The Autism Schism: On causes, cures, and a divided community

April is “autism awareness month”, or better still, “autism acceptance month”, so today is my last opportunity to post a contribution. I do have an idea I want to express but no plan of how to express it, so I’m going to wing it.

This is going to be more of an essay than a blog post. Basically, I intend to touch on the causes of autism, the reason there is no cure, and the schism between the parents of severely autistic children and the autistic adults advocating for neurodiversity – all in one very long post because in my view, they are all connected. (I’ll try not to ramble too much!)

This is all my own opinion. It’s based on a lot of reading on the topic – but I’m not going to provide references; this is not a scientific paper! You are free to disagree.

What is Autism, really?

Well, it’s complicated.

The first thing to understand is that autism is not a disease but a developmental difference. Unlike contagious diseases, there is no single cause and it is present from birth.

Everyone gets the concept of congenital differences such as a club foot or hare lip. But autism is more complicated still. While autism is often referred to as a neurological difference, that can be misleading, as it’s not a single neurological disorder either. Autism is actually a set of common behavioural issues, related to differences in brain development, which occur as a consequence of a neurological problem.

There are actually a variety of problems which can occur in the way neurons communicate with each other. It could be that developing neurons grow too fast or too densely in various brain regions, are affected by changes in the supporting environment (glial cells) or by neurochemical imbalances affecting the synapses. The brain tries to compensate for these various neurological problems by developing in a way that is different from the usual. This developmental difference can later be recognised (through observation of a person’s behavioural challenges) as coming under the umbrella of the autism spectrum.

To summarise: autism is not a single neurological disorder, but a common developmental trajectory of a brain and nervous system which functions differently from the usual. Or:

Various neurological problems –> developmental differences –> common pattern of behavioural issues = autism

This concept is crucial to understanding the rest of this post, as you will see.

Autism Causes

Firstly, when we are talking about what causes autism, we are really referring to the causes of the underlying neurological problem(s). Immediately it is clear that there could be many problems with many causes.

Through studies of twins and families, scientists have identified that genetics factor strongly but environment also plays a role. Again, it’s complicated. Let’s break it down:

  1. Sometimes autism occurs spontaneously in a family with no history, through “denovo” (new) gene mutations.
  2. The environment of previous generations plays a role, as toxin exposures in the father could lead to damaged sperm, and toxin exposures in the maternal grandmother while pregnant could lead to damaged ova in the mother. A link has been established, for example, between autism risk and paternal age – as an older father is more likely to carry mutations in his sperm.
  3. Sometimes a faulty gene or chromosomal abnormalities are already present in parents and directly inherited. This may be the case for certain disorders such as Rett Syndrome and Fragile X Syndrome.
  4. In many cases, no single faulty gene can be identified, instead it is the combination of multiple genes that results in high “polygenic risk”. Between a hundred and a thousand genes are suspected to have links with autism. Fun fact: many of the genes linked to high intelligence also contribute to autism polygenic risk – hence why Asperger’s is known as the Engineer’s disease. (Perhaps this is indicative of a neurology that is stretched to its physio-chemical limits, and more easily tipped over to a malfunctioning state?)
  5. Even with a high polygenic risk, environmental factors will affect gene expression (by epigenetics), which means that autism may not develop, or may develop to varying degrees of severity. For instance, it is known that maternal toxin exposure (such as heavy metals and pesticides) or taking certain medications during pregnancy increases autism risk for the baby. Premature birth is definitely linked. Even maternal stress has been identified as a factor.

OK, enough on autism causes. I think you can see that the wave of increasing autism prevalence can only be addressed by a combined approach, which looks at genetic, environmental, and epigenetic factors on a multi-generational basis. We still have a long way to go to get a full understanding.

Breadth of the Autism Spectrum

Not surprisingly, considering the various root causes of autism, the spectrum is very broad. Many autistics have co-morbid conditions such as epilepsy, dyspraxia, and intellectual disabilities, but even without considering co-morbids, there are wide variations in the severity of autistic traits.

This doesn’t mean that autism is on a continuum with the neurotypical brain or that “we’re all a little bit autistic”. There are commonalities in the way in which a developing brain adjusts to compensate for neurological issues. Hence, everyone diagnosed with autism, at whatever level, will have traits within the common domains: deficits in social communication and interaction; and restricted, repetitive patterns of behaviour, interests or activities. We’re just affected to different degrees, depending on the type and severity of the underlying neurological problem and the way in which our individual brain adapts.

Autism Cures and Treatments

There is much disagreement over whether or not an autism cure, if such a thing could be developed, would be desirable. To me that’s a moot point, because how can we develop a holistic cure for a condition which is not a single disorder? It’s not going to happen.

The way I think of it is this: if autism is not a single neurological disorder but a compensatory developmental trajectory, what does that tell us? We can think of autism as the brain’s attempt to build alternate pathways to work around a neurological issue. This alternative wiring is obviously important in maintaining the autistic person’s cognition. Any attempt to alter or remove autistic cognitive pathways is likely to have a negative effect on that person, unless the root cause of the autism – the underlying neurological issue – can also be resolved. Without understanding this, attempts to cure a person’s autism can actually be perilous.

When presented with a potential autism treatment, it’s important to see where it fits within the equation:

Various neurological problems –> developmental differences –> common pattern of behavioural issues = autism

For any treatment to be a genuine cure, it must address the root cause, that is, the neurological problem. This means that, while we might be able to prevent or treat certain subsets of autism with a common root cause, there can never be a single, definitive cure.

The most common treatments for children, such as ABA therapy, are aimed at lessening autistic behaviours. They target the third and last part of the equation. The obvious problem to this approach is that it neglects consideration of the reason why those behaviours have emerged.

Many of these therapies are somewhat successful, in that an autistic child may learn to modify their behaviours to become less disruptive. While this may seem completely positive to their teachers and carers, there can be a negative impact on the child themselves. Developmental differences are still present, internally, they just become less obvious on the outside.

Imagine, every moment of every day, feeling the itch of a hundred mosquito bites and being told that scratching them is absolutely not acceptable. How exhausting would it be to constantly fight that impulse? So the autistic child is having to actively and constantly work against their own natural impulses in order to keep autistic behaviours in check.

Don’t get me wrong, I’m not against helping autistic children to find work-arounds and alternatives to disruptive behaviours. It is possible to mould young brains to some extent, and the better an autistic can fit into society, the more opportunities and choices they are likely to have in life. In fact, researchers have identified a subset of autistic children who have an “optimal outcome” and actually lose their autism diagnosis.

Has their autism been cured, though? Of course not. The reason they’ve lost the diagnosis is that the diagnostic criteria are based on external observation of autistic behaviours. Such behaviours may be trained out of a person, but will they still experience difficulties due to their autism? Of course they will. The difficulties are likely to become internalised into mental and physical health problems instead, so you no longer see them.

What I’m saying is that we need to be careful when implementing any behavioural treatments to be sure we are always working for the benefit of the autistic person and not solely to extinguish “abnormal” behaviours, at any cost. Which brings me to:

The Autism Schism.

In recent decades, disability advocates have been moving away from the “medical model of disability ” and towards the “social model”. That is, not just seeing disability as a problem within a person which needs to be fixed, as far as medically possible, to allow them to function normally. The “social model of disability” takes the view that society itself needs to adjust and accommodate people with disabilities, so that they can be afforded the the same rights and opportunities as everyone else. That means accepting autistics fully into society, “abnormal” behaviours and all.

Another concept adopted by autistic advocates is that of “neurodiversity”. This is the notion that autism (and other neurological differences such as ADHD) should be recognised as being a part of the natural variety of human brains. The implication is that autism ought not be considered a disorder at all, but a different way of seeing the world which is equally valid.

My understanding of the schism which divides the autism community is this. On the one hand, there are people like myself, the “Level 1” or “Asperger-type” autistics. We have some ability to communicate our difficulties and maybe even advocate for awareness and support. Our aims may be to improve our employment prospects and mental health support, for example. We might use the social model of disability to argue for adjustments at work, and we might adopt the concept of neurodiversity by stressing that autistic brains are different, but not less than, the neurotypical. We may feel that with acceptance of our difficulties and small adjustments by others, we can demonstrate our value to society.

The parent of the severely autistic, intellectually disabled or non-verbal child may see things differently. There may be little comfort for them in the social model of disability because the fact is, there will be many things their child will not be able to achieve due to the severity of their autism. There are limits on how far their difficulties can be offset by societal adjustments.

The neurodiversity concept may also be problematic. It casts a positive light on autism only as far as it is caused by the natural shuffling of genes within the human gene pool. Certainly that may apply to polygenic autism, but when it comes to de-novo mutations or autism triggered by toxic effects, the concept is on shaky ground, and may be unhelpful. It alienates those whose experience of autism is overwhelmingly negative.

In Conclusion

What I’ve tried to illuminate in this post is the heterogeneity of the autistic population, which obstructs us from reaching a common concensus on our needs and advocacy goals. If nothing else, I hope readers will understand to avoid blanket statements with respect to autism causes and treatments.

One person may consider their autism a blessing, another a curse. One may strive for acceptance, another for a cure. Depending on their situations, both views may be equally valid and appropriate.

I think perhaps we’ve missed a step on the road to autism acceptance. To fight a battle an army must be united. If we could recognise and heal the internal divisions within the autism community, maybe we could finally advocate for our multiple and varied needs with one, powerful voice.

Not on the Label, Part 1: Fructans

(Alternative title: Professor Plum in the Dining Room with the Garlic Bread)

Here’s another post on nutrition – thanks to the new food sensitivities I seem to have developed.

Following on from my last post, I’m in the process of removing additives from my diet, as far as I can. But yesterday I had a reaction, once again to (mostly) home-cooked foods, and a google investigation has sent me down another dietary rabbit-hole. So this post is relating to something you don’t see listed on the ingredients label: fructans.

Here I put words into your mouth, and assume you are asking: What are fructans?

I admit, when I first saw the word I confused it with fructose. Fructose is the sugar molecule commonly found in fruit (notorious for causing weight gain when consumed in excess). It is possible to have a fructose intolerance, which leads to digestive distress, but that’s not what I’m talking about here.

Fructans, on the other hand, are complex carbs (that is, longer chain molecules than sugars), comprising several fructose molecules joined together and capped off with a glucose molecule. Just to confuse matters, there are several types of fructans, depending on the length of the chain. Let’s not go down that “wormhole within a rabbithole” here, let’s just lump them all together for now.

Thanks to the internet, here is a picture of some of the shorter-chain fructans which we can pretend to understand. Presumably the little flag-shaped molecule on the lower left is the glucose and the stack of boxes on the right consists of fructose molecules.

Here is a quote from this website:

Fructans consist of soluble fibre. Adding fructans to processed food is a growing trend in the food manufacturing industry. This is because fructans (especially inulin) are considered a functional ingredient that can increase fibre content of processed food. The fermentable fibre is meant to help the growth of ‘friendly’ gut bacteria because they act like prebiotics, which is great for normal people but not so great for people who can’t tolerate FODMAPs!

I’m not going to explain FODMAPs here, but if you read my previous post, you’ll see the link between long-chain fructans like inulin and the thickener guar gum. They are both long-chain carbohydrates which are slow to be digested with our own enzymes, but can be fermented by bacteria in our gut. And supposed to be good for us.

Which foods contain fructans? I hear you asking. (If you’re asking something else, blame the double empathy problem and bear with me!)

All kinds of things, it turns out. While the more simple sugars tend to be confined to particular food groups (such as fructose in fruits and lactose in dairy), fructans can be found in various vegetables, cereals and fruit.

Unfortunately, most lists on the internet just mention foods that are high in fructans but don’t explain exactly how high they are. Which is important. When we’re talking about food intolerances, it’s not like an allergy when even a tiny amount can set off a reaction. With food intolerance, quantity is key – the more of the suspect food is ingested, the greater the reaction.

So I dug a little deeper and found that the foods highest in fructans are: (wait for it…)

Jerusalem artichokes and dandelion leaves.

Er… who eats those anyway?? I’m not sure I’ve ever encountered a Jerusalem artichoke. So I’ve cut things down to the common types of food that I eat (being a self-confessed commoner). Fructans content listed in grams per 100g:

  1. Garlic – 9.8 to 17.4
  2. Leek, bulb – 7.1
  3. Onion powder – 4.5
  4. Leek, whole – 0.5 to 3
  5. Onion, brown – 2.1
  6. Onion, Spanish – 01. to 1.8
  7. Rye – 0.5 to 1.5
  8. Wheat – 0.4 to 1.3
  9. Beetroot – 0.4
  10. Peach, white – 0.4
  11. Banana – 0.0 to 0.7
  12. Brussels Sprouts – 0.3
  13. Zucchini – 0.3
  14. Melon, honeydew – 0.2
  15. Grapefruit – 0.2

If, like me, you’re hopeless at remembering lists like this, I’ve developed a memory aid for you. The foods to avoid if you have a fructans intolerance are: WHITE-ISH STUFF (Plus Beetroot and Plums But not Potatoes).

Hopefully you can see now why it’s important to list by quantity. What would be the point of avoiding that peach or grapefruit, if you followed it with pizza and garlic bread?

Is there a test for fructans intolerance?

Nope. Not as far as I could find online. Seems like it’s only recently they’ve developed tests for fructose and lactose intolerance and they haven’t yet got to fructans.

Are there specific dietary guidelines for fructans intolerance?

Again, nope. At the moment there is only the low FODMAP diet, or the SCD (specific carbohydrate diet), which eliminate all kinds of carbohydrates for a while, not just foods high in fructans but also those high in fructose, lactose, and various long-chain carbs. So those are pretty extreme. The idea is to re-introduce foods gradually and work out which you can tolerate.

Are you intolerant of fructans, Kay?

Honestly, I’m not sure. But remembering things Mum has said I’m wondering if there might be a familial intolerance. There’s her tale of when the neighbour came round asking if we had any garlic and Mum not having any… and then wondering why garlic was not in her cooking repertoire. And there was her disappointed look when I added a heap of chopped raw onion to the tomato salad.

Plus it’s looking like I’ve had issues the morning after eating meals containing onions and garlic. Which is not conclusive since so many meals include onion and garlic and a heap of other veg – but still.

I guess my approach is going to be to cut out onions and garlic for a while and see how that pans out. Possibly I might have overdone the bread a bit, also, once I put it back into my diet, so I might have to limit that to one slice of sourdough per meal. And, of course, eliminate garlic bread!

And finally

If anyone out there has a fructan intolerance, I’d be interested to hear your experiences. Feel free to comment!

Checking Food Labels, Part 1 – Coconut Milk

I’m always open to learning new things about food and nutrition. Just wish my digestive system wasn’t making me learn the hard way! Anyway, this week I got in trouble the morning after eating a (really delicious, if I do say so myself) home-made vegetable curry.

This was a surprise, it being completely home-made – that is, I even formulated the spice mix myself, grinding up coriander seeds, cumin, fenugreek, black pepper, cinnamon and mixing with some turmeric powder and fresh ginger. Mm-mm. So I was puzzled what the issue was.

I’m wondering if it might have been the coconut milk. I used this one, having a lot of faith in the “macro” brand and thinking that “Certified Organic” would be OK:

The ingredients listed are: Organic coconut extract (74%), Water, Thickener (organic guar gum).

So… what exactly is guar gum?

According to Wikipedia, it’s “a galactomannan polysaccharide extracted from guar beans which has thickening and stabilising properties”. In plain(er) English, a polysaccharide is just a carbohydrate in the form of a long chain, which makes it slow to be digested. Galactomannan refers, I believe, to the types of molecules forming the chain. Apparently, guar gum is essentially undigestible by our own enzymes, though it may be partly broken down by our gut microbiota.

Honestly, I wouldn’t expect guar gum would be a problem for most people. Apparently, it might actually have health benefits because it acts like soluble fibre, adding bulk to the stool, and can lower cholesterol. The only issue associated with it was a past link with the pesticide PCP used in India, where it’s grown – but that wouldn’t be an issue if it were certified organic. On the whole, guar gum seems innocuous enough.

Remembering the bad reaction I had to gluten-free bread, though, I looked up the common additives in a popular brand. It lists thickeners (464,412). 464 is a chemical called hydroxypropyl methylcellulose, and 412 is… can you guess?… guar gum. I’m spotting a pattern, here.

Two thoughts pop up:

  1. Guar gum by its nature is undigestible, so it doesn’t feed us so much as it feeds our gut microbiome. It’s a prebiotic. That’s great news for our colon, where most of our helpful bacteria reside, but not good news if we have bacterial overgrowth in our small intestine, a condition called SIBO. Bacteria are not supposed to be hanging out in this part of our gut and are going to compete with us for nutrients and muck up our digestive processes. We don’t want to be feeding them. Conceivably, if I were suffering from SIBO, I might have problems with guar gum (and probably thickeners in general, and prebiotics).
  2. So what am I going to put in my curry?

I found another coconut milk in my store cupboard, this one:

This is another brand I trust, they produce decent Chinese food for the Australian market. Or so I always thought. But the ingredients are listed as: Water, Coconut extract (32%), Emulsifier (435), Thickener and Stabiliser (412,466). Yikes!

So even apart from containing less than half the amount of coconut extract (or double the amount of water, if you prefer), this one has three different chemical additives. 412 we know is guar gum, 466 is carboxymethyl cellulose (which sounds suspiciously like something cooked up in a lab), and the emulsifier 435 is something called polyoxyethylene (20) sorbitan monostearate (which sounds… well, scary). I’m not sure I dare open this tin!

From now on, I’m going with the more expensive brand:

Ingredients listed as: Coconut kernel extract (89%), Water.

No preservatives, no additives, gluten free and BPA-free lining to the tin. And if you were wondering about the downsides of not having emulsifiers and thickeners, there are some notes explaining that: it may solidify below 14 degrees C (without affecting quality); it’s natural colour is light grey; and the fats can separate when boiled (so it should be added in the final 5 minutes of cooking a curry).

So now we know.

It’s not always gluten

Well, I’ve been kind of ill (again) and not doing a whole lot except trying to stay well enough to get on with the basics of life, which is why I haven’t been posting much. Anyway, I thought I might as well give you an update on where I’m at.

So I’ve been having all these minor health issues over the last few years – from mental health issues to joint pains to digestive problems, and recently fatigue and daily headaches. It’s been so hard not knowing what was going on, especially as blood tests usually show me to be pretty healthy (if you don’t look too closely at my cholesterol levels – thanks for those genes, Mum!). And I certainly don’t look ill. As you know if you read this blog, I’ve been to-ing and fro-ing over whether these various issues were related to stress, autism, menopause, a combination of these, or something else.

Recently I’ve been wondering if I might have an underlying auto-immune condition. This is just speculation at the moment, and I could be quite wrong as I have a tendency to convince myself I have all kinds of nasty illnesses (when possibly the only thing I really have is health anxiety!). But I’ve been feeling so wiped out that I decided to try a dietary intervention to see if it helped.

(Don’t worry, I have been talking to my GP about these issues and she was OK with me making dietary changes while we investigate if there’s an underlying medical problem).

Nutrition being an interest of mine, I’ve read quite a few books about what is supposed to be good or bad for our health. Based on these, my first plan was to try eliminating bread/wheat and dairy, avoid processed foods and excess sugar, and reduce intake of starchy foods (nowadays just known as ‘carbs’ – which is stupid, incidentally, because most healthy plant foods are predominantly carbohydrates).

Three weeks in and: (a) it hasn’t exactly worked, but (b) it’s been interesting. It’s led me to try changes to my diet not based so much on conventional wisdom but on what I, personally, am reacting badly to. I’ve learnt that with diet, everyone is different, and we need to have an individual approach.

Here’s what happened:

Ten days of fieldwork in Far North Queensland complicated matters a bit, as the food was provided. Breakfast was tricky, with all the options involving toast and eggs. I tried eggs minus the toast, but didn’t get on with it. They offered me gluten-free toast, on the basis that “it can’t do any harm”.

Oh yes, it can.

That was when I learned my problem is not with the gluten in bread but most likely with additives. Some gluten-free breads contain all kinds of processed nasties like modified starches, canola or palm oil, vegetable gums and preservatives.

A particular nasty to watch out for in bread (in general, not just gluten-free bread) is preservative (282) also know as calcium propionate. Apparently, this chemical has been implicated in developmental delay, headaches, inattention, learning problems, sleep disturbances and more. Definitely one to avoid.

So I ended up having a special order of porridge and bananas for breakfast, which went down OK. For lunch I had meat and salad in a box instead of in a sandwich. I found I could handle this in small quantities, but too much salad disagreed with me. (Huh? Isn’t salad supposed to be healthy?). Dinners were typically meat and veg and went down well, except for one night when we had curry with a yogurt-based sauce. (Wait, yogurt is healthy too, right?)

Back in the office I was stuck for lunch ideas, my usual cheese-and-pickle-sandwich being off the table, so I went with salad again. And sprinkled some sunflower seeds and pepitas over it all for extra goodness. Bad mistake.

Then came the field trip to Collinsville when I was so very careful just to take safe fruits and nuts and salami sticks. Which were fine, but then I bought a coffee to keep me awake for the drive home. Oh boy, another mistake.

So today I’ve re-written my diet plan, to that shown below. Basically, processed foods are still out until I work out exactly which additives I’m reacting to. Seeds and whole grains are out – I don’t know if it’s the fibre or lectins or what, but I just can’t handle them. Salads and raw vegetables need to be limited likewise. And the jury’s still out on dairy and eggs, so I’m being careful there too.

The moral of this tale being, healthy food for one person may be toxic for another. And it’s not always gluten.

Nervous System Dysregulation – ASD vs ADHD

skateboarding picture 1
Sad boy sick of autism. Plays with yellow toy car while his mother is looking at him royalty free stock photography

I’m not an expert on ASD and ADHD – but there seems to be a lot of misunderstanding out there around the connections and differences between these conditions, so thought I’d put forward my 2 cents.

This is just my opinion based on what I’ve read and observed. Observations on ASD courtesy of myself and my son, and those on ADHD based on my (possibly undiagnosed ADHD) daughter and her (definitely ADHD) boyfriend.

So one connection between these conditions is they both involve nervous system dysregulation – but they differ in the details.

Let’s not get too technical. For one thing, I always get confused myself between the sympathetic and parasympathetic nervous systems. And where does autonomic nervous system fit in? Or the somatic? Better limit myself to one paragraph of explanation here.

So our nervous system is what allows our brain to find out what’s going on in the rest of our body and control how we respond. What I’ll be talking about here is the Autonomic Nervous System (ANS). “Auto” is the same root as in “automatic” and “autonomous” – it regulates involuntary processes like heart rate, blood pressure, digestion, and breathing (and yes, we can also exert control over breathing – more on this later*). Oh darn, I need another paragraph. Bear with me…

I’m going to talk about hyperarousal and hypoarousal. “Hyper” refers to an excess and “hypo” refers to a deficit (just like in diabetes, but referring to nervous system activation instead of blood sugar). This is to avoid talking too much about the 3 types of autonomic nervous system: parasympathetic (PNS), sympathetic (SNS) and enteric (ENS? – no idea). Because I figure we’re not doctors, we don’t need to know how it all works, we just need to know how it makes us feel and what it makes us do, right? Oh dear, I need one more paragraph. Or maybe two. But this will be the last technical bit, I promise.

To quote wikipedia:  the sympathetic nervous system is often considered the “fight or flight” system… it is a “quick response mobilizing system”. So when I’m talking about hyperarousal, that generally means the SNS is activated. (See why I’m confused? Why would a system that causes me so much trouble be called “sympathetic”, instead of “uncaring”, or even “downright nasty”?)

Wikipedia again: The parasympathetic nervous system is often considered the “rest and digest” or “feed and breed” system… it is  is a “more slowly activated  dampening system”. So the PNS brings us down from “OMG I nearly crashed the car!” to “let’s vegetate in front of the TV with a bag of crisps”. Hypoarousal would be when the the body stays in this resting state instead of upping its game when needed.

(P.S. “crisps” is “chips” to you Aussies. No, Brits, we don’t mean your kind of chips – those are “hot chips” here. Or “chippies”, which also refers to carpenters, just to make things absolutely clear. So I don’t mean hot chips, otherwise known as french fries, which are actually pommes frites, I mean chips which are cold and come in bags – and just because y’all call them chips doesn’t mean they’re not crisps to me. Glad we got that sorted. Don’t get me started on how to pronounce “yoghurt”.)

So if you’re still here, it seems like the dysregulation in ADHD is easy to understand. Basically, ADHDers spend most of the time in a state of nervous system hypoarousal. So don’t expect the best from them doing a mundane desk job or something repetitive, as they’re going to be hopping from one task to another, or else hopping from one foot to the other, trying to activate their SNS enough to maintain their attention. They probably won’t finish the task but it’s not their fault – it’s the way their brain is wired.

From my observations, it seems like ADHDers can up their attention levels and achieve good performance with a combination of:

  • stimulant drugs or caffeine. These may have a reverse, calming effect on behaviour
  • doing tasks with an active, physical component
  • doing tasks with a stimulating, social component
  • working when motivated by the stress of an approaching deadline, or
  • when intensely interested in the activity

I’ve also found that they crave sugary drinks and snacks – to their detriment, as the sugar rush they need will be followed by a whopping crash. (But try telling teenagers that).

Dysregulation in ASD seems to be a little more complex. I think we can exhibit hypoarousal similar to in ADHD, which is why there can be misdiagnosis, or confusion over whether a dual diagnosis would be applicable. But the difference is that we will also suffer hyperarousal under conditions that stimulate the nervous system. That’s why autistics are prone to meltdowns or shutdowns under conditions of stress or overwhelm. (This is not just my opinion – there’ve been scientific studies showing ANS dysfunction in autistics based on measurement of heart rate and the stress hormone cortisol).

As a personal example, my reaction to caffeine varies depending on the state of my nervous system. Typically I can handle a modest amount of coffee and it usually helps with concentration, but if I am in a hyperaroused state the caffeine will boost the SNS further and make things decidedly uncomfortable.

Autistics generally use repetitive body movements to help regulate our nervous systems. I don’t like the term “stims” (short for “self-stimulatory behaviours”) because it’s a misnomer – the movements may be used either to stimulate or to soothe; they are “regulatory behaviours” (“regs”? “lates”?). For instance, when I’m getting overwhelmed at work I will get up and walk around – but I might also get up and walk around to stimulate myself when I’m feeling bored. I play with my fingers when I’m nervous but might also do so when I’m trying to concentrate. I may not even know whether I’m hypo- or hyper-aroused, I just know that I don’t feel comfortable sitting still at that moment.

You can see that the nature of nervous system dysregulation in ASD means we have different (and often opposite) requirements to ADHDers to achieve good outcomes:

  • avoiding stimulants and caffeine, especially when stressed, angry or upset
  • doing tasks with an active, physical component – for short periods with calming rest breaks in between
  • avoiding or limiting tasks with a stimulating, social component
  • working without the stress of an approaching deadline

The only common factor to achievement within both groups is:

  • being intensely interested in the activity

In other words, whatever your neurotype, do what you enjoy!

*A final word, as promised, on the matter of respiration. Breathing is one of the few processes controlled by the ANS over which we can also exert conscious control. This works both ways – meaning we can use breath control to influence the state of our nervous system. Think of it as respiratory “stimming” (“regging”? “lating”? Hm, I need a better term). That’s why breathing is such an important part of practices such as meditation and yoga – and recommended for anyone who suffers any kind of hyperarousal such as anxiety or panic attacks or PTSD, as well as autism.

That’s all for now; hope this post provided a bit of intellectual stimulation (without triggering too much pacing!)

A tale of ills and pills

Hi all,

Just checking in and saying hi, sorry it’s been so long between blogs.

I’ve been having some issues on the mental health and medication front, which is why I haven’t sufficiently enthused about anything to blog about it. Since I’m here, and feeling a bit more myself now, I might as well tell you the story. If you don’t mind a blog of a personal nature.

So… these last few years something has not been quite right with my mental health but actually pinning down what it was and finding the correct ‘label’ has been challenging. It never fit the diagnostic criteria for anxiety, or depression, or PTSD, or perimenopause, though I would cycle through symptoms common to all of these.

And labels are important, you know? The first time I went to the doctor with foot pain I had to describe to her where the pain was and when it occurred and to what level and how that affected me, from which she gave me the label “plantar fasciitis”. Now if I start limping and someone asks me what’s wrong, I can tell them it’s plantar fasciitis (assuming I can get my tongue around the double i) and am delivered from the need to go through the whole story of when and how much it hurts.

Labels are the shorthand which enable us to give someone a sense of what we are going through and how they can help. Failing that, even when the person doesn’t understand what the label means, stating it with sufficient confidence and finality can still remove the obligation to explain one’s problems further (and place the onus on the other party to go look it up). Plus, of course, the label is important in obtaining the appropriate treatment.

So the story starts with me being given a tentative label of mixed anxiety and depression and being prescribed psychotherapy and antidepressants. The first antidepressant was mirtazapine which was actually quite good (not only for the effect on mood but because it had a sedative effect that helped me get enough sleep). I was on it for a few months, came off when I felt better, went back on when I started feeling bad again, came off again, went back on again. Then it stopped working; it pooped, as they say. I started feeling low and oversleeping and the sedative effect was no longer my friend but making me even more dopey.

Well the doctor was all for upping my dose (why do doctors do this? they push patients onto higher and higher dosages, with no thought of withdrawal symptoms when the poor person tries to come off). Instead I asked if I could switch to something else.

By this time, to be clear, I knew that I was not suffering from clinical depression. Or clinical anxiety, for that matter. After years of trying to find the right label I’ve worked out that it doesn’t exist – so I’m using my own. I’m calling it autistic stress disorder. Autistic because studies have shown that we on the spectrum have differences in the amygdala, the part of the brain responsible for emotional reactions. Stress disorder because it increases during stressful periods and manifests itself in a malfunctioning of the fight-or-flight reaction, which also occurs with anxiety disorders and PTSD, leading to periods of hyperarousal. Only we don’t have panic attacks we have meltdowns. Or we have shutdowns, which look like depression, because it becomes a struggle to engage with people and live our lives. In my case, as you’ve probably worked out by now, it also means losing the energy and motivation to write, or even blog, for long periods.

Getting back to the medication story, if you have any sense you are now wondering why I wanted to go onto another antidepressant, after working out I was not clinically depressed. And the simple answer is that antidepressants seem to help. They level out my mood enough that rather than get upset about anything and everything, the meltdowns get saved for the times when they are, more or less, justified by life events.

The important point in prescribing antidepressants for Apsergers/autism seems to be this: KEEP THE DOSE LOW.

I learnt this the hard way recently when the GP switched me onto an SSRI called escitalopram. This one was not for me, I could not live with the side-effects. At night my jaw was clenching up (out of my conscious control) making it hard to sleep, and I would wake with a headache every day. Apparently jaw-clenching indicates low dopamine levels, similar to Parkinson’s disease. It’s a rare side-effect of SSRI medication, occasionally seen at very high doses – not at the level I was taking, which was supposedly the lowest therapeutic dose.

I switched onto another SSRI called sertraline. As a medication approved for use with anxiety disorders and PTSD as well as depression, I thought it might be a better one for ASD. So far I’ve had no major side-effects, but I’ve learnt my lesson and am taking half the dose the doctor prescribed. And it seems to be working. (For which I am very thankful!)

The other medication I’m taking now is 2mg melatonin in the evening. As one heads into menopause oestrogen levels drop, and apparently oestrogen is important in the production of melatonin in the body (the hormone which makes you feel sleepy when it’s dark). So was it the perimenopause rather than anxiety to blame for me coming wide awake at 3am? Well, the melatonin is certainly helping me sleep through the night. Whether true effect or placebo, I’ll take it.

And the upshot of all this is that I am finally, after a rollercoaster 3 months or so, starting to feel more like myself again. Less overwhelmed by life in general, and looking forward to the drive up to Mareeba tomorrow for 10 days of fieldwork.

So that’s the tale of my adventures with a mysterious mental health condition and my quest for the fabled pill of eternal happiness, leading of course not to eternal happiness but to knowledge and personal growth, in the way of all the best fables. Thank you for reading!

Nothing to See Here

Do you want to know why I haven’t been posting?

Are you sure?

Are you sure you’re sure? It’s not going to be pretty.

OK – if you’re absolutely 100% sure you want to know – here it is, the explanation for my lack of energy / inspiration, complete with the trampling of a self-imposed rule not to talk about my kids online, and a general airing of my dirty laundry. But hey, I’ve got to vent somewhere.

So let’s start with my daughter. Everything always starts with A, she’s like that. So she had a bit of a mental health crisis and ended up spending a few hours at the hospital, and this time I pushed the staff a bit. As in, can someone please assess her for X (a condition she ticks all the boxes for – every single diagnostic criterion)? Oh no, she’s too young to be diagnosed, they tell me. But we can say she has “emotional dysregulation”. Fine, but will that get her the appropriate treatment, the one she needs, which was specially designed for people with X? Blank looks. It’s suggested we try general talk therapy as, after all, she hasn’t actually been diagnosed with X…. you get my drift.

And then there’s the gut issues. She’s always had pretty bad atrocious eating habits, but when she started staying home from school complaining of belly-ache, I thought it was anxiety, or just A being A. But recently it got really bad. As in, belly aches daily, frequent trips to the toilet, not eating properly. The doctor hasn’t been much help so far but after doing a bit of googling myself I can understand why. There are more causes of gut issues than blades of grass in my garden. It’s a big garden.

Anyway, I decided to get her to keep a food diary, and try her on an elimination diet. We knew she was lactose intolerant already but we got stricter with it – no more ice cream or that gunk they call ‘soft serves’, only lactose-free versions of milk and yogurt. Bacon and sausages were out too, because of the preservatives. And we went (mostly) gluten free.

A digression: I’d always thought gluten-free would be incredibly difficult, but once I’d (spent a small fortune and) stocked up on the right food it wasn’t that bad. We even had a bit of fun baking our own g-f muffins and cookies. Which leads me to the next part of the story:

The elimination diet failed to clear up the problem (although it was hard to be sure because A being A, she hadn’t kept the food diary, and she kept breaking the diet). But I did note a particularly nasty episode relating to a multi-coloured iced cookie, which I strongly suggested she not eat after seeing 33 additive numbers listed on the back, and that of course she ate anyway. And my brain went down a different path: food additives <-> processed food <-> excess sugar <-> gut imbalance.

So now we’re onto diet version 2. Gluten is back on, lactose and bacon are still off. Processed and packaged foods are limited, and sweet drinks are not allowed. The idea is to get her eating ‘real food’ – the stuff that comes from plants, or the animals that eat plants (with inspiration from David Gillespie’s book of the same name: Eat Real Food). She hasn’t got the hang of it yet. Thinking to ease her into it, I left a few packaged items on the ‘yes’ list, such as frozen pizza, plain crackers and sesame snaps – so, of course, those are what she’s been eating.

Then on Friday I had one of those (not unusual) calls from the school saying A was feeling ill and could she go home, to which I agreed. Got home from work that evening and she had a very large and obvious tongue-piercing. Can’t say I was very happy about that – even apart from thinking tongue piercings are gross, how exactly is having a painful hole through her tongue going to help get some order into her eating habits? A’s boyfriend proceeded to tell me a colourful story about the drug-using habits of his family, the moral of which seemed to be that he was proud to come from such a family because he loves them for who they are, and hence I should be supportive of all A’s choices because I love her. It was, I have to say, an outstanding piece of Gen Z logical rhetoric. But no. Believe it or not, we Gen Xers are actually capable of separating love of the person from love of the holes they punch through themselves.

As always happens in this household, all the drama with A has resulted in very limited attention being given to my son and his issues – and oh boy, does L have issues. It’s mind-boggling that he recently turned 20. It’s like he stepped into a time-warp at around age 16 and got frozen at the same level of development. So yeah, while I’m first to acknowledge he’s got a brain the size of a planet (with a nod to Douglas Adams), I’m not holding my breath for L to learn anything practically useful in life, such as how to drive or get a job. We’re still working on the regular showers.

Now here I have a bit of good news, a breakthrough! But only if you know the background. That is, the two previous times I’ve enrolled him a course of study, only to have him fail to submit his assignments, from some combination of not understanding what was expected, not wanting to ask, and fear of failure. That last one is a doozy, because every time he fails to submit something it reinforces his belief that he is incapable, which renders him more wary of trying anything, as he is sure to fail. Paralysis by over-analysis!

Anyway, back in February I heard about this TAFE course in Cybersecurity that would be right up his street. I mean, this is a young man who starts conversations by querying one’s method of password protection and wondering whether quantum computers are going to take over the world (or something… it all goes over my head). At first he was like, I don’t want you to waste your money again, but when I pointed out that it was government-subsidised and he only had to pay $48, he reluctantly agreed it might possibly be worth applying.

Fast-forward through 3 torturous months of asking L whether he’d submitted this, reminding him to check his emails, realising he needed to submit that, reminding him to check his emails again, not understanding whether he’d got accepted on the course or not, asking him to actually read through everything in the emails this time, and eventually finding out he was on the course. Then asking him where and when his classes were, discovering he had no idea, reminding him to re-read the emails over again to find out, or call the tutor, and realising he didn’t have a clue who his tutor was either, getting him to watch the orientation video, and now the breakthrough – ta da! He attended his first zoom tutorial.

But Jeez. How long am I going to be managing his life for him?

And speaking of failing to manage one’s life… let’s just say that a lot of L’s personality traits didn’t come from his dad’s side. We’ve got the blind autistic leading the blind autistic here. Which brings us to the ongoing saga of ‘what the heck is wrong with me?’.

I suppose you might think dealing with the aforementioned kids’ issues may be affecting my mental health, and it does get a bit tiring. But A and L have been a constant in my life and I’m used to dealing with their personality quirks; there’s something else going on. My latest theory (and I found a published study to back me up) is that peri-menopausal hormone changes are exacerbating my autism. (Try saying that quickly). So what looks like an anxiety attack followed by depression would be better characterised as a meltdown followed by a recovery period. Biologically, it’s my body not being able to regulate stress properly, so there’s too much cortisol in the body leading to an adrenalin surge (meltdown / freakout), followed by depletion of the adrenals and low mood (recovery period).

Of course, the meltdowns tend to happen in the place where I have least control over stressors or opportunity to self-regulate – the office. If the work is of a nature that keeps my brain happily occupied for hours at a time, the way I like it, I’m usually fine. But recently I’ve had not one project I can concentrate on but a series of requests and emails on multiple projects daily. This completely stresses me out; it’s not what my brain was designed for! At the end of last week I actually got so paralysed by the overwhelm of trying to work out what to do first that I could do nothing useful at all. Then a computer glitch leading to the loss of my timesheet entries (normally not a big deal) triggered me into a freakout, and it took me all weekend and then some to recover.

The conclusion to this long post being, I’ve been too distracted managing my health and that of my kids to get the headspace to post anything here. And I’m only posting this now as a way of processing things for myself.

Especially, right now, I’m processing the latest in the work issue. I admit, I’m proud of my abilities at work – I generally see it as the only aspect of my life in which I function up to a normal standard, or even a superior standard in some aspects. Vested in work is much of my self-esteem. So it was incredibly hard to do what I needed to do and ask for changes to help me maintain my mental health. I basically had to admit that there are aspects of the job that maybe I shouldn’t be doing.

My bosses are great, they really are. I believe we’ve come to an arrangement to get me a long-term project I can concentrate on that will hopefully minimise meltdowns. Plus more help with managing my work in the meantime. It’s a win, of sorts.

But there’s a lot of grief also. Because while I’ve known for a while now that I wasn’t going to get to a higher level at work but would need to stick where I was, I did believe I’d be OK there. I wasn’t expecting it to keep on affecting me like this. Plus I’ve never so openly explained my limitations before; I’ve only ever danced around it in the past, telling them issues I was having with the work but not fully explaining the root problem. I wonder how much respect I’ve lost now, and whether they’ll think of me differently.

Perhaps this was a necessary adjustment. Ultimately, when one is on one’s deathbed looking back, which will feel better: to have achieved success and acclaim at work, or to have put one’s best effort into giving one’s kids the love and attention they deserve? It’s a no-brainer, right?

Still, these last few years have given me a lot to process. And they leave me puzzling even more over how one is supposed to respond when people come up and ask: Hi Kay, how are you?

What on earth does one say? Fine, and leave it there? Do people understand the subtext, that maybe I’m not quite entirely fine, but I’m still alive and taking things a day at a time and remain optimistic for the future, so, I guess… nothing to see here.

Review – When the Body Says No

I just read this book “When the Body Says No (The Cost of Hidden Stress)” by Gabor Mate. It’s a bit old now, published 2003, but I hadn’t seen it before.

This is probably going to be the shortest review ever – because I can’t decide whether the content is profoundly wise or a load of codswallop. I’m actually hoping you, my lovely readers, would read the book and offer your own opinion in the comments.

Anyway, the premise is that modern medicine is problematic in separating the mind and the body, or mental health and physical health. The author uses case studies of patients to illustrate how aspects of their personalities and the ways in which they deal with life stresses may have contributed to the development of physical disease.

So far so good; I know from experience that mental and physical health are connected. The book clarifies how internal stress affects all kinds of neurological, endocrine (hormonal) and immunological pathways and thus can contribute to the development of disease. I can see this might be particularly relevant to autoimmune conditions such as multiple sclerosis (MS), Chrohn’s disease and rheumatoid arthritis, which together with cancers and motor neurone disease / ALS are the main topic of his case studies.

I was also interested in his thoughts on why some people with genetic or environmental risks for cancer and alzheimers disease go on to develop disease and some do not. I have sometimes wondered whether many of us might be carrying around early cancerous changes, and this book explains that we rely on fully functioning immune systems to keep these in check. And certainly it does seem to me as though doctors are still trained towards treating physical diseases without wholistic consideration of the life stress and coping mechanisms of the sufferer.

One thing that I am wary of, however, is drawing any conclusions from the few case studies examined in the book. In places, it reads as though the author is linking particular types of coping style with certain diseases, almost pointing to a “lung cancer personality” as being someone with repressed anger, a “rheumatoid arthritis personality” as being someone who looks after others and shows no weakness, or an “ALS personality” as being a driven perfectionist.

To me, that goes a bit too far. Extracts of his interviews with patients are presented which do illustrate the personality traits and coping mechanisms at play – but I had a niggling feeling that if one was to dive into the childhood/ family experiences of any one of us in a similar fashion, one would be able to find some kind of unhealthy coping mechanism. Do people even exist who have such maturity of outlook as to remain emotionally regulated through any life stress, and able to maintain the perfect balance of security and autonomy in their relationships?

No, I don’t think so either.

On the whole though, I found this book very interesting. It prompted a bit of soul-searching of the “do I have a problem with repressed anger?” type. But there’s no harm in that.

In fact, the book noted that positivity of the kind which stops us from examining the negatives in our lives can actually be harmful and lead to poorer outcomes. It is only by examining our own repressed emotions and harmful coping mechanisms that we can bring about change and healing.

OK, so not such a short review after all – and I’ve now decided I liked the book, even if I’m a bit wary of some aspects. Thoughts, anyone?