definitions) NOTE: The media function on my page is screwed up… can’t size or delete some images – you’ll have to search out “brain parts images” for yourself. 

From: Home » Positive Psychology Articles » What is Self-Awareness and Why Does it Matter? 

So What is Self-Awareness Exactly? / The psychological study of self-awareness can be first traced back to 1972 when Psychologists Shelley Duval and Robert Wicklund developed the theory of self-awareness.

They proposed that: “when we focus our attention on ourselves, we evaluate and compare our current behavior to our internal standards and values. We become self-conscious as objective evaluators of ourselves.”

In essence, they consider self-awareness as a major mechanism of self-control.

Sounds pretty good; a state of “owning” one’s thoughts and intentions and the recognition that one’s behavior is often not congruent with these “values”. NOT the simple act of “mirror recognition” which belongs to the brain’s “visual system”. 

Basic physical def: When you are awake and aware of your surroundings, that’s consciousness. (That “jives with” mirror recognition -type awareness as a property of an active sensory system). 

The most influential modern physical theories of consciousness (there are supernatural theories, of course) are based on psychology and neuroscience. Theories proposed by neuroscientists such as Gerald Edelman and Antonio Damasio, and by philosophers such as Daniel Dennett, seek to explain consciousness in terms of neural events occurring within the brain. Consciousness – Wikipedia

It’s impossible here to present the long-standing and ever-growing confusion over the modern “concepts” of consciousness. It’s a word that is used for the most part, without any meaning whatsoever. Technology also has entered the arena. 

My own idea is this… What we commonly refer to as “being consciousness” is a social interaction, an act of Co-consciousness; the product of language : “In Western cultures verbal language is inseparable from the process of creating a conscious human being.” see previous post: https://aspergerhuman.wordpress.com/?p=9198&preview=true

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Article: https://blogs.scientificamerican.com/brainwaves/does-self-awareness-require-a-complex-brain/

By Ferris Jabr on August 22, 2012

The computer, smartphone or other electronic device on which you are reading this article has a rudimentary brain—kind of.* (uh-oh. Pop-Sci) It has highly organized electrical circuits that store information and behave in specific, predictable ways, just like the interconnected cells in your brain. (No) On the most fundamental level, electrical circuits and neurons are made of the same stuff—atoms and their constituent elementary particles—but whereas the human brain is conscious, manmade gadgets do not know they exist. (WOW! NT nonsense!) Consciousness, most scientists argue, (made up assertion) is not a universal property of all matter in the universe. Rather, consciousness is restricted to a subset of animals with relatively complex brains. The more scientists study animal behavior and brain anatomy, however, the more universal consciousness seems to be. (Confused yet?) (Mirror awareness is a VISUAL phenomenon)

A brain as complex as the human brain is definitely not necessary for consciousness. (!!!)

On July 7 this year, a group of neuroscientists convening at Cambridge University signed a document officially declaring that non-human animals, “including all mammals and birds, and many other creatures, including octopuses” are conscious. (Well, that’s certainly proof that some poorly-defined experiential state in humans is a “thingy” also “in mammals and birds, and many other creatures, including octopuses” !!)

Humans are more than just conscious—they are also self-aware. Scientists differ on the difference between consciousness and self-awareness, (those imaginary Science Elves again, messing us up with “tricky” non specific definitions of “consciousness and self-awareness”) but here is one common explanation: Consciousness is awareness of one’s body and one’s environment; self-awareness is recognition of that consciousness—not only understanding that one exists, but further understanding that one is aware of one’s existence. Another way of thinking about it: To be conscious is to think; to be self-aware is to realize that you are a thinking being and to think about your thoughts. Presumably, human infants are conscious—they perceive and respond to people and things around them—but they are not yet self-aware. In their first years of life, infants develop a sense of self, learn to recognize themselves in the mirror (a phenomenon of the SENSORY SYSTEM) and to distinguish their own point of view from other people’s perspectives.

Notice how a lack of distinction / definition of terms leads to the inevitable “linear-causal-but-hierarchical arrangement of “notions” assumed to be correct (that is, how the brain works as an “isolated” command center, but which are “phrases” merely strung together by “social habit”.

Numerous neuroimaging studies have suggested that thinking about ourselves, recognizing images of ourselves and reflecting on our thoughts and feelings—that is, different forms self-awareness—all involve the cerebral cortex, the outermost, intricately wrinkled part of the brain. The fact that humans have a particularly large and wrinkly cerebral cortex relative to body size supposedly explains why we seem to be more self-aware than most other animals. (This pop-sci blah, blah is unforgivable in a “science” article. 

One would expect, then, that a man missing huge portions of his cerebral cortex would lose at least some of his self-awareness. Patient R, also known as Roger, defies that expectation. Roger is a 57-year-old man who suffered extensive brain damage in 1980 after a severe bout of herpes simplex encephalitis—inflammation of the brain caused by the herpes virus. The disease destroyed most of Roger’s insular cortex, anterior cingulate cortex (ACC), and medial prefrontal cortex (mPFC), all brain regions thought to be essential for self-awareness. About 10 percent of his insula remains and only one percent of his ACC.

Note that “self-awareness” in this article is the “you are awake and aware of your surroundings” definition, and not the Duval, Wickland definition.

Roger cannot remember much of what happened to him between 1970 and 1980 and he has great difficulty forming new memories. He cannot taste or smell either. But he still knows who he is—he has a sense of self. He recognizes himself in the mirror and in photographs. (This would indicate that his VISUAL system / memory is intact) To most people, Roger seems like a relatively typical man who does not act out of the ordinary. (That’s NTs for you; minimal evidence, inattentional blindness, social convention = “must be a normal person”) LOL

Carissa Philippi and David Rudrauf of the University of Iowa and their colleagues investigated the extent of Roger’s self-awareness in a series of tests. In a mirror recognition task, for example, a researcher pretended to brush something off of Roger’s nose with a tissue that concealed black eye shadow. 15 minutes later, the researcher asked Roger to look at himself in the mirror. Roger immediately rubbed away the black smudge on his nose and wondered aloud how it got there in the first place.

Philippi and Rudrauf also showed Roger photographs of himself, of people he knew and of strangers. He almost always recognized himself and never mistook someone else for himself, but he sometimes had difficulty recognizing a photo of his face when it appeared by itself on a black background, absent of hair and clothing. (Visual system)

Roger also distinguished the sensation of tickling himself from the feeling of someone else tickling him and consistently found the latter more stimulating. When one researcher asked for permission to tickler Roger’s armpits, he replied, “Got a towel?” As Philippi and Rudrauf note, Roger’s quick wit indicates that in addition to maintaining a sense of self, he adopts the perspective of others—a talent known as theory of mind. (Hmmm… a man without an insular cortex, anterior cingulate cortex (ACC), and medial prefrontal cortex is capable of “mind-reading” and subtle social thinking and interaction. BUT, ASD Asperger people who have these “parts” intact, are not capable of “mind-reading” and social communication) He anticipated that the researcher would notice his sweaty armpits and used humor to preempt any awkwardness.

Just where is the “mythic social brain” located? In a textbook perhaps?

In another task, Roger had to use a computer mouse to drag a blue box from the center of a computer screen towards a green box in one of the corners of the screen. In some cases, the program gave him complete control over the blue box; in other cases, the program restricted his control. Roger easily discriminated between sessions in which he had full control and times when some other force was at work. In other words, he understood when he was and was not responsible for certain actions. (Aye, yai, yai. What a “stretchy” conclusion!) The results appear online August 22 in PLOS One.

Given the evidence of Roger’s largely intact self-awareness (visual recognition)despite his ravaged brain, Philippi, Rudrauf and their colleagues argue that the insular cortex, anterior cingulate cortex (ACC), and medial prefrontal cortex (mPFC) cannot by themselves account for conscious recognition of oneself as a thinking being. (Well, congratulations!) Instead, they propose that self-awareness is a far more diffuse cognitive process, relying on many parts of the brain, including regions not located in the cerebral cortex. (Why no recognition of VISUAL processing??)

In their new study, Philippi and Rudrauf point to a fascinating review of children with hydranencephaly—a rare disorder in which fluid-filled sacs replace the brain’s cerebral hemispheres. Children with hydranencphaly are essentially missing every part of their brain except the brainstem and cerebellum and a few other structures. Holding a light near such a child’s head illuminates the skull like a jack-o-lantern. Although many children with hydranencephaly appear relatively normal at birth, they often quickly develop growth problems, seizures and impaired vision. Most die within their first year of life. In some cases, however, children with hydranencephaly live for years or even decades. Such children lack a cerebral cortex—the part of the brain thought to be most important for consciousness and self-awareness—but, as the review paper makes clear, at least some hydranencephalic children give every appearance of genuine consciousness. They respond to people and things in their environment. When someone calls, they perk up. The children smile, laugh and cry. They know the difference between familiar people and strangers. They move themselves towards objects they desire. And they prefer some kinds of music over others. If some children with hydranencephaly are conscious, then the brain does not require an intact cerebral cortex to produce consciousness. (Which “consciousness” are we discussing?)

Hydranencephaly: “conscious” by definition “awake and aware of its surroundings” – there seems to be a consistent error in equating this definition (which is true of any animal that is not “asleep, dormant, anesthetized, or comatose” and includes automatic reflexes) and being aware that one is aware, or self-awareness). 

Whether such children are truly self-aware, however, is more difficult to answer, especially as they cannot communicate with language. In D. Alan Shewmon‘s review, one child showed intense fascination with his reflection in a mirror (visual system), but it’s not clear whether he recognized his reflection as his own. Still, research on hydranencephaly and Roger’s case study indicate that self-awareness—this ostensibly sophisticated and unique cognitive process layered upon consciousness—might be more universal than we realized. (Totally ridiculous statement. Mixing simple visual recognition with Duval, Wickland definition. Still no clue as to what “consciousness” is. 

References

Merker B (2007) Consciousness without a cerebral cortex: A challenge for neuroscience and medicine. Behavioral and Brain Sciences 30: 63-81.

Philippi C., Feinstein J.S., Khalsa S.S., Damasio A., Tranel D., Landini G., Williford K.5, Rudrauf D. Preserved self-awareness following extensive bilateral brain damage to the insula, anterior cingulate, and medial prefrontal cortices. PLOS ONE. Aug 22.

Shewmon DA, Holmes GL, Byrne PA. Consciousness in congenitally decorticate children: developmental vegetative state as self-fulfilling prophecy. Dev Med Child Neurol. 1999 Jun;41(6):364-74.

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Self Awareness / OMG What a Hornet’s Nest

What made me awaken this morning with the question of self awareness dancing in my head? It’s both a personal and social question and quest, and so almost impossible to think about objectively. And like so many “word concepts” there is no agreed-upon definition or meaning to actually talk about, unless it’s among religionists of certain beliefs, philosophical schools of knowledge, or neurologists hunched over their arrays of brain tissue, peering like haruspices over a pile of pink meat.

My own prejudices lean toward two basic underpinnings of self-awareness:

1. It is not a “thing” but an experience.

2. Self awareness (beyond Look! It’s me in the mirror…) is learned, earned, created, achieved.

From a previous post –

Co-consciousness; the product of language : “In Western cultures verbal language is inseparable from the process of creating a conscious human being.

A child is told who it is, where it belongs, and how to behave, day in and day out, from birth throughout childhood. In this way culturally-approved patterns of thought and behavior are implanted, organized and strengthened in the child’s brain. 

Social education means setting tasks that require following directions, and asking children to ‘correctly’ answer with words and behavior, to prove that co-consciousness is in place.

This is one of the great challenges of human development, and children who do not ‘pay attention’ to adult demands, however deftly sugar-coated, are rejected as defective, defiant, and diseased.

Punishment for having early self awareness may be physical or emotional brutality or abandonment and exile from the group.”

Who am I? is a question that most children ask sooner or later – prompted obviously by questions from adults (no child is born thinking about this) such as “What do you want to be when you grow up?” (Not, Who are you now?) The socially acceptable menu is small: “A famous sports star” for boys, ” For girls? “A wonderful mom and career woman who looks 16 years old, forever”.

How boring and unrealistic. How life and joy killing. Adults mustn’t let children in on the truth, which is even worse. We know at this point that a child can look in a mirror and say, “That’s me! I hate my haircut,” but he or she is entirely unaware that someday firing rockets into mud brick houses, thereby blowing human bodies to smithereens, may be their passion. Or she may be a single mom with three kids, totally unprepared for an adequate job. Or perhaps he or she may end up addicted to pills and rage and stuffing paper bags with French fries eight hours a day.

If a child were to utter these reasonably probabilistic goals, he or she would be labeled as disturbed and possibly dangerous. And yet human children grow up to be less than ideal, and many  dreadful outcomes occur, but these are the result of the individual colliding with societal fantasies and promises that are not likely outcomes at all.

The strangest part of this is that we talk about self awareness as a “thing” tucked into a hidden space, deep with us, but it isn’t. It is a running score on a test, that once we are born, starts running: the test questions are life’s demands, both from the environment into which we are born, and the culture of family, school, work and citizenship. The tragedy is that few caregivers bother to find out enough about a child to guide them toward a healthy and happy self-awareness. This requires observing and accepting the child’s native gifts and personality, AND helping them to manage their difficulties. This is not the same as curing them of being different, or inflicting life long scars by abandoning them, or diligent training so that like parrots, they can mimic conformist behavior and speech.

Self awareness comes as we live our lives: self-esteem is connected to that process, not as a “before” thing, but an “after” thing: a result of meeting life as it really is, not as a social fantasy. Self awareness is built from the talents and strengths that we didn’t know  we possessed. It also arises as we see the “world” as its pretentions crumble before us. Being able to see one’s existence cast against the immensity of reality, and yet to feel secure, is the measure of finally giving birth to a “self”. 

 

 

 

I’m satisfied that loving the land is my talent and that this is not a small thing, when there are so many human beings who don’t.

Adult Aspergers discuss bullies and manipulators / Re-Post

Adult AS discussion about Asperger individuals having a talent for setting off “typical” humans, specifically, becoming targets for bullies and the recipients of angry responses from “nice” people.

Edited and paraphrased to protect identities.

Topic: It seems that being Asperger’s means that I have SUCKER tattooed across my forehead. Anyone else agree? Any advice? 

Me too – since the day I was born and the result has been a very difficult life.

Aspies seem strange to other people: people fear what they don’t understand. The sad thing is, most Aspies are honest and sensitive and pay attention to other people and their needs. Guess this is what makes us so strange. The normal majority are not honest or sensitive to other people’s needs. We are strange because we love and care. We are hated because we are non violent; honesty and fairness make us unpredictable and that intimidates the average SOB. There is no way we can change ourselves to be as mean as most NTs.

It will be a long wait until society gets better and can make room for honest and intelligent people with good intentions. It could be a very long wait.

Asperger’s can put you at higher risk for this sort of thing (bullying, deception) but unfortunately (or I guess fortunately if it helps you feel better) anyone with low self esteem and poor social skills, and not Asperger’s, is at risk for all of those things. Also, I would bet that these so called “normal” people are only acting nice because society pushes them to be. Anyone who is a bully will bully lots of people, but they feel safe doing it to people like Asperger’s. Bullies aren’t nice people who are being mean, they are cowards being mean to people who won’t fight back.

Very true – “nice” people gave me hell most of my life. Nice normal people get angry at my very prescence in a room. It is hell to deal with our very complicated soul, while at the same time having to be confronted by unjustified cruelty in the  normal social environment. But is there a solution ?

I stay away from people as much as it is possible. it’s very hard, sad, and lonely but at least I’m alive and I don’t get beat up.

I do whatever “works”. I don’t care about being “socially appropriate”. Is there a reason to be ethical around unethical people, who create corrupt systems? Wouldn’t it be more unethical to allow them to get away with being unfair? Doing what is effective is only logical.

I also have never cared about what is considered to “socially appropriate” behavior because underhanded tactics are what is be socially appropriate. To play the game – to inspire fear or to manipulate people – is not something I’ll recommend to Aspies as it doesn’t fit our personality.

NTs are good at and like manipulating people because they seek power above anything else. Most Aspies don’t care about that stuff: power is for idiots

I don’t want power over people or social status. I want do as I please, as long as it’s fair, which isn’t always possible. My experience is that an Aspie must use strategic thinking to break free of the malevolent actions and unjust rules that NTs use to attack a person with ASD.

You know how hard it is to “read” NTs, and how their behaviour is so confusing? It’s the same for many NTs too, but we’re that lone nail that stands out from the masses. I don’t understand bullying, but I know it’s a survival thing, like an animal picking out the weakest in the litter and kicking it out. But, since humans don’t live in the forest and stuff, there’s nowhere for “one of us” to go – we become withdrawn, even die, or stay and try to take the blows.

Sounds sad and sombre, and it is.

I’d like to say that a common myth about Asperger people is that our lack of manipulation skills is because we’re weak or naive. Just the opposite is true – nothing terrifies NTs more than someone who expresses himself directly with no hidden agenda, or irony, or double meaning. With an Aspie, what you see is what you get. I think that assertiveness it is much better; use your natural strengths so you can be more creative and spontaneous.

I served in the military and everyone thought I was weird, but also very good at my job. And even though I was called “a freak of nature” they knew they could count on me no matter what.  An Aspie should count on his “native” strength and skills instead of wasting them on NT games. In short – be yourself

For me, Hell is the waste of time and energy that having to deal bullies takes. The bully demands my time … how dysfunctional is that? “

I don’t think there’s any doubt that we bring out the worst in some people. I assumed it was because there’s some “body language” thing that we’re doing or not doing. People  react as if we’re a threat or something. My attitude is to be extremely wary. I’ve become attuned to the signs that someone is getting annoyed or aggressive, and say something like … “it’s not necessary to get angry”. Of course, there’s a big risk saying that will cause some people to get even angrier.

Unfortunately, confronting people wears me out. Always warring with people leaves me more vulnerable to meltdowns – I end up being tired and over-stimulated.

Actually, I don’t really believe that normal nice people are bullies. Normal nice people do not do these things to people. It’s the bullies against everyone else. They hurt anyone that they think will let them get away with it.

Why Asperger Types Exist / Videos LOL

No, I’m not “diagnosing” these lecturers as Asperger, but the topics discussed are an important part of the Asperger “realm of” (supposedly) bizarre, annoying, antisocial and dangerous “obsessions.”

What would mankind do without these people?

Hey, Neurotypicals: GROW UP. It’s called SCIENCE.

Paper / Climate Effects on Birds and Mammals (That’s Us)

Despite persistent belief, both inside and outside the supposed “science / religion” boundary, that humans are “a special supernatural creation,” and therefore require magical and murky socio-supernatural explanations for our behavior, we are animals. Thanks to the work of “animal scientists” we do have access to REAL information about Homo sapiens: mammal, primate, ape. Via papers such as this, we can understand how physical parameters (not manmade social constructs) drive physiology and behavior in Homo sapiens, just as in any other mammal.   

Calculating Climate Effects on Birds and Mammals: Impacts on Biodiversity, Conservation, Population Parameters, and Global Community Structure

https://academic.oup.com/icb/article/40/4/597/101662

Integrative and Comparative Biology, Volume 40, Issue 4, 1 August 2000, Pages 597–630, https://doi.org/10.1093/icb/40.4.597

INTRODUCTION

A brief history

Ever since the era of Charles Darwin biologists have been intrigued by how and why animals live where they do and what is it about their properties that makes them appear where they do, and appear in the species associations that they form. Hutchinson (1959) defined the concept of the niche. MacArthur et al. (1966), Roughgarden (1974) and many others explored aspects of how size and habitat may influence community structure. Norris (1967) and Bartlett and Gates (1967) were the first to calculate explicitly how climate affects animal heat and mass balance and the consequences for body temperature in outdoor environments. The climate space concept emerged from steady state heat and mass balance calculations and was used to explore how climates might constrain animal survival outdoors (Porter and Gates, 1969).

Those early animal models of the 1960s were limited by the lack of models for distributed heat generation internally, distributed evaporative water loss internally, and a first principles model of gut function. Batch reactor, plug flow and other models were already in existence in the chemical engineering literature (Bird et al., 1960) and it would take time for the biological community to rediscover them. Also missing were a first principles model of porous insulation for fur or feathers, an appendage model, and a general microclimate model that could use local macroclimate data to calculate the range of local microenvironments above and below ground. It became possible to estimate convection heat transfer properties knowing only the volume of an animal (Mitchell, 1976). Another useful development was the appearance of a countercurrent heat exchange model for appendages (Mitchell and Myers, 1968) and the measurement of heat transfer characteristics from animal appendage shapes (Wathen et al., 1971, 1974). It also became possible to deal with outdoor turbulence effects on convective heat transport (Kowalski and Mitchell, 1976). A general-purpose microclimate model emerged in the early 1970s (Beckman et al., 1971; Porter et al., 1973; Mitchell et al., 1975) that calculated above and below ground microclimates. The ability to deal with local environmental heterogeneity and calculate percent of thermally available habitat came later (Grant and Porter, 1992). Over time general-purpose conduction–radiation porous media models for fur appeared in the biological literature (Kowalski, 1978) and it became possible to refine and test them in a variety of habitats and on many species (Porter et al., 1994). The extension of the models to radial instead of Cartesian coordinates and the implementation of first principles fluid mechanics in the porous media (Stewart et al., 1993; Budaraju et al., 1994, 1997) added important new dimensions to the models, which could now calculate temperature and velocity profiles and therefore heat and mass transfer within the fur from basic principles. A test of the ectotherm and microclimate models to estimate a species’ survivorship, growth and reproduction at a continental scale appeared in the mid 1990s (Adolph and Porter, 1993, 1996).

Thanks to these developments and the ones reported in this paper, such as the temperature dependent behavior linked to the new thermoregulatory model, it is now possible to ask: “How does climate affect individual animals’ temperature dependent behavior and physiology and what role(s) does it play in population dynamics and community structure?” This paper attempts to address some of these questions.

We approach the problem from the perspective of a combination of heat and mass transfer engineering and specific aspects of morphology, physiology and temperature dependent behavior of individuals. We show how this interactive combination is essential to calculate preferred activity time that minimizes size specific heat/water stress.

Preferred activity time is a key link between individual energetics and population level variables of survivorship, growth and reproduction, since it impacts all three population variables. Both individual and population level effects may place constraints on community structure. At the individual level, climate at any given time and food type and quality affect the optimal body size that maximizes discretionary mass and energy, the resources needed for growth and reproduction. Climate also affects community structure by affecting individual survivorship directly (heat balance/metabolic costs) and indirectly (activity time overlap of predator and prey). Climate affects seasonal food availability, distribution of food in space and time, and the cost of foraging for that food at different times during a day. Survivorship is affected by temperature dependent behavior changes that allow animals to move to less costly microenvironments at any time. For small mammals, underground burrows or under snow tunnels provide temperatures that never stay below 0°C due to local heating effects of the animal’s metabolic heat production.

At the population level,climate plays a very important role in population numbers. Each species interacts in its own way with climate, affecting its abundance, and community structure. As Ives et al. (1999 p. 546) have pointed out

Our main result is that interspecific competition and species number have little influence on community-level variances; the variance in total community biomass depends only on how species respond to environmental fluctuations. This contrasts with arguments (Tilman and Downing, 1994; Lawton and Brown, 1993) that interspecific competition may decrease community-level variances by driving negative covariances between species abundances. We show that negative covariances are counteracted by increased species-level variances created by interspecific competition.

Consequently, assessing the effect of biodiversity on community variability should emphasize species-environment interactions and differences in species’ sensitivities to environmental fluctuations (for example, drought-tolerant species and phosphorus-limited species) (McNaughton, 1977, 1985; Frost et al., 1994). Competitive interactions are relatively unimportant except through their effects on mean abundances. We have focused on competitive communities, because much current experimental work has addressed competition among plants. Nonetheless, the same results can be shown to hold for more complex models with multiple trophic levels.

Exactly how climate variation, vegetation differences, animal morphology, and foraging behavior all interact to constrain multiple functional types’ existence as a community is still largely unknown. Very little is known about temperature dependent foraging in mammals, although this has been well studied in reptiles and insects. Quantitative consequences of functional morphology on encounter probability and food handling time also are relatively unexplored as yet in mammals.

Temporal climate variation in a locality creates the opportunity for multiple optimal body sizes over annual cycles. The spatial local variation in topography and vegetation creates multiple local climates. Thus temporal and spatial variation in climate creates opportunities for multiple functional types (sizes) to coexist as communities, because as we shall see below, different body sizes interact differently with climate. Qualitatively, this idea is not new. However with likely major shifts in global climates and the rapid global changes in land use, there is urgent need to move these qualitative ideas to a quantitative framework for protection of biodiversity, conservation biology, and a number of other applications. We focus in this paper on applications to mammals and birds.

An overview of this paper

The structure of the paper begins with an overview of how macroclimate drives microclimates, which in turn impact individual animal properties. We then show how key individual properties determine population level parameters that can be used to calculate population dynamics variables. We then illustrate how individual properties also impact on community structure, that in turn feed back to temperature dependent animal properties of individuals.

The initial overview provides a context for an analysis of the model components and their interactions in hierarchical contexts. We start with the model components from the core to the skin, then from the skin through the insulation to the environment. We demonstrate how these components collectively can define the metabolic cost to mammals ranging in size from mice to elephants. We show how the empirical mouse-to-elephant metabolic regression line for animals of different sizes changes depending upon the animal’s climate and posture.

Then we explore how changing mammal body size affects discretionary energy across all climates. Once the mammal model is explored, we repeat the process for the bird model. We demonstrate how we can estimate metabolic cost across bird sizes ranging from hummingbirds to ostriches. We show how postural changes and air temperature can alter metabolic cost estimates for birds.

Once sensitivity analyses are completed, we explore how temporal and spatial variation in global climate impact body size dependent discretionary energy assuming no food limitation and thereby place constraints on the potential combinations of body sizes (community structure) of mammals at the global scale.

Finally, we show how these models can be applied to estimate for the first time from basic principles the metabolic costs and food requirements of an endangered species of bird, the Orange-bellied Parrot of Tasmania and Australia. We show these results for body sizes ranging from hatchling to fully mature adult for a wide range of environmental conditions.

MATERIALS AND METHODS

(go to original paper for text and figures; topics and some sample text follow) 

Survivorship (mortality) probability/hour

Growth and reproduction potential

Different sizes of animals

Model cross section

Inside the body

Heat generation models

Respiration

Temperature regulation model

The gut

Temperature dependent feeding

Porous insulation

Fur vs. feathers

Finite elements and flow through the fur

Appendages

Modeling an individual

Internal body temperature profiles

The insulation

Flow at very low wind

Scaling across mammal body sizes

Mouse to elephant metabolic rate

Mouse to elephant discretionary energy uptake

Diet effects on optimal body size

Bergmann’s Rule

These results are reminiscent of Bergmann’s rule, an empirical observation that as climates get colder, animal sizes tend to get larger. Body size increases with decreasing temperature provide the greatest advantage at small size (Steudel et al., 1994). At larger body sizes, changes in fur insulation confer a greater advantage Steudel et al., 1994). Experimental data from different types of fur on a flat plate (Scholander et al., 1950) suggested this, but animals of larger size also have thicker boundary layers. A thicker boundary layer reduces convective heat loss and simultaneously enhances radiation temperature effects (Porter and Gates, 1969). Larger animals are taller, which means exposure to greater wind speeds higher above the ground. Higher wind speed reduces boundary layer thickness and may engender greater wind penetration of the fur. A first principles fur model can separate boundary layer effects due to size and wind from fur properties effects and provide better estimates of combined effects.

Assessment of consequences of Bergmann’s rule have pointed out that larger animals have the advantage of longer fasting ability under conditions of climate or food availability stress (Morrison, 1960). However, smaller animals have the advantage of lowering body temperature and seeking much more favorable microclimates, especially underground habits in severe cold. Careful transient modeling analyses of these two strategies in the animals’ microclimates would yield a testable hypothesis of the relative benefits of these different solutions to the same problem of dealing with cold.

Of course, survival in extreme temperature events is also important in affecting community structure. However, extreme temperature survival may be overrated in terms of its effects on community structure, at least for mammals. Temperature dependent behavior and selection of microhabitats by both small and large animals can greatly reduce cold or heat stress. For example, moving under or into trees and modifying the solar and infrared radiation and wind protection they provide can change equivalent local microenvironment temperatures by 20°C or more. Underground burrows or tunneling beneath the snow can provide habitats that typically do not drop below 0°C in winter when an animal is present, due to local heat from metabolism. Photoperiod-induced temperature dependent physiology, such as hibernation or estivation is another way that mammals can persist in habitats during periods of extreme heat or cold stress and thereby maintain community structure. Birds typically opt to migrate from extremely cold habitats in winter that they occupy in the summer. By exercising temperature dependent behavioral selection of microclimates through migration, the scale of their selection movements is simply larger due to the short time and lower costs of long distance bird transport.

Scaling across bird body size

Hummingbird to ostrich metabolic rates—Air temperature effect

Global communities-climatic constraints

Figure 16 shows temporal and spatial variation in optimal body size based on discretionary mass/energy for mammals for the months of January and July on a global scale. In January (winter) in the Northern Hemisphere, the optimal sizes are larger as one moves north. Large topographic features, such as the Rocky Mountains, are also predicted to have larger animals with their optima. In the Southern Hemisphere, where it is summer, topographic features do not stand out as strongly.

In July (winter) in the Southern Hemisphere there is somewhat of a “mirror image” effect on optimal body size. However, different topographic and latitudinal features create somewhat different patterns. In general, though, the model suggests that larger animals have the advantage. In the Northern Hemisphere at the same time smaller animals should have the advantage. Large topographic features like the Tibetan plateau with its cool weather in summer still show up fairly clearly as affecting optimal body size. For clarity, variation in vegetation type and food quality were not included in these graphs.

The criteria for optimization were maximum discretionary energy uptake for a given temperature at all possible body sizes. This figure was generated from the endotherm model driven by global weather data at half-degree intervals in latitude and longitude.

The map of optimal body size is different at different seasons of the year. This suggests that climate places important constraints on what functional types can coexist in a locality. Because the environment is constantly changing, it creates a constantly changing optimal body size in any locality. Changing environments create the opportunity for multiple functional types to coexist in the same area.

What is unknown at present is over what time intervals does natural selection integrate time and environmental conditions to “choose” body size? Figure 16 represents the beginnings of the effort to understand climatic constraints on community structure from basic principles. The vegetation on the landscape is certainly a very important variable that will modify the current version of the model. The spatial and temporal distribution of available food places important additional constraints on optimal body size. These constraints include encounter probabilities, handling time, food energy value and metabolic cost to get to the food. Three of these variables are related to body size and the “packaging” and “distribution” of food on the landscape. It is clear that this construct can also be applied to species of birds to study migratory patterns and other aspects of bird ecology.

It is important to note, as one reviewer did, that “evolution may select less for optima under average daily climate cycles and more for adaptations that increase survivorship during winnowing events. At any given time a population may consist of individuals with below or above optimal body sizes, should recent history include high mortality linked to extreme climate, with availability, or predation.” These important considerations have not been added to these models yet.

Conservation application: The Orange-bellied Parrot, Neophema chrysogaster

Ontogeny of metabolic costs

DISCUSSION

Surrogates for size in modeling metabolism

Body weight is a surrogate for body radius. Posture is a surrogate for body geometry. Empirical metabolism data collected since the time of Benedict in the 1930s have related metabolic heat production to body mass. However, mass is only one of the variables that drive metabolic heat production. A key variable is the radius of the trunk of the animal, which is in turn a function of the posture. Most of the analyses of metabolic scaling in the literature that we know ignore this important aspect. Furthermore, the role of a variety of environmental variables and different types of porous insulation in modifying metabolic demand have not been predictable because of the lack of reliable quantitative models.

However, our new animal models and the microclimate model that links them to macroclimate data have changed the outlook for understanding the quantitative relationships of these variables. Fortunately, there have been some careful experiments on endotherm heat loss in wind tunnels with solar radiation. They make it possible to test these models in much more realistic settings than metabolic chambers (Bakken, 1991; Bakken and Lee, 1992; Bakken et al., 1991; Hayes and Gessaman, 1980, 1982; Rogowitz and Gessaman, 1990; Walsberg, 1988a, b, c; Walsberg and Wolf, 1995).

Climate/body size effects on biodiversity

Body size affects discretionary mass and energy intake. Growth and reproduction potential affects fitness. As Figures 11 through 15 demonstrate, body size has important impacts through geometric form and radial dimensions on energy expenditure and intake. The surrogate for these primary variables is body weight (mass). We have pointed out here how air and radiant temperature and posture can make important modifications in energy cost in different environments. These energy costs are not linear with body size. Heat transfer mechanisms are not all linear with body size and neither are temperature regulation responses. Scaling of the gut is not linear with body size, either (Calder, 1984). The combinations of these nonlinear functions result in calculations that suggest discontinuous optimal body size with temperature. This is consistent with empirical data (Brown et al., 1993; Brown and Maurer, 1987; Brown and Nicoletto, 1991; Holling, 1992; Maurer et al., 1992; Peterson et al., 1998). However, there is an important reanalysis questioning these empirical results (Siemann and Brown, 1999). Our results of climate/body size/gut modeling suggest that whether or not animal sizes are clumped in nature may depend on the digestive efficiencies of foods consumed and the locations of those foods. High quality foods suggest greater clumping, low quality foods suggest very little in the way of body size clumping (Fig. 13a–d).

Body size effects on cost of foraging: temperature dependent foraging/activity time

Body size has multiple effects on cost of foraging. It affects heat and mass balance (Figs. 12, 13, 15, and 16). Body size affects cost of locomotion, which is constrained by the respiratory and mitochondrial systems of animals, as Taylor and his colleagues have so eloquently demonstrated (Mathieu et al., 1981; Taylor et al., 1982; Weibel et al., 1991). Their studies interface very nicely with recent work on animal scaling (Enquist et al., 1998; West et al., 1997, 1999).

The work presented here explains that changes in boundary conditions, such as environmental constraints on heat and mass exchange, alter fluxes and therefore alter internal scaling requirements that must adapt to changing needs. Thus, we suggest that temperature dependent behavior may be an important response to environmental change that tends to keep the organism as close as possible to optimal function as dictated by its internal and external anatomy, thereby maximizing fitness.

Body size determines whether a species can be fossorial or not, which affects diurnal microclimates and heat and mass balances. Body size affects likelihood of predation, which can be cast as a cost of foraging (Brown et al., 1994). Body size affects competition, which alters temperature-dependent activity time, which also affects cost of foraging.

Body size effects on total annual activity time

Body size effects on total annual activity time are mediated through heat and mass exchange with the environment. The onset of heat or cold stress appears to be an important constraint in limiting activity. That is, temperatures that force skin temperatures below 3°C or conditions where evaporative water loss must be elevated to protect organism integrity are bounds on activity time that impact animal fitness.

The boundary layer thickness in the air next to the animal surface constrains mass and heat transfer from an animal. Boundary layer thickness is a function of the friction between the animal surface and the air. The amount of friction depends on the dimension of the animal, fluid and animal speed relative to each other, and fluid properties of density, viscosity and thermal conductivity. On the one hand small animals have thin boundary layers and are more responsive to convective environments than to radiant heat exchange (Porter and Gates, 1969). On the other hand, large animals have thicker boundary layers and are more sensitive to the diurnal changes in infrared radiation and solar radiation fluxes in the environment. For large animals, absorption of radiant energy is a much greater challenge, since cooling by convective heat transfer is diminished because of the thicker insulating boundary layer around the larger animal.

Body size affects competitive success, hence temperature-dependent behavior including habitat utilization, which impacts on total annual activity time.

Vegetation/body size effects on biodiversity

Vegetation modifies microclimate conditions available to animals in predictable ways. Animal body size determines where animals spend their time in the wind patterns near the ground. Figure 16 is based on empirical climate data. Those empirical data reflect how vegetation may modify local microclimates. Vegetation also affects animal energetics either by direct shading of the animals or by providing cool surfaces that radiate back to animals. Thus, by directly and indirectly affecting the animal heat fluxes, vegetation impacts optimal body size and constrains functional types that might coexist in a community.

The distribution and quality of food in space and time changes in an annual cycle. Animal food encounter probabilities, and food handling time are consequences of vegetation structure and type. The calculations used in Figure 16 do not yet incorporate various possible distributions of food of various types in the environment. Diverse food distributions have not yet been explored using our models. Food encounter probabilities and handling times, which are a key part of food intake, are only beginning to be explored. The different food types, sizes and spacing also place important constraints on the range of body sizes of animals, which can efficiently utilize them.

Body size, cost of locomotion, and home range size are also interconnected. Home range size must be a function of body size, cost of locomotion, and the foraging thermal and vegetative environment. The minimum time and cost to forage for a particular type, distribution and size of food should be calculable for a broad range of body sizes and environments.

Feathers and plumage

When we watch the development of feathers through the ontogeny of a bird, it is apparent that the down structure is very much like the extremely dense fur of some mammals. Both types of fibers emerge from single openings in the skin as multiple fibers and then “fan out” in three dimensions as multiple fibers as they grow. In so doing they extend the layer of still air above the skin (and in the insulation) substantially. The second stage of plumage development with the eruption of feathers that tend to seal off air flow even further from the skin is unique in its efficiency of cross linking elements to hold complex units together and seal out air flow. The only fur that seems even closely comparable is that of the snowshoe hare that has fur tips that are flattened like tiny shovels (Porter, unpublished data). These structures probably assist in minimizing air and snow penetration into the coat.

The restriction of feather tracts to portions of a bird’s skin provide for flexibility in opening up skin areas to much more rapid heat transfer is also unique to birds. Some mammals like polar bears have inguinal regions that are highly vascularized and lightly furred. Polar bears sometimes apply them to the snow to dissipate heat, but mammals, unlike birds, have not evolved the ability to open large areas of nearly bare skin to dissipate or absorb heat.

CONCLUSIONS

1. Temporal and spatial variation in physical environments impose important constraints on functional types of animals that can coexist in biological communities. These constraints are further refined locally by food diversity representing different digestive qualities.

2. Morphology, physiology, and temperature-dependent activity in animals link individual energetics to population dynamics and community structure by specifying total annual activity time and mass/energy available for growth and reproduction.

3. Porous insulation in birds at rest can be modeled with current state-of-the-art fur models. Resting birds have feather positions that tend to seal off convective transport. This creates a conduction–radiation heat transfer environment. This is simpler to calculate than an environment where three heat transfer mechanisms are all important.

4. Posture plays an important role in metabolic heat loss. This is true mainly because posture affects the radial dimension of the animal, which is a key variable in the equation governing an animal’s total heat generation requirements. Posture is typically ignored in metabolic chamber metabolism studies. The model presented here allows the calculation of the upper and lower limits of metabolic expenditure for a wide variety of climatic conditions.

5. Animal geometry and posture, insulation properties, and environmental conditions influence “thermal conductance.” Thermal conductance is a term implying a passive transport of heat through a non-heat-generating medium. Thus, it is inappropriate for describing fluxes through flesh, where heat generation is occurring. It is also inappropriate in porous media that “act alive” by absorbing solar radiation in the insulation. Thermal conductance is affected by properties and boundary conditions that can have nonlinear effects on heat transport through the medium in question. It can be useful as a descriptive concept for heat source-free systems if all of the relevant boundary conditions and properties are specified.

6. The novel thermoregulatory model in conjunction with user specifications for diurnal/nocturnal/crepuscular activity allows for estimates of activity time that are in good agreement with published data.

7. Climate/body size/gut model calculations for different food types suggest that optimal body size (maximizing discretionary mass/energy) changes with different food types and their associated digestive efficiencies and the temperature. This suggests that vegetation diversity in a locality allows for specific multiple body sizes to coexist at the same point in time. As food quality declines from high digestive efficiencies of flesh/seeds to lower digestive efficiencies of grasses/leaves, optimal body size increases, lowest survival temperature rises, and the degree of clumping predicted for species in nature declines. Land use changes that tend toward monocultures would appear to dictate that fewer species would survive as vegetation diversity declines. Global warming trends would lead to smaller optimal body sizes with no change in vegetation. However vegetation changes associated with climate warming would specify larger or smaller body sizes depending on whether vegetation digestive qualities decrease or increase respectively.

8. Application of the microclimate and endotherm models to rare or endangered species requires relatively few, easily measured data to estimate food and water requirements, potential for activity time, growth, and reproduction for a wide variety of habits. This information will be useful as an aid for identification of potential reserves/transplantation sites and modification/management of existing habitats.

1

From the Symposium Evolutionary Origin of Feathers presented at the Annual Meeting of the Society for Integrative and Comparative Biology, 6–10 January 1999, at Denver, Colorado.

 

Phrenology and Brain Scans / Ancient Tools of Psychology

We’re sure lucky that brain scans came along to put an end to this nonsense!

goodhealthv1-paperrelicsbipolar_transverse_4 fru4_ant

From Frontiers of Psychology: Fifty psychological and psychiatric terms to avoid: 

(4) Brain region X lights up. Many authors in the popular and academic literatures use such phrases as “brain area X lit up following manipulation Y” (e.g., Morin, 2011). This phrase is unfortunate for several reasons. First, the bright red and orange colors seen on functional brain imaging scans are superimposed by researchers to reflect regions of higher brain activation. Nevertheless, they may engender a perception of “illumination” in viewers. Second, the activations represented by these colors do not reflect neural activity per se; they reflect oxygen uptake by neurons and are at best indirect proxies of brain activity. Even then, this linkage may sometimes be unclear or perhaps absent (Ekstrom, 2010). Third, in almost all cases, the activations observed on brain scans are the products of subtraction of one experimental condition from another. Hence, they typically do not reflect the raw levels of neural activation in response to an experimental manipulation. For this reason, referring to a brain region that displays little or no activation in response to an experimental manipulation as a “dead zone” (e.g., Lamont, 2008) is similarly misleading. Fourth, depending on the neurotransmitters released and the brain areas in which they are released, the regions that are “activated” in a brain scan may actually be being inhibited rather than excited (Satel and Lilienfeld, 2013). Hence, from a functional perspective, these areas may be being “lit down” rather than “lit up.”

Phrenology: Examining The Bumps of Your Brain

PSYCHCENTRAL Website, By Associate Editor 

The next time you say, “so and so should have her head examined,” remember that this was literally done in the 19th century.

Phrenology, as it became known, is the study of brain function. Specifically, phrenologists believed that different parts of the brain were responsible for different emotional and intellectual functions. Furthermore, they felt that these functions could be ascertained by measuring the bumps and indentations in your skull. That is, the shape of your skull revealed your character and talents.

Viennese doctor and anatomist Franz Josef Gall originated phrenology, though he called it cranioscopy. He was correct in saying that brain function was localized (this was a novel idea at the time), but unfortunately, he got everything else wrong.

When Gall was young, he noticed a relationship between people’s attributes and behaviors and the shape of their heads. For instance, he observed that his classmates who had better memories had protruding eyes.  This inspired him to start forming his theories and collecting anecdotal evidence. It’s this type of evidence that is the foundation of phrenology.

The problem? Phrenologists would simply dismiss cases that didn’t support their principles, or just revise their explanation to fit any example.

It was also thought that criminals could be identified by the shape of their brains.

It was also thought that criminals could be identified by the shape of their brains.

Phrenology’s Principles

Johann Spurzheim collaborated with Gall on his brain research, and he is the one who actually coined the term phrenology. He eventually went out on his own. He believed that there were 21 emotional faculties (the term for abilities or attributes) and 14 intellectual faculties.

Phrenology had five main principles, which Spurzheim laid out in Outlines of Phrenology (Goodwin, 1999):

  1. “The brain is the organ of the mind.”
  2. The mind consists of about three dozen faculties, which are either intellectual or emotional.
  3. Each faculty has its own brain location.
  4. People have different amounts of these faculties. A person that has more of a certain faculty will have more brain tissue at that location.
  5. Because the shape of the skull is similar to the shape of your brain, it’s possible to measure the skull to assess these faculties (known as the “doctrine of the skull”).

In this text, Spurzheim featured highly detailed descriptions of the faculties and their locations. Spurzheim popularized phrenology in the U.S. While he was on a lecture tour in America, he passed away. Former attorney turned phrenologist George Combe took over Spurzheim’s work and kept his categories.

Phrenology’s Popularity

Phrenology was particularly popular in the U.S. because it fit so well with the idea of the American dream–the notion that we can accomplish our goals despite a humble heritage. Spurzheim believed that the brain was like a muscle that could be exercised. Like weights for your biceps, a good education could strengthen your intellectual faculties. Plus, phrenology promised to improve the public’s everyday lives with simple solutions.

Soon, phrenology became big business and spread to various areas of life. Phrenologists would test couples for compatibility, potential suitors for marriage, and job applicants for different positions.

Brothers Lorenzo and Orson Fowler (who, as an Amherst college student, actually charged students two cents a head) became phrenology marketing gurus. They opened up phrenology clinics, sold supplies to other phrenologists and even started the American Phrenological Journal in 1838. (Its last issue was published in 1911.) Sound familiar?

The Fowler brothers sold pamphlets on a variety of subjects. A few of the titles: The Indications of Character, Wedlock and Choice of Pursuits. They also gave lectures and offered classes to phrenologists and the public.

They even created a faculties manual that a person would take home after being examined by a phrenologist. The phrenologist would indicate the strength of a faculty from two to seven and then check either the box that said “cultivate” or “restrain.” Then, the person would refer to the necessary sections of the 175-paged book.

While much of the public was fascinated by phrenology, the scientific community wasn’t impressed. By the 1830s, it was already considered pseudoscience. Pierre Flourens, a French physiologist and surgeon, questioned the movement and discredited it by performing experimental studies. He experimented on a variety of animals by observing what happened when he’d remove specific sections of their brains.

But science didn’t cause phrenology to fall out of favor. Psychology professionals offering new methods did.

Phrenology’s Influence on Psychology

If you’ve ever read an introductory psychology book, you might remember that phrenology was depicted as basically a fraud.  It was viewed “as a bizarre scientific dead end in which charlatans read character by looking at the bumps on someone’s head,” wrote C. James Goodwin in A History of Modern Psychology.

But as Goodwin said in his book, that’s a simplistic explanation. In fact, phrenology helped move American psychology forward in various ways. (And while there were charlatans, there were phrenologists who truly wanted to help.)

For instance, the basis of phrenology was individual faculties, and thereby individual differences. Phrenologists were interested in analyzing and measuring individual differences, like psychologists do today.

As mentioned above, phrenology also proposed that one’s DNA didn’t predetermine their life. The environment, including education, played a big role, too. You could improve upon your skills and talents. You — not your genes — had control over your future, and that was a hopeful and exciting notion. It still is!

 

 

The Debate Over Sensory Processing Disorder vs. Autism / Aye, yai, yai!

This debate is just one more “Catholics vs. Protestants” type religious war over “who owns the hearts, minds and fates of children” – and their $$ insurance coverage. I wish for once that genuine scientific thinking – and compassion had some influence on reproduction and the health of fetuses, infants, children, young adults and their families. (We adults are on our own in this NT – produced nightmare of irrational – supernatural thinking) LOL

Sensory processing disorder is a condition in which the brain has trouble receiving and responding appropriately to information that comes in through the senses.

Well! That’s certainly a well-defined “thingy”

Here is a list of links:

https://childmind.org/article/the-debate-over-sensory-processing/

http://chan.usc.edu/academics/sensory-integration/history-and-theory

https://www.spdstar.org/basic/symptoms-checklist

https://www.frontiersin.org/articles/10.3389/neuro.07.022.2009/full

https://autismawarenesscentre.com/the-dsm-v-and-sensory-processing-disorder/

http://blogs.discovermagazine.com/crux/2014/04/04/floating-away-the-science-of-sensory-deprivation-therapy/#.WvyIl0xFyUk

https://www.spectrumnews.org/features/talking-sense-what-sensory-processing-disorder-says-about-autism/

https://www.psychologytoday.com/us/blog/creative-development/201107/sensory-processing-disorder

http://www.ascentchs.com/developmental/sensory-processing/symptoms-signs-effects/

and many, many more….

HAVE FUN!

Note the “similarities” between SPD and ASD – and the “socio-religious message” that any child who falls on either side of socially conformist behavior on a Bell curve is “defective” 

This extensive chart sums it up well: AMERICANS HATE CHILDREN and other living things. LIFE is a sin.

Environmental Influences on Gene Expression / Social Human Denial

One of the most mind-boggling aspects of Autism research is the insistence that ASD /Asperger types have “defective sensory systems” because they “react negatively” to “toxic” modern social environments: This is so backwards! “Autism experts” expect human fetuses, infants and children to develop “normally” in what are ANTI-LIFE artificial environments. This is simply ignorant “social blindness” to the fact that “toxic environments” are wreaking havoc on human physiology, which evolved over millions of years in Nature, and not in polluted, unhealthy and high stress “concentration camps” of millions of people, denied clean air and water, nutritious food, privacy and autonomy and self-preservation. Attempts are made to “drug” and medically intervene in the catastrophic so-called “mental illness” epidemic and the failing health of millions; drastic medical intervention is resorted to, in order to “artificially adapt” Homo sapiens to killer environments. Not even the cascade of species extinctions caused by modern human degradation of the environment can “penetrate” the ignorance of   social humans. 

Internal and external environmental factors, like gender and temperature, influence gene expression.

https://www.nature.com/scitable/topicpage/environmental-influences-on-gene-expression-536

By: Ingrid Lobo, Ph.D. (Write Science Right) © 2008 Nature Education

The expression of genes in an organism can be influenced by the environment, including the external world in which the organism is located or develops, as well as the organism’s internal world, which includes such factors as its hormones and metabolism. One major internal environmental influence that affects gene expression is gender, as is the case with sex-influenced and sex-limited traits. Similarly, drugs, chemicals, temperature, and light are among the external environmental factors that can determine which genes are turned on and off, thereby influencing the way an organism develops and functions.

Sex-Influenced and Sex-Limited Traits

 Sex-influenced traits are those that are expressed differently in the two sexes. Such traits are autosomal, which means that the genes responsible for their expression are not carried on the sex chromosomes. An example of a sex-influenced trait is male-pattern baldness. The baldness allele, which causes hair loss, is influenced by the hormones testosterone and dihydrotestosterone, but only when levels of the two hormones are high. In general, males have much higher levels of these hormones than females, so the baldness allele has a stronger effect in males than in females. However, high levels of stress can lead to expression of the gene in women. In stressful situations, women’s adrenal glands can produce testosterone and convert it into dihydrotestosterone, which can result in hair loss.

Sex-limited traits are also autosomal. Unlike sex-influenced traits, whose expression differs according to sex, sex-limited traits are expressed in individuals of only one sex. An example of a sex-limited trait is lactation, or milk production. Although the genes for producing milk are carried by both males and females, only lactating females express these genes.

Drugs and Chemicals

The presence of drugs or chemicals in an organism’s environment can also influence gene expression in the organism. Cyclops fish are a dramatic example of the way in which an environmental chemical can affect development. In 1907, researcher C. R. Stockard created cyclopean fish embryos by placing fertilized Fundulus heteroclitus eggs in 100 mL of seawater mixed with approximately 6 g of magnesium chloride. Normally, F. heteroclitus embryos feature two eyes; however, in this experiment, half of the eggs placed in the magnesium chloride mixture gave rise to one-eyed embryos (Stockard, 1907).

A second example of how chemical environments affect gene expression is the case of supplemental oxygen administration causing blindness in premature infants (Silverman, 2004). In the 1940s, supplemental oxygen administration became a popular practice when doctors noticed that increasing oxygen levels converted the breathing pattern of premature infants to a “normal” rhythm. Unfortunately, there is a causal relationship between oxygen administration and retinopathy of prematurity (ROP), although this relationship was unknown at the time; thus, by 1953, ROP had blinded approximately 10,000 infants worldwide. Finally, in 1954, a randomized clinical trial identified supplemental oxygen as the factor causing blindness. Complicating the issue is the fact that too little oxygen results in a higher rate of brain damage and mortality in premature infants. Unfortunately, even today, the optimal amount of oxygenation necessary to treat premature infants while completely avoiding these complications is still not clear.

How much devastating and life long damage continues to be suffered by infants due to the “promotion” of premature birth as the new normal? 

Yet another example of the way in which chemicals can alter gene expression involves thalidomide, a sedative, antiemetic, and nonbarbiturate drug that was first manufactured and marketed during the mid-1950s. While thalidomide has no discernable effect on gene expression and development in healthy adults, it has a profoundly detrimental effect on developing fetuses. When the drug was first created, however, its impact on fetuses was not known. Moreover, because of its apparent lack of toxicity in adult human volunteers, thalidomide was marketed as the safest available sedative of its time and rapidly became popular in Europe, Australia, Asia, and South America for countering the effects of morning sickness. (In the United States, the drug failed to receive Food and Drug Administration approval because its side effects included tingling hands and feet after long-term administration, which led to concerns that the drug might be associated with neuropathy.) Not until 1961 did Australian researcher William McBride and German researcher Widukind Lenz independently report that thalidomide was a teratogen, meaning that its use was associated with birth defects. (How many of today’s medical drugs and treatments will be / are being “discovered” to be dangerous, due to ignorance and lack of diligent testing, when “rush to market” profitability is the motivation, not human benefit)  Another study associated thalidomide use with neuropathies. Sadly, the drug was withdrawn too late to prevent severe developmental deformities in approximately 8,000 to 12,000 infants, many of whom were born with stunted limb development. Interestingly, despite the fact that thalidomide is dangerous during embryonic development, the drug continues to be used in certain instances yet today. For example, it has therapeutic potential in treating leprosy, and in recent years, it has also been used to treat cancers and enhance the effectiveness of cancer vaccines (Bartlett et al., 2004; Fraser, 1988).

Nature is packed full with evidence for the wide-ranging and specific effects of environment! Why do “researchers” cling to the socio-religious fantasy that humans, as “special creations” are somehow “exempt” from the consequences of animal reality?

Temperature and Light  A pigment gene is influenced by temperature.

© 2013 Nature Education Adapted from Pierce, Benjamin. Genetics: A Conceptual Approach, 2nd ed. All rights reserved.

In addition to drugs and chemicals, temperature and light are external environmental factors that may influence gene expression in certain organisms. For example, Himalayan rabbits carry the C gene, which is required for the development of pigments in the fur, skin, and eyes, and whose expression is regulated by temperature (Sturtevant, 1913). Specifically, the C gene is inactive above 35°C, and it is maximally active from 15°C to 25°C. This temperature regulation of gene expression produces rabbits with a distinctive coat coloring. In the warm, central parts of the rabbit’s body, the gene is inactive, and no pigments are produced, causing the fur color to be white (Figure 1). Meanwhile, in the rabbit’s extremities (i.e., the ears, tip of the nose, and feet), where the temperature is much lower than 35°C, the C gene actively produces pigment, making these parts of the animal black.

Light can also influence gene expression, as in the case of butterfly wing development and growth. For example, in 1917, biologist Thomas Hunt Morgan conducted studies in which he placed Vanessa urtica and Vanessa io caterpillars under red, green, or blue light, while other caterpillars were kept in the dark. When the caterpillars developed into butterflies, their wings showed dramatic differences. Exposure to red light resulted in intensely colored wings, while exposure to green light resulted in dusky wings. Blue light and darkness led to paler colored wings. In addition, the V. urtica butterflies reared under blue light and V. io butterflies reared in the dark were larger than the other butterflies.

As these examples illustrate, there are many specific instances of environmental influences on gene expression. However, it is important to keep in mind that there is a very complex interaction between our genes and our environment that defines our phenotype and who we are.

And yet “autistic” children are blamed for physical effects that originate in unhealthy human-created and imposed toxic environments. Which, not surprisingly, are also negatively impacting ALL HUMANS. 

Widespread Bias Large Genetic Studies / Implications for ASD Asperger’s

Pleiotropy: This certainly has implications for the endlessly repeated assertion that heritable genetic pathologies account for symptoms that include everything from “being antisocial” to being interested in subjects that bore neurotypicals” to female ASDs “preferring to wear clothing with lots of pockets”. It is acknowledged that ASD / Asperger’s are a highly ‘heterogeneous’ bunch of individuals; no two are alike. Claims for “discovery” of scads of “autism-linked genes” are highly suspicious to begin with, and now this unsurprising report, in which “causal” links are over- and under- estimated, or MISSED COMPLETELY.  

Source of Potential Bias Widespread in Large Genetic Studies

A new statistical method finds that many genetic variants used to determine trait-disease relationships may have additional effects that GWAS analyses don’t pick up.

By Diana Kwon | May 15, 2018

Genome-wide association studies, which scan thousands of genetic variants to identify links to a specific trait, have recently provided epidemiologists with a rich source of data. By applying Mendelian randomization, a technique that leverages an individual’s unique genetic variation to recreate randomized experiments, researchers have been able to infer the causal effect of specific risk factors on health outcomes, such as the link between elevated blood pressure and heart disease. (And all those supposed “links” between ASD / Autism “genes” and a bizarre selection / collection of “manifestations” in ASD / Asperger behavior, brain function and even in apparel choices)

The Mendelian randomization technique has long operated on the key assumption that horizontal pleiotropy, a phenomenon in which a single gene contributes to a disease through more than one pathway, is not happening. However, a new study published last month (April 23) in Nature Genetics finds that when it comes to potentially causal trait-disease relationships identified from genome-wide association studies (GWAS), pleiotropy is widespread—and may bias findings.

The “no pleiotropy” assumption was reasonable when scientists were examining only a few genes and much more was known about their specific biological functions, says Jack Bowden, a biostatistician at the University of Bristol’s MRC Integrative Epidemiology Unit in the U.K., who was not involved in the study. Nowadays, GWAS, which include many more genetic variants, are often conducted with little understanding about the precise mechanisms through which each gene could act on physiological traits, he adds.

Although researchers have suspected that pleiotropy exists in a large number of Mendelian randomization studies using GWAS datasets, “no one has actually tested how much of a problem this was,” says study coauthor Ron Do, a geneticist at the Icahn School of Medicine Mount Sinai.

To address this question, Do and his colleagues developed the so-called MR-PRESSO technique, an algorithm that identifies pleiotropy in Mendelian randomization analyses by searching for outliers in the relationship between the genetic variants’ effects on the trait of interest, say, blood pressure, and the same polymorphisms’ effects on the health outcome, such as heart disease. Outliers suggest that some genetic variants may not only be acting on the outcome through that particular trait—in other words, that pleiotropy exists. 

The team used this method to test all possible trait-disease combinations generated from 82 publicly available GWAS datasets and found that pleiotropy was present in approximately 48 percent of the 191 statistically significant causal relationships they identified. (Yes, statistics are only as good as the quality of the “thinking” of the people manipulating the process) 

When the researchers compared the Mendelian randomization results before and after correcting for pleiotropy, they discovered that pleiotropy could lead to drastic over- or underestimations of the magnitude of a trait’s influence on a disease. (And ASD / Autism is NOT A DISEASE; it’s a collection of symptoms – which have multiple sources including WESTERN socio-cultural prejudice) Approximately 10 percent of the causal associations they found were significantly distorted, and by as much as 200 percent.

For example, the team identified an outlier variant in one of the significant causal relationships they found using Mendelian randomization—a link between body mass index (BMI) and levels of C-reactive protein, a marker for inflammation and heart disease. Further examination revealed that this variant, found in a gene encoding apolipoprotein E—a protein involved in metabolism—was associated with several traits and diseases, including BMI, C-reactive protein, cholesterol levels, and Alzheimer’s disease. After removing this outlier, the effect of BMI on C-reactive protein dropped by 12 percent, still statistically significant, but obviously to a lesser degree.

“There is growing awareness that there’s widespread pleiotropy in the human genome in general, and I think these findings suggest that there needs to be rigorous analysis and careful interpretation of casual relationships when performing Mendelian randomization,” (One would have thought that this was the conservative baseline in “science-based” research) Do says. “I think what’s going to have the biggest impact is not just saying whether causal relationships exist, but actually showing that the magnitude of the causal relationship can be distorted due to pleiotropy.”

Bowden notes that the presence of pleiotropy does not mean that Mendelian randomization is necessarily a flawed technique. “Many research groups around the world are currently developing novel statistical approaches that can detect and adjust for pleiotropy, enabling you to reliability test whether a [gene] has a causal effect on an outcome,” he tells The Scientist. For example, he and his colleagues at the University of Bristol recently reported another method to identify and correct for pleiotropy in large-scale Mendelian randomization analyses. (Are these “novel statistical approaches” proven to correct a problem that has much to do with the “reductive mindset” of those who place prime value on “any positive results” for their research agenda, above scientific discipline?)

“I hope that this paper will raise people’s attention to the potential problems in the assumptions behind [these studies],” says Wei Pan, a biostatistician at the University of Minnesota who was not involved in this work. “Large genetic datasets give researchers the opportunity to use a method like this to move the field forward, and as long as they use the method carefully, they can reach meaningful conclusions.” (Is this true, or social blah, blah?)

M. Verbanck et al., “Detection of widespread horizontal pleiotropy in causal relationships inferred from Mendelian randomization between complex traits and diseases,” Nature Genet, doi:10.1038/s41588-018-0099-7, 2018.

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 A chicken with the frizzle gene
© 2004 Richard Blatchford, Dept. of Animal Science UC Davis. All rights reserved. View Terms of Use

Pleiotropy: 

https://www.nature.com/scitable/topicpage/pleiotropy-one-gene-can-affect-multiple-traits-569

The term pleiotropy is derived from the Greek words pleio, which means “many,” and tropic, which means “affecting.” Genes that affect multiple, apparently unrelated, phenotypes are thus called pleiotropic genes Pleiotropy should not be confused with polygenic traits, in which multiple genes converge to result in a single phenotype.

Examples of Pleiotropy

In some instances of pleiotropy, the influence of the single gene may be direct. For example, if a mouse is born blind due to any number of single-gene traits (Chang et al., 2002), it is not surprising that this mouse would also do poorly in visual learning tasks. In other instances, however, a single gene might be involved in multiple pathways. For instance, consider the amino acid tyrosine. This substance is needed for general protein synthesis, and it is also a precursor for several neurotransmitters (e.g., dopamine, norepinephrine), the hormone thyroxine, and the pigment melanin. Thus, mutations in any one of the genes that affect tyrosine synthesis or metabolism may affect multiple body systems. These and other instances in which a single gene affects multiple systems and therefore has widespread phenotypic effects are referred to as indirect or secondary pleiotropy (Grüneberg, 1938; Hodgkin, 1998).

Other examples of both direct and indirect pleiotropy are described in the sections that follow.
Chickens and the Frizzle Trait

In 1936, researchers Walter Landauer and Elizabeth Upham observed that chickens that expressed the dominant frizzle gene produced feathers that curled outward rather than lying flat against their bodies (Figure 2). However, this was not the only phenotypic effect of this gene — along with producing defective feathers, the frizzle gene caused the fowl to have abnormal body temperatures, higher metabolic and blood flow rates, and greater digestive capacity. Furthermore, chickens who had this allele also laid fewer eggs than their wild-type counterparts, further highlighting the pleiotropic nature of the frizzle gene.

See article for Pigmentation and Deafness in Cats, and Antagonistic Pleiotropy and much much more on genetics….  https://www.nature.com/scitable/topicpage/pleiotropy-one-gene-can-affect-multiple-traits-569

Human Pleiotropy

As touched upon earlier in this article, there are many examples of pleiotropic genes in humans, some of which are associated with disease. For instance, Marfan syndrome is a disorder in humans in which one gene is responsible for a constellation of symptoms, including thinness, joint hypermobility, limb elongation, lens dislocation, and increased susceptibility to heart disease. Similarly, mutations in the gene that codes for transcription factor TBX5 cause the cardiac and limb defects of Holt-Oram syndrome, while mutation of the gene that codes for DNA damage repair protein NBS1 leads to microcephaly, immunodeficiency, and cancer predisposition in Nijmegen breakage syndrome.

One of the most widely cited examples of pleiotropy in humans is phenylketonuria (PKU). This disorder is caused by a deficiency of the enzyme phenylalanine hydroxylase, which is necessary to convert the essential amino acid phenylalanine to tyrosine. A defect in the single gene that codes for this enzyme therefore results in the multiple phenotypes associated with PKU, including mental retardation, eczema, and pigment defects that make affected individuals lighter skinned (Paul, 2000).

The phenotypic effects that single genes may impose in multiple systems often give us insight into the biological function of specific genes. Pleiotropic genes can also provide us valuable information regarding the evolution of different genes and gene families, as genes are “co-opted” for new purposes beyond what is believed to be their original function (Hodgkin, 1998). Quite simply, pleiotropy reflects the fact that most proteins have multiple roles in distinct cell types; thus, any genetic change that alters gene expression or function can potentially have wide-ranging effects in a variety of tissues.

Somewhat ironic, that large genetic studies REMOVE PLEIOTROPY, a “fact” in human genetics that may provide real progress in finding genetic links to physical conditions that are at present lumped together under a phony  “autistic pathology” that is based in the “social brain” of neutrotypicals – and not in scientific reality.

 

Video Lecture / Time, the brain and visual processing – wild reality

As an Asperger (?) or visual thinker, my attention to time is highly variable; when concentrating on a “visual” object or scene, time does not seem to exist. Time “markers” (these really are social in origin) such as calendars, schedules, appointments, fixed places and dates in time, are irritating interruptions to this highly pleasant lack of “feeling” for time. When these social “markers” are inevitable, as many are, I don’t feel well; anxiety may accompany the commitment to “be there” “show up” “put in an appearance.” This “regulation of time” by social entities feels alien.

My experience of the natural environment is fluid; determined by sensory “cues” – light, the motion of the atmosphere, color changes, sounds that merge and pass smoothly. The “human environment” is by contrast, incoherent; abrupt interruptions of sound, artificial light, space confined by walls and obstacles, jagged stop and go movement, no “time” to “enjoy” the senses. No peace.

In short, when in a natural environment I am within the ‘time sense’ of that environment; sensory embedded-ness, might be a description. In a human environment (except those few highly aesthetically conscious spaces), the sensory input is simply “all wrong”.

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