Autoimmune Thyroid Disease

An Unfortunate and Lengthy Adventure in Misdiagnosis

Archive for December 2008

Food chemical intolerance medical and scientific references

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Food chemical intolerance medical and scientific references for intolerance to salicylates, amines, glutamates and additives are now available on CiteULike.

It’s half past three in the morning and I’ve just finished adding them all! There are almost six hundred and fifty abstracts available as of this moment.

There are a handful of full text PDFs available too under the tag ‘fulltext’.

These are mostly taken from the Feingold website, Fed up with food additives, and the RPAH website, but I keep stumbling across new ones all the time.

Phew. What a way to spend boxing day. This has been epic. I’m going to get some sleep now!


Written by alienrobotgirl

27 December, 2008 at 4:34 am

Posted in The Science of FCI

The default brain network and autism

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Following on from the previous two posts, here’s a little more about the default network and how it relates to autism.

Several regions of the brain (including medial prefrontal cortex, rostral anterior cingulate, posterior cingulate, and precuneus) are known to have high metabolic activity during rest, which is suppressed during cognitively demanding tasks. With functional magnetic resonance imaging (fMRI), this suppression of activity is observed as “deactivations,” which are thought to be indicative of an interruption of the mental activity that persists during rest. Thus, measuring deactivation provides a means by which rest-associated functional activity can be quantitatively examined. Applying this approach to autism, we found that the autism group failed to demonstrate this deactivation effect. Furthermore, there was a strong correlation between a clinical measure of social impairment and functional activity within the ventral medial prefrontal cortex. We speculate that the lack of deactivation in the autism group is indicative of abnormal internally directed processes at rest, which may be an important contribution to the social and emotional deficits of autism. Failing to deactivate: Resting functional abnormalities in autism

The above link includes a free full text.

Recent studies of autism have identified functional abnormalities of the default network during a passive resting state. Since the default network is also typically engaged during social, emotional and introspective processing, dysfunction of this network may underlie some of the difficulties individuals with autism exhibit in these broad domains. In the present experiment, we attempted to further delineate the nature of default network abnormality in autism using experimentally constrained social and introspective tasks. Thirteen autism and 12 control participants were scanned while making true/false judgments for various statements about themselves (SELF condition) or a close other person (OTHER), and pertaining to either psychological personality traits (INTERNAL) or observable characteristics and behaviors (EXTERNAL). In the ventral medial prefrontal cortex/ventral anterior cingulate cortex, activity was reduced in the autism group across all judgment conditions and also during a resting condition, suggestive of task-independent dysfunction of this region. In other default network regions, overall levels of activity were not different between groups. Furthermore, in several of these regions, we found group by condition interactions only for INTERNAL/EXTERNAL judgments, and not SELF/OTHER judgments, suggestive of task-specific dysfunction. Overall, these results provide a more detailed view of default network functionality and abnormality in autism. Functional abnormalities of the default network during self- and other-reflection in autism

So if I’m interpreting this correctly, autistics don’t switch off their default networks like neurotypicals do when they are asked to focus on tasks. They are also using their default networks slightly differently than neurotypicals, regardless of whether they are being asked to focus or not: “In the ventral medial prefrontal cortex/ventral anterior cingulate cortex, activity was reduced in the autism group across all judgment conditions and also during a resting condition, suggestive of task-independent dysfunction of this region.”

I am sure there would be much clearer results with regards the default network if autistics were divided into ADD and non-ADD types and studied.

Whilst researching the default network, I read an interesting comparison on an attention deficit disorder forum. The ADD author related how people with ADD are constantly daydreaming and imagining, and drew a comparison with the “insulated inner world of the autistic”. The autistic is in effect daydreaming all of the time, not rousing themselves to pay attention to the world around them. So much for autistics lacking imagination! This certainly confirms my belief that autistics are deep thinkers. I suspect in severe classic autism, one never emerges from this daydream world long enough to learn how to speak.

Written by alienrobotgirl

24 December, 2008 at 5:54 pm

Posted in The Brain

Jumping to conclusions bias

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Jumping to conclusions bias is an actual real name for a psychological state. Unfortunately I can’t find any tests online to direct you to so that you can measure your own bias, but I can tell you about a test called the “beads in a jar test” that I saw on the television.

Recently my partner and I were watching a BBC programme called “how mad are you?” in which psychiatrists subjected a mixed group of normal people and people with diagnosed psychiatric disorders to a variety of tests, to see whether they could figure out who had what disorders. The idea was to demonstrate how blurry the lines are between psychiatric disorders and regular personality types. They certainly demonstrated this well during the course of the series.

In this particular test, the psychiatrists were searching for jumping to conclusions bias because it is a known feature of schizophrenia. Schizophrenics and individuals suffering from delusions, for whatever reason, tend to leap to conclusions based on very, very little evidence.

One might suggest that this may simply be a feature of how the delusions are interpreted, for example, if someone hears a voice in their head, someone with jumping to conclusions bias might assume the voice is God, whereas someone without jumping to conclusions bias might assume they are hearing a voice and employ informal CBT techniques to suppress it, thus avoiding acting on the voice, and escaping diagnosis.

However, because there is such strong evidence of this reasoning bias in people with delusions, it is more than likely that there is a very real, very direct link between jumping to conclusions bias and schizophrenia and other delusional states. This cognitive style is thought to actually form part of the fundamental process of developing and maintaining delusional beliefs.

So anyway, the individuals were set the following test: in a jar there are eighty red or blue beads. Twenty of them are one colour, and sixty of them are another colour. The task is to tell us whether there are more blue beads or more red beads in the jar. We will hide the jar and pull out coloured beads one by one, and you stop us when you feel you know the answer.

At this point my partner and I shared a joke with each other that we would probably wait for twenty one coloured beads of either colour to be pulled from the jar, as this would absolutely confirm which colour was in the majority.

The sneaky thing was, the psychiatrists weren’t pulling the beads from a jar, but from a standard sequence of beads laid out in a tray. The beads appeared quite evenly, being red, blue, red, blue, until eventually there were three beads of the same colour in a row, at which point most of the participants took a decision.

One woman, however, decided on the first bead.

My partner and I sat there with our mouths open and both declared “that’s nuts!”

The woman in question did not turn out to have schizophrenia, just a very strong jumping to conclusions bias. When questioned she could not really explain why on earth she had made this rash choice. It didn’t seem irrational to her.

Unfortunately, people with jumping to conclusions bias are simply not aware that they are, well, jumping to conclusions. I suppose at this point one could invoke the saying “there’s such a thing as being so open minded that your brain falls out.”

A lot (most?) of the people I encounter on the internet seem to be prone to jumping to conclusions too swiftly. I don’t know whether this is just because of my former association with WAPF, who have, sadly, mutated into a bit of a bonkers CAM organisation in recent years, and are as a result attracting people with extreme thinking styles. This thinking style makes me fairly uncomfortable because my own style is so cautious.

The moral of the story is: make sure you are really sure about what you are saying. Look before you leap. Being prone to delusional thinking makes you a bad scientist. Slow down. Do the job properly. Try to be more self-aware of your shortcomings. Don’t believe everything you read on the internet.

Written by alienrobotgirl

23 December, 2008 at 6:45 pm

Posted in Psychology

The default brain network and ADD

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So in the previous post I published some New Scientist articles about the ‘default network’ in the brain. This network kicks into action as soon as we stop focusing our attention on a task.

The default network is where we think. Imagine living like this:

People who suffer damage to their medial prefrontal cortex become listless and uncommunicative. One woman who recovered from a stroke in that area recalled inhabiting an empty mind, devoid of the wandering, stream-of-consciousness thoughts that most of us take for granted.

No default network, no thoughts.

The default network is aberrant in schizophrenia, and schizophrenic subjects appear to have problems accessing their default network properly.

In the healthy subjects, the default mode network resonated slowly and regularly as observed by blood flow. In the patients with schizophrenia, the activity in the brain increased and was significantly more irregular, although they performed equally well on the task. Brain’s ‘Default Mode’ Awry In Schizophrenia

Schizophrenia is interesting because it is treated with dopamine antagonists. No direct correlation can be found between schizophrenia and high dopamine levels, though high dopamine is known to cause delusions. However, some scientists believe schizophrenia may be an autoimmune condition in which autoantibodies trigger dopamine receptors in the brain. The fact is, dopamine antagonists control and treat delusions and hallucinations.

In Alzheimer’s, not only is there a loss of dopamine D2 receptors in the brain, but the default network areas specifically accumulate plaques. Alzheimer’s patients appear to turn on their default network when asked to concentrate on a task, while normal subjects turn off their default network.

In terms of neurotransmitters, at the direct opposite end of the spectrum from schizophrenia is attention deficit (hyperactivity) disorder. AD(H)D is considered a condition characterised by low dopamine levels. Low dopamine levels lead to a lack of attention – to daydreaming.

Whilst attention deficit is typically thought to be something that affects children, adults experience it too – though perhaps not so obviously, possibly because the default network is something that matures into a complex and cohesive network during one’s lifetime.

In recent years, the brain’s “default network,” a set of regions characterized by decreased neural activity during goal-oriented tasks, has generated a significant amount of interest, as well as controversy. Much of the discussion has focused on the relationship of these regions to a “default mode” of brain function. In early studies, investigators suggested that, the brain’s default mode supports “self-referential” or “introspective” mental activity. Subsequently, regions of the default network have been more specifically related to the “internal narrative,” the “autobiographical self,” “stimulus independent thought,” “mentalizing,” and most recently “self-projection.” However, the extant literature on the function of the default network is limited to adults, i.e., after the system has reached maturity. We hypothesized that further insight into the network’s functioning could be achieved by characterizing its development. In the current study, we used resting-state functional connectivity MRI (rs-fcMRI) to characterize the development of the brain’s default network. We found that the default regions are only sparsely functionally connected at early school age (7–9 years old); over development, these regions integrate into a cohesive, interconnected network. The maturing architecture of the brain’s default network

What is really fascinating about the default network to me, is that the more I read about it, the more it seems to be how my brain functions.

I’ve been so busy studying autism, perhaps I should have been paying more attention(!) to attention deficit disorder. I have always had ADD. It is the cause of many of my problems, but also the cause of a lot of my talents.

Since being a child I have been chided for being in a permanent daydream. My imagination is constantly in action. I frequently take on the look of the gormless because I disappear off onto my own planet, open-mouthed, as I speculate about some possible future, or some possible theory about the universe. I burn the dinner, I leave tasks half-finished for other tasks, I don’t pay attention to where I am going, I get lost in the supermarket and make six laps because I am too busy pondering the universe, and at any given second I can break off half way through a sentence or a line of code to go google whatever question pops into my head.

I have evolved a lot of coping mechanisms for these traits: I have an OCD level of strictness about making sure I have locked the door, I have thought about the items I need to buy, I have checked my keys are in my bag, I have looked both ways before crossing the road, and I have set the kitchen timer. I often have to make a conscious effort to switch off the wireless internet connection so I can get on with my writing. The OCD is not real: it is simply my conscious way of dealing with my short attention span.

Whilst most of the world may regard this as a disorder, I prefer to regard it as a difference.

When I am not on the failsafe diet (which is never), my attention deficit disorder is very serious indeed, to the point where it could be dangerous for me to drive a car (my driving instructor always chided me for not paying enough attention). Sometimes it has been so bad that I have felt I cannot be gainfully employed due to the time I waste doing everything except working. My brain buzzes, throws disjointed thoughts at me, and repeats itself again and again.

When I am on the failsafe diet, however, I think quite clearly. I can focus when I need to, but I still go off on massive reveries and have epiphanies about things. So what? What’s wrong with spending your time thinking? I’m sure Sir Isaac Newton wouldn’t have discovered all those laws of physics if he hadn’t spent so much time daydreaming.

My big theory about the default network is that it is suppressed by dopamine, and activated when dopamine is low. I’ve found a couple of studies that back up this theory, here and here. Indeed, this blog describes how the use of stimulants like ritalin deactivate the default network.

The default network is where my consciousness lives. I’ve tried meditation before and I find it tremendously difficult to switch off my stream of consciousness. I have no patience for meditation or yoga. Switching off is something that I can perhaps do when I am watching television or reading very intensely, where I just have words going in that I process without thinking about them, though it only lasts a few seconds before the stream of consciousness reasserts itself again.

I find it incredibly uncomfortable to try to switch off that stream of consciousness, like holding one’s breath. It seems to me that being asked to concentrate can make me irritable and tired.

Music is something I have a real problem with. I rarely listen to music. When in the right mood, I like listening to music, but it tends to take over my brain. If it is too loud (i.e. speaking volume), it actually interferes with my stream of consciousness. I find this very, very uncomfortable. If I’m forced to sit in a car and listen to music that is loud enough to interfere with my thoughts, it’s like torture, and I can get really irritable. It’s like I’m being forced to concentrate against my will.

So ADD is not so much a case of “I can’t concentrate,” it’s a case of my dopamine being low and as a result my default network is constantly reasserting itself over the rest of my mind. This is not an unpleasant experience, in fact, I prefer things that way.

The things that the default network is good at doing are the same things that I am good at doing, for example:

Planning: whether a route, or a future event. I always plan things. I am uncomfortable if I don’t plan things. It seems to me that when I get irritated by something, it is almost always because a plan has gone awry and my brain has to re-plan at short notice. I am very good at envisaging future scenarios, even totally unexpected ones. If a conversation is happening where future possibilities are being discussed, I can guarantee to have thought up each of the future possibilities long before someone else suggests them. When I listen to politics on the radio, I am frequently annoyed by the lack of foresight politicians have for the consequences of their policies. I’m an “I told you so,” kind of person. I like to think this trait makes me a good scientist, because when I observe a phenomenon, I can imagine many possible causes and therefore have many theories to suggest and test.

Remembering: particularly autobiographical memories. This elephant never forgets. I often recall scenarios to other people, only to find they have forgotten them. My memory is very reliable, and it’s very rare that I have forgotten something that someone else remembers. I am also a terrifying fact machine, as long as I can relate the facts to myself in some way.

Imagining: I write fantasy and science fiction. I share my big imagination with one grandparent in my family who used to tell us stories when we were kids. This grandparent also has ADHD and can’t sit still.

Moral decision making: I am a very principled, moral person with a complex set of standards that I adhere to. I don’t blindly follow rules however, I think about the consequences of actions and consider the greater good.

Self-awareness: things simply don’t get by me unnoticed the way they seem to get by other people. I always used to wonder why people didn’t understand obvious things about themselves. Now I guess I do know. They aren’t using their default networks as much as I am.

The default network also explains the things I am not very good at, for example – it answers that question I have been asking myself for years – why am I so slow at everything? How come it takes me twice as long to do any task as it takes someone else? How come on those silly facebook quizzes, I always take twice as many minutes to complete them as everyone else?

Though I have a big imagination, I’ve struggled to actually get on and do the process of writing for years and years. I have to go to some unusual extremes in order to write. I can’t concentrate during the day, if there is background noise, if there is anyone else around. I basically have to closet myself in a dark room in the dead of night in order to put down all my ideas on paper.

I see now that my default network is getting in the way, it’s reasserting itself all the time and slowing me down when I have to focus. It’s almost like a kind of epilepsy, I’m just switching off for a few seconds here and there all the time, my mind wandering without me even being aware of it.

Do other people experience conciousness differently to me? When they are concentrating on a task, do they simply stop thinking? I can’t imagine what that feels like.

There is one major anomaly though. According to this (free) review of the studies done on the default network so far, the default network is activated during theory of the mind tasks. Considering how commonly autism and attention deficit disorder occur together in the same individual, this is very odd.

Regarding the function of the default network in autism, the review implies mixed results so far, with some studies suggesting increased brain volume in default network areas, whilst others suggesting absence of activity during passive tasks when the mind would usually wander. This suggests the autistics in question were concentrating very hard on the task they were given! Still other information in the review points out to a complex interaction with the amygdala, which is known to contribute to social cognition, and interacts with the default network.

An intriguing possibility suggested by the authors of the study […] is that the failure to modulate the default network in ASD is driven by differential cognitive mentation during rest, specifically a lack of self-referential processing […] Another recent study using analysis of intrinsic functional correlations showed that the default network correlations were weaker in ASD (Cherkassky et al. 2006). Of note, the individuals with ASD showed differences in a fronto-parietal network that has been recently hypothesized to control interactions between the default network and brain systems linked to external attention (Vincent et al. 2007b). These data in ASD suggest an interesting possibility: the default network may be largely intact in ASD but under utilized perhaps because of a dysfunction in control systems that regulate its use. The Brain’s Default Network

Now I’m the first to point out I’m not a typical aspie. Many other aspies seem a lot whackier than me (higher dopamine?), and as far as the theory of the mind goes, I do pretty good (but then, I’m female). I’ve never fitted the Baron-Cohen “extreme male brain” theory. I’m rubbish at maths, but great at logic, pattern-spotting and programming.

However, I’m not alone in being anomalous. Fifty to sixty percent of autistics also qualify for a diagnosis of ADD/ADHD,  see this reference. Yet autism can also occur together with schizophrenia, as can schizophrenia and ADHD occur together.

So what’s going on here?

Written by alienrobotgirl

22 December, 2008 at 6:38 pm

Posted in Neurotransmitters

The default brain network

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More amazing revelations from the New Scientist magazine.

The default network in action

The default network in action

IN 1953 a physician named Louis Sokoloff laid a 20-year-old college student onto a gurney, attached electrodes to his scalp and inserted a syringe into his jugular vein.

For 60 minutes the volunteer lay there and solved arithmetic problems. All the while, Sokoloff monitored his brainwaves and checked the levels of oxygen and carbon dioxide in his blood.

Sokoloff, a researcher at the University of Pennsylvania in Philadelphia, was trying to find out how much energy the brain consumes during vigorous thought. He expected his volunteer’s brain to guzzle more oxygen as it crunched the problems, but what he saw surprised him: his subject’s brain consumed no more oxygen while doing arithmetic than it did while he was resting with his eyes closed.

People have long envisaged the brain as being like a computer on standby, lying dormant until called upon to do a task, such as solving a Sudoku, reading a newspaper, or looking for a face in a crowd. Sokoloff’s experiment provided the first glimpse of a different truth: that the brain enjoys a rich private life. This amazing organ, which accounts for only 2 per cent of our body mass but devours 20 per cent of the calories we eat, fritters away much of that energy doing, as far as we can tell, absolutely nothing.

“There is a huge amount of activity in the [resting] brain that has been largely unaccounted for,” says Marcus Raichle, a neuroscientist at Washington University in St Louis. “The brain is a very expensive organ, but nobody had asked deeply what this cost is all about.”

Raichle and a handful of others are finally tackling this fundamental question – what exactly is the idling brain up to, anyway? Their work has led to the discovery of a major system within the brain, an organ within an organ, that hid for decades right before our eyes. Some call it the neural dynamo of daydreaming. Others assign it a more mysterious role, possibly selecting memories and knitting them seamlessly into a personal narrative. Whatever it does, it fires up whenever the brain is otherwise unoccupied and burns white hot, guzzling more oxygen, gram for gram, than your beating heart.

“It’s a very important thing,” says Giulio Tononi, a neuroscientist at the University of Wisconsin-Madison. “It’s not very frequent that a new functional system is identified in the brain, in fact it hasn’t happened for I don’t know how many years. It’s like finding a new continent.”

The discovery was slow in coming. Sokoloff’s experiment 55 years ago drew little attention. It wasn’t until the 1980s that it started to dawn on researchers that the brain may be doing important things while apparently stuck in neutral.

Eavesdropping on the mind

In those days a novel brain scanning technique called PET was all the rage. By injecting radioactive glucose and measuring where it accumulated, researchers were able to eavesdrop on the brain’s inner workings. In a typical experiment they would scan a volunteer lying down with their eyes closed and again while doing a mentally demanding task, then subtract one scan from the other to find the brain areas that lit up.

Raichle was using PET to find brain areas associated with words when he noticed something odd: some brain areas seemed to go at full tilt during rest, but quietened down as soon as the person started an exercise. Most people shrugged off these oddities as random noise. But in 1997 Raichle’s colleague Gordon Shulman found otherwise.

Shulman sifted through a stack of brain scans from 134 people. Regardless of the task, whether it involved reading or watching shapes on a screen, the same constellation of brain areas always dimmed as soon as the subject started concentrating. “I was surprised by the level of consistency,” says Shulman. Suddenly it looked a lot less like random noise. “There was this neural network that had not previously been described.”

Raichle and Shulman published a paper in 2001 suggesting that they had stumbled onto a previously unrecognised “default mode” – a sort of internal game of solitaire which the brain turns to when unoccupied and sets aside when called on to do something else. This brain activity occurred largely in a cluster of regions arching through the midline of the brain, from front to back, which Raichle and Shulman dubbed the default network (Proceedings of the National Academy of Sciences, vol 98, p 676).

The brain areas in the network were known and previously studied by researchers. What they hadn’t known before was that they chattered non-stop to one another when the person was unoccupied but quietened down as soon as a task requiring focused attention came along. Measurements of metabolic activity showed that some parts of this network devoured 30 per cent more calories, gram for gram, than nearly any other area of the brain.

All of this poses the question – what exactly is the brain up to when we are not doing anything? When Raichle and Shulman outlined the default network, they saw clues to its purpose based on what was already known about the brain areas concerned.

One of the core components is the medial prefrontal cortex (see diagram), which is known to evaluate things from a highly self-centred perspective of whether they’re likely to be good, bad, or indifferent. Parts of this region also light up when people are asked to study lists of adjectives and choose ones that apply to themselves but not to, say, Britney Spears. People who suffer damage to their medial prefrontal cortex become listless and uncommunicative. One woman who recovered from a stroke in that area recalled inhabiting an empty mind, devoid of the wandering, stream-of-consciousness thoughts that most of us take for granted.

Parts of the default network also have strong connections to the hippocampus, which records and recalls autobiographical memories such as yesterday’s breakfast or your first day of kindergarten.

To Raichle and his colleague Debra Gusnard, this all pointed to one thing: daydreaming. Through the hippocampus, the default network could tap into memories – the raw material of daydreams. The medial prefrontal cortex could then evaluate those memories from an introspective viewpoint. Raichle and Gusnard speculated that the default network might provide the brain with an “inner rehearsal” for considering future actions and choices.

Randy Buckner, a former colleague of Raichle’s now at Harvard, agrees. To him the evidence paints a picture of a brain system involved in the quintessential acts of daydreaming: mulling over past experiences and speculating about the future (New Scientist, 24 March 2007, p 36). “We’re very good at imagining possible worlds and thinking about them,” says Bucker. “This may be the brain network that helps us to do that.”

There is now direct evidence to support this idea. Last year, Malia Mason of Dartmouth College in Hanover, New Hampshire, reported that the activity of the default network correlates with daydreaming. Using the brain imaging technique fMRI, Mason found that people reported daydreaming when their default network was active, but not when it dimmed down. Volunteers with more active default networks reported more wandering thoughts overall (Science, vol 315, p 393).

Daydreaming may sound like a mental luxury, but its purpose is deadly serious: Buckner and his Harvard colleague Daniel Gilbert see it as the ultimate tool for incorporating lessons learned in the past into our plans for the future. So important is this exercise, it seems, that the brain engages in it whenever possible, breaking off only when it has to divert its limited supply of blood, oxygen and glucose to a more urgent task.

“Daydreaming may sound like a mental luxury but its purpose is deadly serious”

But people are starting to suspect that the default network does more than just daydream. It started in 2003 when Michael Greicius of Stanford University in California studied the default network in a new way. He got his subjects to lie quietly in an fMRI scanner and simply watched their brains in action. This led him to find what are called resting state fluctuations in the default network – slow waves of neural activity that ripple through in a coordinated fashion, linking its constellation of brain areas into a coherent unit. The waves lasted 10 to 20 seconds from crest to crest, up to 100 times slower than typical EEG brain waves recorded by electrodes on the scalp.

Until then scientists had studied the default network in the old-fashioned way, subtracting resting scans from task scans to measure changes in brain activity. But Greicius’s work showed that you could eavesdrop on the network by simply scanning people as they lay around doing nothing. This allowed scientists to study the network in people who weren’t even conscious, revealing something unexpected.

Raichle reported last year that the network’s resting waves continued in heavily anaesthetised monkeys as though they were awake (Nature, vol 447, p 83). More recently, Greicius reported a similar phenomenon in sedated humans, and other researchers have found the default network active and synchronised in early sleep (Human Brain Mapping, vol 29, p 839 and p 671).

It threw a monkey wrench into the assumption that the default network is all about daydreaming. “I was surprised,” admits Greicius. “I’ve had to revamp my understanding of what we’re looking at.”

Given that the default network is active in early sleep it’s tempting to link it with real dreaming, but Raichle suspects its nocturnal activity has another purpose – sorting and preserving memories. Each day we soak up a mountain of short-term memories but only a few are actually worth adding to the personal narrative that guides our lives.

Raichle now believes that the default network is involved, selectively storing and updating memories based on their importance from a personal perspective – whether they’re good, threatening, emotionally painful, and so on. To prevent a backlog of unstored memories building up, the network returns to its duties whenever it can.

In support of this idea, Raichle points out that the default network constantly chatters with the hippocampus. It also devours huge amounts of glucose, way out of proportion to the amount of oxygen it uses. Raichle believes that rather than burning this extra glucose for energy it uses it as a raw material for making the amino acids and neurotransmitters it needs to build and maintain synapses, the very stuff of memory. “It’s in those connections where most of the cost of running the brain is,” says Raichle.

With such a central role, it shouldn’t be surprising that the default network is implicated in some familiar brain diseases. In 2004, Buckner saw a presentation by William Klunk of the University of Pittsburgh School of Medicine. Klunk presented 3D maps showing harmful protein clumps in the brains of people with Alzheimer’s. Until then people had only looked at these clumps in one brain location at a time, by dissecting the brains of deceased patients. So when Klunk projected his whole-brain map on the screen, it was the first time many people had seen the complete picture. “It was quite surprising,” says Buckner. “It looked just like the default network.”

Raichle, Greicius and Buckner have since found that the default network’s pattern of activity is disrupted in patients with Alzheimer’s disease. They have also begun to monitor default network activity in people with mild memory problems to see if they can learn to predict who will go on to develop Alzheimer’s. Half of people with memory problems go on to develop the disease, but which half? “Can we use what we’ve learned to provide insight into who’s at risk for Alzheimer’s?” says Buckner.

The default network also turns out to be disrupted in other maladies including depression, attention-deficit hyperactivity disorder (ADHD), autism and schizophrenia. It also plays a mysterious role in victims of brain injury or stroke who hover in the grey netherworld between consciousness and brain death known as a minimally conscious or vegetative state. Steven Laureys, a neurologist at the University of Liège in Belgium, has used fMRI to look at patterns of activity in the default networks of people in this state. “You can really see how this network breaks down as coma deepens,” he says. He is now looking for a link between default network activity and whether patients will regain consciousness after, say, 12 months. “We’re hoping to show that it will have prognostic value,” he says.

All of this has been a long time coming since Sokoloff’s surprising observation 55 years ago. Watching the brain at rest, rather than constantly prodding it to do tricks, is now revealing the rich inner world of our private moments. So the next time you’re mooching around doing nothing much, take a moment to remind yourself that your brain is still beavering away – if you can tear yourself away from your daydreams, that is.

Sidebar: The meditating mind

WHEN Zen Buddhists meditate, they may be deliberately switching off their default network, a recently discovered system within the brain that has been strongly linked with daydreaming (see main story).The goal of Zen meditation is to clear the mind of wandering, stream-of-consciousness thoughts by focusing attention on posture and breathing. Giuseppe Pagnoni, a neuroscientist at the University of Modena and Reggio Emilia in Italy, wondered whether this meant they had learned to suppress the activity of their default network.He recruited a group of volunteers trained in Zen meditation and put them in an fMRI scanner. He presented them with random strings of letters and asked them to determine whether each was an English-language word or just gibberish. Each time a subject saw a real word, their default network would light up for a few seconds – evidence of meandering thoughts triggered by the word, such as apple… apple pie… cinnamon. Zen meditators performed just as well as non-meditators on word recognition, but they were much quicker to rein in their daydreaming engines afterwards, doing so within about 10 seconds, versus 15 for non-meditators (PLoS ONE, vol 3, p e3083). The Secret Life of the Brain

Not only is the default network the place where we daydream, it’s also becoming a way to define our consciousness:

Daydreaming your way out of a coma? Unlikely as it sounds, keeping track of a wandering mind may one day help doctors to discover whether a brain-damaged individual is still “in there”.

When a healthy person is daydreaming, their brain is not occupied with specific tasks and the “default network”, a series of specific, connected regions in the brain’s cortex, kicks in. The network’s purpose is still hotly debated but recent evidence suggests it keeps the brain primed and ready to take on new tasks. Problems activating the default network have been linked to cognitive diseases like Alzheimer’s and schizophrenia.

Now Steven Laureys and colleagues at the University of Liège in Belgium have used brain scans to measure the activity of the default network in 13 brain-damaged people whose levels of consciousness were different.

Their study, presented at this week’s meeting of the European Neurology Society in Nice, France, found that activity varied in proportion to the amount of brain damage. Minimally conscious patients had a 10 per cent reduction compared with healthy individuals, while activity was reduced by 35 per cent in coma patients and those in a persistent vegetative state (PVS). There was no activity at all in the default network of a brain-dead patient.

Laureys concludes that such a scan could act as a “consciousness meter”. “This could turn into an utterly useful way to diagnose residual consciousness in brain-damaged patients,” he says. Such a test could dramatically affect the fate of brain-damaged patients, by helping to determine whether to treat them with drugs or therapies, and in some cases, whether to keep them alive at all, says Laureys.

Usually, consciousness is measured by running a battery of behavioural tests. But these may miss some people who are minimally conscious. Two years ago, researchers at the University of Cambridge, together with Laureys’s group, investigated an alternative. They found that the correct brain areas lit up in someone they thought was in a PVS when she was asked to imagine playing tennis. This indicated that she must in fact be conscious (New Scientist, 7 July 2007, p 40).

However, the test is difficult to carry out and negative results are hard to interpret as the patient may simply not be able to think about a particular task. Measuring activity in the resting brain is quicker – and doesn’t depend on the patient responding. “We just scan someone for 10 minutes and get an easily quantifiable read-out,” says Laureys.

John Whyte at the Moss Rehabilitation Research Institute in Philadelphia, Pennsylvania, who is testing drugs that may help restore consciousness, says that although larger studies are needed to determine how reliably the default network indicates consciousness, assessing awareness in the resting brain is crucial to treating unresponsive, brain-damaged patients: “To find the right treatments, we need to be able to classify patients better, and resting assessments like this one should help with that.”

Joseph Giacino at the JFK Medical Center in Edison, New Jersey, agrees: “If this can help us to sort patients by how well connected their brains are, we might be able to use it one day to better predict who will wake up and who won’t.” ‘Consciousness meter’ may predict coma recoveries

The default network is where we imagine the future and the past.

[…] Much of that work has been documented by Gilbert in his book Stumbling on Happiness. “Every time you say, ‘I think I’ll go have lunch’, you’ve just thought about the future,” he says. That is just one small example of a general tendency to project ourselves forwards in time. According to Gilbert, psychologists studying stream of consciousness have found that the average person reports spending about 12 per cent of their waking hours thinking about the future.

It is easy to see the benefits of spending so much time in reverie. Running through future scenarios helps us achieve outcomes we want – and avoid ones we do not, perhaps as a direct result of learning from memories of past mistakes. We can maximise the enjoyment of future events by looking forward to them, while envisioning negative events helps us minimise their impact: volunteers’ hearts beat faster and they sweat more over lesser, but unpredictable, electric shocks than over larger, predictable ones.

In fact, there is evidence that mental time travel is such an important part of our inner lives that our brain will engage in it whenever it gets the chance. For more than 50 years, neuroscientists have known that even when your brain is apparently at rest, there is something important going on inside it. This comes from experiments showing that as the brain shifts gear from a passive, undirected state to an active, directed one – such as solving a puzzle – overall blood flow and oxygen uptake stay the same. So the “default” brain is up to something – but what?

A number of recent studies have tried to answer this, by scanning subjects who are doing nothing in particular. These studies always find the same surprising pattern of brain activity: the brain’s default state shows remarkable overlap with the mental time-travel network discovered in recent brain scans, according to Randy Buckner, another Harvard psychologist (Trends in Cognitive Sciences, vol 11, p 49). It seems that unless called upon to do something specific, your brain is busy recalling the past or projecting into the future. So next time you catch yourself staring into space instead of getting on with your work, or drifting into reverie as you try to read a book, don’t beat yourself up about it. Your daydreams will pay off in the long run. Future recall: your mind can slip through time

I’m very excited about the default network. I’ll post some comments about why in a separate blog.

Written by alienrobotgirl

21 December, 2008 at 11:47 pm

Posted in Neurotransmitters

The problem with the low oxalate group

with 6 comments

I have so many more important things to do than this. Internet wars are just tiresome. However, when something upsets me, I tend to dwell on it and I can’t do anything else until I have had my right of reply. Hence I am writing this instead of writing one of the final chapters of my novel. I would much rather be writing my novel, I was working on a killer scene but because of this it’s fizzled out like a damp squib. This is why I don’t do the internet anymore.

I wrote a criticism of the low oxalate diet some time ago. Looking back on the article now, I can see I spent a lot of time waffling, ranted off on other subjects like gluten, and wasn’t clear enough in my conclusions. In actual fact, the article should have been entitled “the problem with the low oxalate yahoo group,” since that is really what I was criticising.

So, I’ll state my conclusions about the low oxalate diet here:

1. A low oxalate diet is helpful to some people, particularly those with kidney stones or vulvodynia. I have recommended people consider oxalates along with other theories on the occasions when their symptoms are anomalous and/or do not resolve on the failsafe diet.

2. There are many, many people on the low oxalate diet group who are clearly affected by salicylates, amines and glutamates, and may not be reacting to oxalates at all.

3. These salicylate/amine/glutamate responders are helped somewhat by the low oxalate diet because it cuts out a very, very similar list of foods to those cut out on the failsafe diet, in particular, the very high chemical foods failsafers see reactions to, like chocolate, nuts, leafy greens, “too much protein” (i.e. amines) and so on.

4. These individuals falsely draw the conclusion that they are responding to oxalates. When they react to anomalous low oxalate/high salicylate/amine foods, they believe they are “dumping” oxalates. This is the equivalent of a candida “herx”. It is something that people use to explain away anomalies rather than reconsider that their hypothesis may be false.

5. It is damaging that people who are not responding to oxalates are continuing to believe that they are. It is damaging to themselves, and damaging to others with the same constellation of symptoms. It is also damaging to the science of the low oxalate diet, because it is really messing up the perception of what symptoms are and are not caused by oxalates, and it is really messing up their variables.

6. This kind of group, like so many other yahoo health groups, is what I call an aspie-trap. Aspies see patterns in things. Sometimes those patterns aren’t really there. Aspies can get attached to things and hate to move on, and they will keep on trying for years without concluding that they are on the wrong track.

7. I wish these people would try the failsafe diet FIRST, before trying a low oxalate diet. Unfortunately, most of these people have not heard of the failsafe diet.

I wrote the post because I was SO TIRED of having people come to my group who had tried the low oxalate diet and it didn’t work properly for them, or they were really, really confused about what they were reacting to and trying to cut out too many foods at once.

My problem is not with a low oxalate diet per se, it is with the really big goof-ups people testing a low oxalate diet have been making in the scientific method. My main point was this: unless you have tried the failsafe diet first, there is absolutely no point going on a low oxalate diet. Unless you have first established whether you react to salicylates, amines and glutamates, you are failing to control your variables properly!

I’ve had some moderate hostility in response to that post. It doesn’t help that I waffled a lot.

I have a nifty RSS feed that notifies me when other people link to my blog, and it turns out that someone from the trying low oxalates yahoo group recently discovered the post.

First I found a blog post with a copy and paste of Susan Owen’s response, along with the following comment:

Below from Susan, list owner of the oxalate list. The low oxalate diet works for me and I continue to read the list to find out more info. I suggest the list to clients who know someone with problems which seem like low oxalate diet might help. Lots of success stories on the list of people with kids with Autism or Asperger’s syndrome who had to deal with temper tantrums, rage, etc. Low Oxalate diet does not cure all problems from Autism, but it sure seems to help a lot. [my emphasis]

Unfortunately this is exactly what I mean by point 6. on my list. The low oxalate diet is an aspie-trap. It helps, but it does not cure all the problems. That’s because oxalates are unlikely to be the problem! The diet is simply working by cutting out most salicylates, amines, and glutamates. Think about it: why would cutting out oxalates fix temper tantrums? Oxalates don’t affect neurotransmitters, unless you are SO toxic that they have disturbed your blood mineral levels. Salicylates do affect neurotransmitters, and amines and glutamates ARE neurotransmitters.

So here’s what happened on the trying low oxalates group.

Someone posts a link to my blog post along with the following comment:

I think the author is a bit hostile to anything that does not fit with her diet 26202

I think this is a bit of an unfair introduction, don’t you? The only thing I’m hostile to is pseudoscience. I’m very hostile to morgellon’s disease, for example, or chronic lyme disease. I recognise very much that different people have different dietary needs, that’s why I don’t go out of my way to criticise carbohydrates even though I prefer to low carb. The only diet I’m actively hostile to is the candida diet, because it is such utter CAM tosh.

Says the next poster:

I looked at this point, and the person seems to have a bone to pick. Too bad – telling people a diet doesn’t work just because she thinks they don’t have data is like saying the sun isn’t shining because it’s behind the clouds.

Nowhere in my original post did I suggest people not try the low oxalate diet because of  “a lack of data”. This is an odd thing to say. I clearly spend most of the post telling people to control their variables – i.e. to clarify their data by first testing an established diet – the failsafe diet – which known to clear up the symptoms that are claimed by the trying low oxalates group to be caused by oxalates.

There are lots of folks who are pro and con all sorts of things, and when they are pro or con because of a personal bone to pick (my guess with this blogger) then you aren’t going to change their minds. That’s fine: I’ve got my results with my daughter, and that’s all that I need.

A personal bone to pick? This individual is now inventing stuff to explain my actions away. Of course, I can’t be making a rational argument, I must have some sort of emotional hostility to the low oxalate diet. Obviously I have been personally offended by the low oxalate diet and bear it a grudge. Perhaps I really, really like rhubarb or something.

However, she’s aggressive and nasty so I’m not likely to put a comment on her blog. 26207

I can only say WTF?! I will certainly dish it out in the comments section when people write me anonymous insults (as someone chose to on that post), but there’s nothing aggressive or nasty about my criticisms of the low oxalate diet group.

This time it’s Susan Owens’ turn:

This particular blog is pretty clearly what is called an “argumentum ad hominem” […] Ad hominem argumentation is along the lines of “You’re ugly and your mother dresses you funny”.

Notice how much space this blog piece gives to characterizing the personality of the people on our list (not just me). Her own diagnosis of us as being Aspergers seems to be what invalidates, in her eyes, what we do here, or any need on her part to address specific points of research we’ve brought in from pubmed. I wonder when (if ever) she was on our list because she must have been busy diagnosing us rather than paying attention to the scientific details!

Why would having Asperger’s invalidate “what we do here”? I have Asperger’s. If I was out to invalidate people with Asperger’s, I would be invalidating the whole of my own blog and the whole of my personality. I have a pro-aspie bias and generally think of aspies as being smart, technical people like me, with a few unfortunate weaknesses, in that, untrained, they can get really carried away with things. There was no ad hominem attack involved. My own group is full of smart aspie people too, many of whom have the same weaknesses. I am always trying to get them to control their variables and not jump to conclusions on too little evidence (apologies community members!).

The problem in interpretation here, is that Susan has assumed that being an aspie is a negative thing. It isn’t. It’s the best thing that ever happened to me. I’m GLAD I was born this way. If you told me I could eat what I want and have loads of friends, I would not give it up in exchange. Susan thinks I am criticising the low oxalate group members for being weird. I’m so not.

Instead, what I was trying to do was to point out the horrible ways in which internet health forum aspies can get trapped in styles of thinking and end up in the wrong place. It is no different with the candida diet. I am so tired of seeing these individuals turn up at my group believing they have an oxalate problem (or a candida problem) having been low oxalate (or on the candida diet) for ages, and after proper testing on my group, THEY DON’T have a problem with oxalates (or candida). I have certainly had individuals turn up who DO have a problem with oxalates (or candida), but they are in the minority and have specific conditions like vulvodynia (or thrush).

In actual fact I devote very little space in the post to this characterisation of aspieness (four paragraphs out of around twenty five), the vast majority of the post describes the flaws in people’s reasoning that can lead them to false conclusions about what diet they need, and scientific criticisms, which are not addressed by Susan.

Susan may wonder, but I have been lurking on trying low oxalates for a long time now. I found the group a couple of months after I first went failsafe. I thought “hmm, there’s a variable I ought to test for, maybe it explains some of my anomalous reactions,” and so I did test for it. I discovered that I do not respond to dietary oxalates. I am just very sensitive to food chemicals (and only mildly responsive to the opioid peptides in gluten and A1 casein, while we’re at it, and no I don’t have leaky gut either). I still sometimes suggest oxalates as a cause if I see a rare anomalous reaction in myself or someone else. However, I usually trace anomalous reactions to sulphites.

Most people don’t have the luxury of variable-controlled testing like I did, because they are unaware that there is more than one diet. The longer I lurked on the oxalates group, the more I realised that there were so, so many people there who were responding to salicylates and amines and attributing this to oxalates, and they were all getting trapped in the same confirmation-bias style of thinking that plagues so many CAM groups, whether they be GFCF, candida, lyme, or whatever.

Next Susan goes on to write:

Interestingly, she says in the “about me” section of her blog that she has Aspergers. She also says:

>I have a variety of chronic genetic health problems and peculiarities, including asperger’s traits, ADD/concentration problems/brainfog, cyclothymia symptoms, fibromyalgia (I do have an official diagnosis for that), reactive hypoglycaemia, back and neck pain, ear ache, heart palpitations, insomnia and hypnic jerking, allergies, asthma, and eczema. Messy, huh?

I don’t know what listmates think as they read her list of health
complaints, but to me, she sounds like a pretty good candidate for trying LOD, but I doubt she will try it because of her loyalty to the Failsafe model.

Can you imagine how much this remark irritates me?

It presumes I am too prejudiced and close-minded to try the low oxalate diet. In fact, I have already tried the low oxalate diet and I have discovered that I do not react to oxalates.

It is a beautiful example of confirmation bias. Susan has quoted this list of health problems from my about me page. The very next paragraph on my about me page goes on to describe how I follow the failsafe diet. It then concludes with the following phrase:

[T]he above health problems have all but vanished as a result.

In spite of clearing up my health problems by going on failsafe, Susan still believes I am a candidate for the low oxalate diet. Unbelievable. This is a very strong indication of confirmation-bias in her thinking style.

Susan goes on to make a couple of statements I totally agree with:

Her blog gives me the opportunity to say here that I’m thrilled to hear about the improvements people have seen on this diet, but there isn’t a good reason to develop a loyalty to the diet outside of what it has been capable of changing. Any diet should rest on its own merits in being able to help people, but it shouldn’t acquire a life of its own.


I am confident LOD has many specific niches and can stand on its own merits and can compete “in the open market place” (as if that were a goal?). My goal is to get people better and I see LOD as one very interesting and capable tool which has its own relevancy and reason to study carefully.

And some points I don’t agree with:

When people criticize THIS STAGE of the diet’s history, I guess they are expecting RESEARCH at the beginning stage of its life, to pop, as it were, out of the womb already dressed in academic gowns, carrying a Ph.D. diploma, sporting a full beard and speaking in a voice that is already low, mellow and mature!

The problem is, Susan, you have a very good opportunity to do some of this research, albeit informally, with your group members. But unless you actually tutor them to control their variables properly, everything you are doing on trying low oxalates is invalidated by the existence of the failsafe diet, and specialist allergy/food intolerance doctors are not going to take it seriously.

You need to tell your audience to test for salicylate, amine and glutamate reactions. Because all of the symptoms you claim to be caused by oxalates – with the notable exception of kidney stones, vulvodynia, and one form of arthritis – are already established by the Royal Prince Alfred Hospital Allergy Unit to be caused by salicylate, amine and glutamate sensitivity. Unless you are going to weed out all of the people on your group who ought to be failsafe, then you are not going to be able to discover those individuals who have actual real problems with oxalates. Control your variables!

Susan finishes with the following remarks:

It seems LOD’s philosophical critics tend to think the only way to stop the LOD from spreading like a plague (and offering competition to other diets with loyal followings) is by discouraging people on the front end from ever joining our list to consider what we present here. I guess that is why this lady wants to characterize our list as

>so systemised and technical, it tends to attract aspies, rather like flies into a big sticky spider web. Whee, thinks the aspie, I like this; technical language, orthomolecular medicine, smart people like me, and lots of complicated theories!

So I will state again, clearly, the objective of my original post was not to discourage people from trying the low oxalate diet. It was to encourage them to try it whilst controlling their variables. It was to encourage them to avoid that big sticky spider web of thought that results from confirmation-bias, from being over-loyal to diets that only half-fix the problem, and from assuming that what appears at first glance to be scientific is actually fully grounded in science.

I am not sure why this message did not get through in the first place, but I suspect it has something to do with people reading things the way they would like to read them instead of reading what is actually written.

I am not sure why Susan wants to characterise me as someone who is afraid of a diet which “offers competition to other diets with loyal followings” – i.e. that I am somehow afraid that the low oxalate diet would take over from failsafe. This is not a marketplace and diets are not wares. I have no financial interest in the failsafe diet.

I also have no credibility or reputation invested in the failsafe diet, which is already very well established and used widely in Australia (unlike Susan’s diet). On my group, if I think someone is not sensitive to salicylates and amines, I will suggest a different course of action, whether that is a different diet, or a trip to a doctors to be diagnosed with a completely different condition. For example, frequently when individuals present with digestive problems, the first thing I will ask is if they have been tested for celiac disease, despite the fact that many people intolerant of salicylates and amines have digestive problems. The only reputation I have invested in is in remaining scientific and open minded, and in steering individuals towards the right cure for their problems, not in steering them towards what I would like to be the cure for their problems.

At any rate, I hope ths woman hasn’t ad-hominem argued herself out of trying something that would get her well, or at least better! That would be sad, wouldn’t it? 26225

Were it true, it would be very sad. But it is not, because I have actually controlled my variables properly.

Susan focusses almost entirely on what she regards as the “ad hominem attack on aspies” at the start of my post and doesn’t address any of my actual criticisms. Once Susan has had her say, everyone else goes along:

I sure won’t give her a thought. You have helped so many of us. We must just ignore posters like this. […] just let the nuts go spread their nonsense and we’ll continue to get our health back. 26226

So now I’m a nut. I’m not making any rational criticisms at all.

Funny that the criticism characterizes us all as “aspies” when there are some of us here who have arrived due to vulvar pain and chronic yeast […] Her post is personality assassination of a group based on very little evidence. 26228

All I said was that the group was “very aspie”, not that everyone on it had Asperger’s syndrome. Why do some people think in absolutes? Keep ignoring the 20+ paragraphs of logical criticism that followed the characterisation, in the hopes that they will go away.

sounds like this lady suffers from the same thing other closed-minded people do when it comes to health issues. it’s sad that some get an *attitude* when they feel like they have more education under their belt and start belittling everyone else, even though they may have no experience whatsoever in what they’re writing about. 26240

When criticised, people like to console themselves by turning the critic into an emotionally driven character rather than a rational one in an effort to undermine their arguments.

People don’t like to countenance ideas and theories that haven’t been constructed in their own minds. Maybe it’s a matter of personal pride. Such a pity. It is in my opinion one of the greatest barriers in the development and proliferation of new ideas and the greatest impedance to helping our kids. 26242

Strange, because I didn’t construct the failsafe diet in my own mind, or the GFCF diet in my own mind, or the Atkins diet in my own mind… but I countenanced them. I’ve countenanced a whole lot of ideas in the past. At one point (when I was really ill and desperate) I thought I had candida or lyme and I was juicing green vegetables and eating apricot kernels like I had cancer or something. I disagree with the poster. I personally feel the greatest barrier to helping autistic kids is the sheer lack of scientific reasoning displayed by the biomed community. A lot of active harm is being done to autistic kids this way.

Being an aspie might be beneficial. 26243

Says someone who has got trapped in this odd idea that I think being an aspie is a bad thing.

This blog sounded to me like an intelligent critical opinion – albeit a shallow one. […]

Her website is difficult to comb for salient information, given her tendency to write on about absolutely everything she knows […]

However, she makes a good point that people can get overly fixated on a single problem like gluten sensitivity, yeast dysbiosis, etc and can tend to blame every physical and even emotional problem on their pet cause. She seems to feel the same way about salicylates, amines and glutamates… and because this listgroup is specifically about oxalates, it’s easy to get the idea that we’re all obsessed with that alone as the source of all our problems. 26250

The comment “she seems to feel the same way about salicylates, amines and glutamates” could be interpreted in two ways. I’m choosing to interpret it generously, in that this individual believes I do not blame everything on salicylates, amines and glutamates, which would be correct.

But yey for me! I may be shallow and in need of an editor, but at least one  on the low oxalate list actually read what I had written instead of what they wanted to read!

I would not have felt the need to reply to any of this if I had not been so wildly misrepresented and the criticisms I actually made were taken seriously. Instead what results is a character attack on me, and no answer at all to the arguments I put forward.

I didn’t say anything half as nasty in my original post as these people have written in response. Girls, act more like ladies and less like bitches, huh? If you’ve got a problem with what I write, keep it on a logical and a scientific level please.

Written by alienrobotgirl

6 December, 2008 at 1:48 am