Diagnosis creep
This is one for the ‘autism epidemic’ crowd.
I watched Rain Man last week for the first time in years.
This is an extract from the Rain Man script:
Doctor: (To Charlie) In his case, he’s pretty well off. He’s very high-functioning. Most autistics can’t speak or communicate. (To Raymond) Do you know what ‘autistic’ is?
Raymond: Yeah.
Doctor: You know that word? Are you autistic?
Raymond: I don’t think so. (Pause) No. Definitely not.
If you watch Rain Man today you probably regard Raymond as suffering from ‘severe’ autism. Rain Man was released in 1988. When Rain Man was released, Raymond was regarded as unusually high functioning because he could talk.
These days anyone who has more IQ points than facebook friends is regarded as autistic. Well, not quite. But you get my point.
This is a phenomenon sometimes referred to as ‘diagnosis creep’. It happens a lot in medicine. Diagnosis criteria are revised and expanded all the time, funnelling in larger and larger segments of the population. Acceptable cholesterol levels and blood glucose levels have been revised downwards repeatedly during the last thirty years or so. Not so long ago anyone with a diagnosis of ‘manic depression’ was locked up in an asylum. Nowadays it’s almost trendy to be bipolar. ADHD and dyslexia have followed a similar pattern. When I was a child only the most severe cases were diagnosed – anyone else was just a poor learner.
ACE and premenstrual tension
ACE – it stands for angiotensin converting enzyme. People with a common deletion in their ACE gene secrete more angiotensin II and aldosterone than people with the common insertion variant.
Emotional upsets related to changes in ovarian hormones are highly prevalent and are responsible for psychiatric morbidity and mortality. Significant increases in acute psychiatric hospitalizations, suicidal activity, and other psychopathology occur during the premenstruum and during menstruation.
This paper reviews evidence indicating that menstrual cycle psychopathology may be mediated by the effects of estrogen, progesterone, and possibly the renin—angiotensin—aldosterone system on the brain monoamines, norepinephrine, dopamine, and serotonin.
During the menstrual cycle, psychopathology often begins with the onset of luteal estrogen—progesterone—angiotensin—aldosterone secretion and intensifies as these hormone levels later fall, prior to and during menstruation. Aldosterone is reported elevated in cases of premenstrual tension syndrome.
There are numerous reports of affective upsets occurring with the use of estrogen—progestin oral contraceptives and following their withdrawal. Contraceptives stimulate the renin—angiotensin—aldosterone system and are reported useful in alleviating premenstrual—menstrual emotional upsets and postpartum depressive episodes.
What a counter-intuitive conclusion – aldosterone increases PMT, but if you increase aldosterone even further whilst nuking the menstrual cycle, it ‘alleviates’ the problem. It certainly didn’t work that way for me. When I was on the pill my ‘premenstrual’ tension went away – I just had massive chronic tension all the time instead! My PMT always went away immediately that my period started.
Affective lability, prevalent at parturition, occurs when estrogen, progesterone, and aldosterone levels are first high and later falling. Exogenous estrogen and progesterone profoundly affect mating activity in castrated rhesus monkeys, and cyclic fluctuations in sexual activity in humans may occur during the menstrual cycle. Much information links manic and depressive reactions with alterations in brain monoamines. Lithium, monoamine oxidase inhibitors, and tricylic antidepressants, specifically used to treat affective disorders, are reported useful in treating ovarian hormone—linked upsets. Similarities exist between changes in animal behavior caused by drugs altering affective states and the effects of ovarian hormones.
Like certain antidepressants, estrogen induces hyperactivity in rats. Like reserpine, progesterone exhibits sedative and soporific effects. Sexual behavior in female rats is reported linked to changes in brain monoamines. Agents increasing brain monoamine levels and availability decrease mating responses, and monoamine depletors, such as reserpine may be substituted for progesterone in activating mating behavior.
Serotonin and dopamine appear to be important in the regulation of ovulation. Brain norepinephrine varies with the phases of the rat estrus cycle. Castration increases brain norepinephrine and decreases brain dopamine. Exogenous estrogen decreases rat brain norepinephrine content. The monoamine-destroying enzymes, monoamine oxidase, and catechol O-methyl transferase are affected by ovarian steroids and show fluctuating levels during the reproductive cycle. The effects of reserpine, monoamine oxidase inhibitors, tricyclic antidepressants, and lithium on monoamines in neurophysiological preparations have been used as evidence supporting theories linking monoamine changes with human affective disorders. Estrogen, progesterone, and angiotensin also exhibit effects on in vitromonoamine systems.
Like the tricyclic antidepressants, uptake of norepinephrine and dopamine by nerve endings is inhibited in the presence of estrogen, progesterone, and angiotensin. As with reserpine, the flow of these monoamines from nerve endings is increased by progesterone. Estrogen slows the flow of norepinephrine from nerve endings and decreases the electrically induced release of serotonin and norepinephrine from brain slices. The above information provides clues that ovarian hormone—linked psychopathology, like affective disorders in general, may be related to alterations in brain monoamines. Monoamines and ovarian hormone-linked sexual and emotional changes: A review
Aldosterone is also responsible for water retention, by acting on the central nervous system to release vasopressin, the hormone which tells the kidneys to conserve water.
For the poo people
There is a dirty obsession with poo and bowel movements amongst some alties.
Here are a couple of excellent debunking articles for those people who feel the need to examine their stool.
Colon “cleanses”: A load of you know what…
They are written by doctors.
GAPS: a pile of…
Dr. Natasha Campbell-McBride, quacktitioner extraordinaire and author of Gut and Psychology Syndrome (GAPS) believes that salicylates and SLAs are ‘high in antioxidants’ and ‘help the body to detox’. Apparently ADHD and other behavioural symptoms are the result of the ‘detox’ which is of course ‘good for you’. She recommends a gluten-free, casein-free, high salicylate/amine/glutamate diet to ‘cure’ autism and ADHD.
I came across a few blog posts from some poor soul who has been duped into doing GAPS by the bloody idiots at the Weston A. Price Foundation for various symptoms of ill health that rightly ought to be treated with a hospital monitored failsafe elimination diet. I’ll run through the sorry tale:
I had no idea that doing the GAPS diet would be so hard for me and on my family. I have lived without gluten for almost two years and dairy for 6 months so I thought…”hey I can live on soup for awhile”….hahaha….yeah right! I totally underestimated the power food has over my life and the power of the bad bacteria in my gut. This has truly been the hardest week of my life (besides giving birth).
[...]
I belive the reason this has been so hard for me was because my body had great difficulty expelling the toxic waste from my body (constipation) and going into the diet thinking that I would be able to add new things quickly.
When I began feeling some constipation issues I immediately noticed my skin starting to itch terribly (I think the toxins were trying to get out any way possible), my nursing daughter woke up with bumpy skin rash/eczema, and I experienced severe mood swings and terrible gas. I literally felt like the dead bacteria in my body were producing some sort of gas that was rocketing into my brain. I almost went to the hospital yesterday to get on anti-depressants. I was really starting to freak my self out. Thankfully my husband has been supportive but there has been some very hard times for us all. Oh another thing….my 12month old wakes every two hours at night crying. I’ve tried letting her cry herself to sleep but she literally continues to cry for hours so I finally go in to nurse her and she sleeps for a few hours and wakes again. This type of sleep is NOT good for either of us. In case we were not already feeling crappy, now we are purely exhausted. This is enough reason for me to want to get us better. I know her sleep troubles are diet related. I’m starting over
Despite this appalling and perhaps even dangerous reaction to the diet, this poor woman persists:
It has been a solid two weeks since beginning our probiotic Bio-Kult by Dr. Natasha Campbell McBride. And at least 4 weeks since beginning the GAPS diet of bone broth soups, veggies, meat, beet kvass, ginger tea, fermented veggies, ghee galore, coconut oil, cod liver oil, some nuts, apple/pear sauce and fresh veggie juices.
Could this diet be any higher in food chemicals? I can just imagine what they are going to do to this poor woman.
I’ll list the positive improvements for Ani and I first: I’ve gained 12lbs, Ani only wakes twice a night and my bowel movements are pretty regular, coming once a day.
Because I began with two bio-kults per day and lots of coconut oil (major candida killer), Ani and I have had head cold type symptoms for last two weeks. Yesterday I began only taking 1 capsule per day and really cut down on the coconut oil. Today we both seem better but I really have to stay consistent with detoxing. We drink a small glass of fresh carrot/celery/beet/cilantro/garlic juice after waking (btw….beets are the best liver cleansers in the world, cilantro is known to expel metal toxicity and garlic kills bad bacteria), I’m drinking lots of beet kvass, and bone broth with ginger (another powerful anti-microbial) and of course eating lots of soups!! Despite these measures, I’ll admit that both Ani and I have die-off coming out of every area in our bodies. Ani has eczema on her legs and neck, she has a runny nose, watery eyes, and some emotional issues every so often. I have a runny nose, my ear aches a little, sporadic mood swings, and exhaustion.
You would think that these classic food chemical intolerance symptoms would clue this poor woman in that perhaps she should avoid these unpleasant and reactive foods. Her child has broken out in eczema for heaven’s sake. But no:
But these are all good signs really, because they present that things are taking place internally. They show me that I really need to work on my liver health and encourage the bad bacteria to be flushed out before traveling into my blood stream. I’m amazed that one capsule of bio-kult is doing so much when Dr. McBride encourages working up to 8 capsules per day and then tapering back down to 4 for maintenance. I’m also amazed by the power of coconut oil in killing candida.
With all my discoveries on this diet I really am beginning to think that probiotics should be slowly administered after a few weeks eating an SCD or anti-candida diet otherwise there is too much die-off at one time causing the body to be overloaded with toxins.
Well anyways, I must end by saying that I’m so happy to be getting better even though at times it seems like we are just suffering. Detoxing and Die-off
The alleged ‘power of coconut oil in killing candida’ is actually this poor woman experiencing horrible physical reactions to coconut oil, which are brought on because it is very high in salicylates and SLAs. In the cult of candida-land, this translates as being ‘a herx’ and ‘it means you are getting better’. I am just amazed how people do such horrible things to their bodies and still think they are doing themselves some good.
What happens a week later?
Though, I thoroughly love Dr. Natasha Campbell McBride and her work and her probiotics, I have currently disowned her procedure for healing leaky gut. Why? A few reasons, firstly, doing the diet as well as the probiotics (even in the tiniest amount) was too harsh on my body. Maybe a young child who has not had candida for very long could handle her method very well but for my own damaged gut, my body had difficulty expelling the toxins. Instead, the toxins were hitch-hiking through my blood stream. And somehow into my nursing daughter’s system too.
The author has been recruited by bonkers Bee Wilder and her anti-candida diet and is now eating a high fat, low carbohydrate diet. The diet is lower in food chemicals, but still relatively high compared to a normal diet.
After just a day or so on this new path, I felt so energized, strong and capable, so happy! It took a little while to balance my blood sugar levels until I learned that I wasn’t getting enough fat. I no longer have any blood sugar issues and my impulsive food cravings (usually for a handful of nuts) has disappeared. I can go longer between meals (I had been eating every other hour). I went running yesterday with my babe and daughter. Jason said I’m much more delightful. No more intense die-off, just a little here and there. A shift
I also experience the same energy rush and increased tolerance to food chemicals on a high fat, low carbohydrate diet. And I assure you it has nothing to do with candida and everything to do with the reasons the ketogenic diet is used to treat intractable epilepsy in children. But just like me, this woman is never going to feel truly ‘right’ on this diet.
How are things going lately?
Last week we went out to dinner and I ordered a thai salad. Though everything on it was ok (besides the dressing which I’m sure had sugar in it) the lettuce was raw and my gut is not ready for raw greens. I seem to do ok with a small amounts of fermented veggies like pickled ginger root and pickled garlic and any sauted veggies. But eating raw greens while healing a damaged gut is like eating sand paper, it is very irritating. I felt terrible for about 36 hours after that dumb mistake. My stomach hurts
She’s blaming all of her problems on tiny mistakes like slightly too many carbohydrates or too much fibre, just like I used to. Actually, the problem is the extremely high chemical Thai dressing she has eaten.
Another tragic victim of WAPF’s promotion of quack cures over science.
Food additives in the UK
The UK is continuing to make slow but positive progress on banning six of the fifty food additives known to cause negative effects in failsafers.
Artificial food colours are set to be removed from hundreds of products after a team of university researchers warned they were doing as much damage to children’s brains as lead in petrol.
Academics at Southampton University, who carried out an official study into seven additives for the Food Standards Agency (FSA), said children’s intelligence was being significantly damaged by E-numbers. After receiving the advice last month, officials at the FSA have advised their directors to call for the food industry to remove six additives named in the study by the end of next year.
The advice, which will be put before the FSA board next week, would be voluntary. However, manufacturers would be expected by the regulator to remove the additives, replacing them with natural alternatives if possible. Some sweetmakers have unilaterally agreed to remove the suspect colours following the latest scientific evidence.
Researchers have linked E-numbers to behavioural problems since the 1970s but the debate has intensified after the Southampton study, published last September, found that seven additives such as sunset yellow (E110) and tartrazine (E102) were causing temper tantrums among normal children.
The FSA, which funded the £750,000 study, was criticised by health groups for failing to ban the additives after taking the advice of the Committee on Toxicology, which said they had only a moderate effect on some children.
Instead, the FSA said it would work with manufacturers to see if they would remove the additives and awaited an assessment of its research by the European Food Safety Agency (Efsa).
While conceding there was “limited” evidence that the additives caused the children problems, Efsa decided the study was not a good enough reason to change the safe limits of the E-numbers.
Apparently stung by the failure to act, Professor Jim Stevenson, who led the Southampton study, wrote to the FSA demanding immediate action.
His letter dated 20 March is included in the bundle of documents forwarded to the board, which were published yesterday.
In an 18-page rebuttal of criticism of his study, Professor Stevenson and three colleagues wrote: “The position in relation to AFCs [Artificial Food Colours] is analogous to the state of knowledge about lead and IQ that was being evaluated in the early 1980s … Needleman [a researcher] found the difference in IQ between high and low lead groups was 5.5 IQ points … This is very close to the sizes obtained in our study of food additives.”
Politicians finally phased out leaded petrol from all petrol stations in 2000, almost two decades after researchers warned that the toxin was stunting the development of young brains.
Professor Stevenson’s team warned: “We would argue that the findings from our own study and the previous research overviewed by the Efsa would lead to the same conclusion as was reached by Professor Sir Michael Rutter in relation to lead in 1983. Namely that for food colours there is ‘justification for action now’.”
They advised that there be more research on a seventh additive they studied, the preservative sodium benzoate, which stops mould growing in fizzy drinks such as Diet Coke.
The FSA’s board, which meets on Thursday, will make a recommendation to ministers on what to do about additives.
Officials have warned that some products such as mushy peas, tinned strawberries and Battenberg cake might not be able to be reformulated in time and might have to be withdrawn from the shelves.
* A list of more than 900 products containing the additives is published on the Food Commission’s website actiononadditives.com. Food additives ‘could be as damaging as lead in petrol’
I thought something like this might happen with sodium benzoate. Whilst artificial food colourings like tartrazine can be written off as frivolous and unnecessary (being replaced easily with what the industry are eagerly calling ‘natural fruit and vegetable colourings’), benzoates are absolutely everywhere and in everything, so there’s considerable pressure to keep them in the food supply. Not to sound too gloomy, but as soon as benzoate does get removed, it will be replaced by equally nasty ‘natural’ alternatives like the rosemary and oregano oils used ubiquitously by the health/wholefood industry. Just like if they ever remove nitrates, they will get replaced by the ‘natural nitrate free’ alternative – concentrated celery extract – a natural source of nitrates. The only real change is that these ingredients will appear on the food label under the euphemism ‘natural preservatives’.
Until the food standards agency actually recognises and accepts that natural food chemicals like salicylates cause hyperactivity in children too (which will involve dismantling the five-a-day advice and actually making an effort to diagnose and treat affected children properly with diet via local hospitals as they are in Australia), we’ll just be continuing that false belief we middle classes are so eager to indulge – in which ‘natural’ equates with ‘good’ and ‘wholesome’.
ACE interactions
Angiotensin I-converting enzyme (ACE) is a zinc metallopeptidase whose main known functions are to convert angiotensin I into the vasoactive and aldosterone-stimulating peptide angiotensin II, and to inactivate bradykinin. ACE is believed to have other physiological roles because of its wide enzymatic specificity and wide distrubution. An insertion/deletion polymorphism in the angiotensin I-converting enzyme gene accounting for half the variance of serum enzyme levels.
Analysis of ACE genotypes reveal[s] that patients with the wild type ACE gene (ACE I/I) have normal angiotensin II levels, while patients with a deletion in both alleles (ACE D/D) have far higher levels, and those with a single allele deletion have intermediate levels. New Approaches to Heart Failure: From Pharmacogenomics to Drug Development
Mild quantitative changes in the expression of ACE do not affect plasma angiotensin II level or BP because of the concomitant changes in the level of angiotensin I. However, plasma [bradykinin] level changes with changes in ACE expression. Minireview: Computer Simulations of Blood Pressure Regulation by the Renin-Angiotensin System
D/D homozygotes have a 25% increase, and I/I homozygotes have a 25% decrease in plasma ACE activity relative to the I/D heterozygotes. In otherwords, feedback causes angiotensin I levels to lower to maintain correct angiotensin II levels. Examine Figure 3B in the minireview linked to above. It displays D/D types as having lower angiotensin I levels whilst maintaining relatively normal angiotensin II levels.
Now check out the interaction with monoamine oxidase:
It is concluded that diminished [angiotensin I] receptor stimulation decreases cardiac MAO activity, probably by regulating MAO expression, since ANG, ACE inhibitors, and AT(1) antagonists had no effect on MAO activity in vitro. Angiotensin I-converting enzyme inhibition increases cardiac catecholamine content and reduces monoamine oxidase activity via an angiotensin type 1 receptor-mediated mechanism.
Stressed all the time?
Angiotensin II increases thirst sensation[...] It also potentiates the release of norepinephrine by direct action on postganglionic sympathetic fibers. Angiotensin Wiki
Another interaction with COMT:
Angiotensin-converting enzyme (ACE) modulates dopamine turnover in the brain and catechol-O-methyltransferase (COMT) enzyme is an important agent in the metabolic inactivation of dopamine and norepinephrine. Functional polymorphism in the COMT and ACE genes causes variation in enzyme activities. We investigated the relationship of COMT and ACE gene polymorphism with response to conventional neuroleptic treatment in schizophrenia. In this study population we had earlier detected that COMT genotype is associated with unsatisfactory drug response. A total of 94 schizophrenic patients were evaluated either as responders (n=43) or non-responders (n=51). The responders had experienced a fair and steady response to conventional neuroleptics. The non-responders had failed to achieve an acceptable response to conventional neuroleptics. We also used a control population of 94 age- and gender-matched blood donors. Genotyping of the COMT and ACE genes was performed by polymerase chain reaction. The risk of having both low activity COMT and high activity ACE genotypes was over 10 times higher (odds RATIO=10.89, 95%CI 1.14–103.98, P=0.04) in the non-responders compared to responders. ACE genotype alone did not differ between any groups. This finding may suggest a possible interaction with low activity COMT and high activity ACE genotype in association with poor response to conventional neuroleptics. Interaction between angiotensin-converting enzyme and catechol-O-methyltransferase genotypes in schizophrenics with poor response to conventional neuroleptics
One interesting fact I stumbled upon recently is that a low sodium diet increases monoamine oxidase activity in rats, and this operates via an angiotensin II mechanism. So does a high sodium diet decrease monoamine oxidase activity?
And check out the interaction with vitamin D receptors:
Mice lacking the Vitamin D receptor (VDR) have elevated production of renin and angiotensin (Ang) II, leading to hypertension, cardiac hypertrophy and increased water intake. These abnormalities can be prevented by treatment with an ACE inhibitor or AT(1) receptor antagonist. Vitamin D: a negative endocrine regulator of the renin-angiotensin system and blood pressure
In fact the lower your vitamin D levels the higher your whole renin-angiotensin sytem. Vitamin D is an extremely effective way to lower your blood pressure.
The extermination of the savant
NEW YORK (CNN) — He’s only 5½ years old, and yet he’s practically memorized the entire New York subway grid.He reads at the fourth-grade level, plays two-handed piano compositions and is better versed than most adults about the Fibonacci code, a complex mathematics sequence.
Dylan loves Italian music and draws pictures that artist Jackson Pollock would be proud of.
He also happens to be autistic.
Gwenyth Jackaway, Dylan’s mother, is a professor at New York’s Fordham University. She’s single but had always wanted to have a child. So she contacted California Cryobank, one of the largest sperm donor banks in the country.
Cryobank doesn’t reveal the identities of donors but allows people to choose based on the traits they’d like their child to have. Jackaway decided on “Donor X” because he appeared philosophical and intelligent on paper. He liked music, loved to travel and had a high IQ and a degree in economics.
What she couldn’t know then is that her son would have autism. So she started to wonder whether Donor X might carry a gene that could have contributed.
The cause or causes of autism are not known and are hotly debated. Most experts believe that genetics are a component, making a child predisposed to autism or responsive to an environmental trigger.
“It’s a combination of being genetically vulnerable and then having some kind of social or toxicant exposure that tips you over,” according to Dr. Gary Goldstein of the Kennedy Krieger Institute.
Researchers have found some genetic areas associated with autism, but it could take years before the gene or genes that cause autism or contribute to it will be determined.
Until then, Geri Dawson, chief science officer for the Manhattan-based advocacy group Autism Speaks, says there’s no way to screen for those genes and prevent them from being passed to a child.
“We wouldn’t be able to screen a donor for autism because we don’t yet know the specific genes that are contributing to autism,” Dawson said. “But there is a lot of research going on, and I would say in the next five to 10 years, we will have identified between five and 10 genes that we know raise the risk for autism.”
Once the autism gene or genes have been identified, it would theoretically be possible to screen for those genes, according to Dawson.
Jackaway says she went into a period of mourning when Dylan’s autism was diagnosed at age 2.
“When you’re handed a diagnosis of some sort of developmental disorder, you have to let go of the child you thought you were going to have,” Jackaway said. “There’s a sense of loss of the child, a grieving process. There’s denial, there’s rage, and then there’s the tremendous sadness, and hopefully you get to a place of accepting.”
Jackaway says she had to accept that “I don’t have that child I thought I was going to have. But I have this child instead, who’s right here in front of me.”
Through a Web site called Donor Sibling Registry, she reached out to other women who used Donor X. She found six families who had used the same donor.
Two years ago, she visited Theresa Pergola in the New York area; she had given birth to triplets using sperm from Donor X. Just minutes into their meeting, Jackaway noticed Pergola’s son, Joseph, 2, exhibiting some of the same behavior as her son.
“He was walking on his toes; he was flapping his hands. There seemed to be eye contact issues,” recalled Jackaway, who immediately suggested screening Joseph for autism.
“She told me that she saw characteristics of autism, and it was very upsetting to me at that time,” Pergola said. “I didn’t know what to expect from that point on. I know I was scared, and she was there to let me know that it was going to be OK.”
Pergola says she was afraid because she had an image of autism in her head and believed her son would be “in the corner and rocking and not talking.”
She says Jackaway reassured her that wouldn’t be the case.
One month later, a test confirmed what Pergola already knew: Joseph was autistic. The diagnosis brought her to tears, and now these two women whose sons share a father were immediately connected by another bond: autism.
“She was terribly upset,” Jackaway remembered. “That moment is a terribly frightening moment. You get handed a diagnosis, and you get handed an entirely new future.”
In six families Jackaway contacted that had used Donor X, three of the children are autistic, and one is showing signs of autism.
But would Jackaway be happier today if there had been a way to screen Donor X for an autism gene?
“I’ve done a lot of thinking about this, and to say yes to that is to say that I wish Dylan isn’t Dylan,” Jackaway said. “I love my son and everything about him, and that means loving his autism also. Loving your children means loving everything about them. Our children don’t have autism; they are autistic. It’s part of who they are.”
There is currently no way to screen for autism, and in a statement, the company said in part:
“There is no current genetic test to detect autism. California Cryobank (CCB) employs one of the most thorough and rigorous donor screening processes in the industry, with less than 1% of all applicants actually becoming donors. The standard CCB procedure for screening donors involves extensive physical, genetic and health screening …”
Since the discovery of autism in some of the families that used Donor X, Cryobank had this to say about his samples:
“… per CCB policy, the donor’s samples were removed from the general catalog. These vials may only be sold to a client who has previously used specimens of this donor and is interested in ordering additional specimens. In this case the client is made aware of the new medical information and potential issues …”
The families don’t blame the sperm bank. In fact, Theresa Pergola says she’s still uncertain about an autism screening process, if and when it ever becomes available.
“It can go either way, on the one hand it could be helpful so that people could make choices about what risks they want to take,” says Pergola. “On the other hand it’s like, what else are they going to screen for, you know? Are they going to screen for certain personality traits? It’s hard to say. It’s really hard to say.” Autistic children linked to same sperm donor
Would it be silly of me to point out that I am not at all surprised that the offspring of a female professor and an economics graduate who likes music and has a high IQ ends up with an autism diagnosis?
Boy, you NTs really want to live in a Brave New World. Says Bev of Asperger Square 8:
It’s the fact that a mother can express such positive regard, and that a child can so clearly have much to offer, far from being a burden on society, and still…this is how the story ends:
“Per CCB policy, the donor’s samples were removed from the general catalog.”
Not just identified or labeled. Removed. As if another child like this one would be unacceptable. For anyone who doubts the implications of potential prenatal screenings, here is a wakeup call. Autism, even “shiny autism,” even when attached to obvious brilliance and supported by a loving and accepting family, is still judged to have no place in the “general catalog” of humanity. The Point of Awareness
No more Vincent Van Gogh, Leonardo Da Vinci, Andy Warhol, Jane Austen, Emily Dickinson, HP Lovecraft, Hans Christian Andersen, Lewis Carroll, George Bernard Shaw, George Orwell, Isaac Asimov, Ludwig van Beethoven, Wolfgang Amadeus Mozart, Bob Dylan, Michael Jackson, Woody Allen, Michael Palin, Alexander Graham Bell, Thomas Edison, Henry Ford, Howard Hughes, Bill Gates, Immanuel Kant, Charles Darwin, Albert Einstein, Isaac Newton… These are just some of the individuals who have been attributed today as having asperger’s syndrome or autism.
What would a world be like without autism? No more inventors, innovators, computer programmers, mathematicians, engineers, doctors, surgeons, artists, designers, composers, authors, actors, geniuses, entrepreneurs. It takes vital little traits from each of these personalities to coincide and produce autism. To exterminate autism, you need to exterminate all the genes that cause autism. Most intelligence genes would be erradicated in one fell swoop. Women who terminate their pregancies because their foetuses have a high chance of developing autism are going to have a big shock when they find that autism or ASDs repeatedly show up in the foetus whenever they become pregnant. That’s going to be a bit of a downer.
What would you have left if you took away all the autistic genes? Builders. Telephone sales people. Jocks. Cheerleaders. Administrators. Soccer moms. Hairdressers. HR managers. Radio Discjockeys. People who get liquored up and go to clubs. Oh my god, the Golgafrinchans! Nooo!
Good luck with the future of the human race. Be sure to preserve a few of our genes so you have something to fall back on when you remember you need some rocket scientists for that moon landing.
leave a comment