This post is all about those stomach problems typical of many kids with ASD and some of their neuro-typical close relatives. Since Monty, aged 10 with ASD, does not have any of these problems, it is not something I have looked into earlier. As you will see later in this post, by understanding the underlying science, we can move another step towards inhibiting systemic inflammation, which affects all people with ASD.
Irritable
bowel syndrome (IBS) and Inflammatory Bowel Disease (IBD),
First of all
we need to differentiate two common conditions with very similar symptoms. IBS is the less serious condition, though it causes
lots of discomfort.
Irritable Bowel syndrome - IBS
Irritable bowel syndrome (IBS)
sufferers show no sign of disease or abnormalities when the colon is examined.
IBS does not produce the
destructive inflammation found in IBD. It does not result in permanent harm to
the intestines, intestinal bleeding, or the harmful complications often
occurring with IBD. People with IBS are not at higher risk for colon cancer,
nor are they more likely to develop IBD or other gastrointestinal diseases
The exact cause of IBS is unknown. The
most common theory is that IBS is a disorder of the interaction between the
brain and the gastrointestinal tract, although there may
also be abnormalities in the gut flora and immune system.
Inflammatory Bowel Disease - IBD
Inflammatory bowel disease is a
group of inflammatory conditions of the colon
and small intestine. The major types of IBD are Crohn's
disease and ulcerative colitis
Crohn’s
disease has a strong genetic component and is far more prevalent among smokers. The usual onset is between 15 and 30 years
old.
Ulcerative
colitis is an auto-immune disease with no known cause. The symptoms are very similar to Crohn’s
disease, but there are some stark differences. Ulcerative colitis is far less prevalent among smokers
Autistic Colitis / Ulcerative Colitis
The
Inflammatory Bowel Disease (IBD) that seems to be relevant in Autism is
ulcerative colitis, so much so that Wakefield and Krigsman sought to name a
sub-type Autistic Enterocolitis. Due to
all the furore about vaccinations and autism, the research of these two gastroenterologists
has been blacklisted.
Dr Krigsman
has an informative website and has published some interesting research.
If you spend
all day looking via the endoscope at
children with ASD, you are bound to notice a thing or two. Ignoring what Krigsman observes is bizarre.
In case you
are wondering what he does, he is going through the mouth to do an Upper Endoscopy; for the Colonoscopy
he goes in from below. He does both
procedures under general anaesthetic. That
will be painless; I once had an endoscopy under general anaesthetic and you have no bad
effects. I had the misfortune to have
another one without any anaesthetic,
which was one of the most unpleasant experiences of my life.
Ulcerative
colitis looks like a nasty condition but Krigsman finds it is generally treatable
with some combination of
anti-inflammatory medication, antimicrobials, probiotics, digestive enzymes and
dietary restriction.
One thing he
does not mention is nicotine, more of that later.
GERD
Gastroesophageal reflux disease (GERD) is a very common disease. The acid within the stomach rises up into the
esophagus and in doing so, damages its lining.
Most children will outgrow their reflux by their first
birthday. However, a small but significant number of them will not outgrow the
condition. This is particularly true when a family history of GERD is present. It is
estimated that 15% of adults of adults are affected by GERD.
Krigsman
find that in kids with ASD and their siblings, GERD is relatively common.
Mechanisms linking IBS and IBD to
Autism
I have already
written about the link between food allergies, autism and behaviour. In those posts it was histamine released from
mast cells (along with cytokines and other nasties) that was the culprit. The treatments included antihistamines and
mast cell stabilizers (Ketotifen, Intal etc).
I would presume this would fall into the IBS category.
When it
comes to IBD, things get interesting.
In 1936 the
Nobel Prize for Physiology was awarded to Sir Henry Dale and Otto Loewi. One had identified the neurotransmitter acetylcholine
and the other had shown how the vagus nerve releases acetylcholine to control heartbeat.
It later became apparent how
important the vagus nerve is. The vagus nerve is a modulator of inflammation throughout
the body. Acetylcholine, the principle neurotransmitter released by the
vagus nerve, can exert its anti-inflammatory effect via binding to nicotinic
acetylcholine receptors (nAChRs), which are expressed on macrophages and other
immune cells.
In a recent post I showed that autistic brain samples have diminished acetylcholine and nicotinic receptor activity. I showed how this could be corrected either by drugs that mimic acetylcholine (eg nicotine or acetylcholine) or with an acetylcholinesterase inhibitor (Galantamine or Donepezil).
I found it
very interesting that IBD can be successfully treated by mild smoking (3
cigarettes a day) or with nicotine patches.
This then
connects various comorbidities in a very useful way and opens up therapeutic directions. The vagus nerve is also key to epilepsy. Vagus nerve stimulation is currently used to
treat epilepsy and depression.
Experimentally,
vagus nerve stimulation is already used in autism.
CONCLUSIONS:
Patients with ASD and intractable
epilepsy respond as favorably as all other patients receiving VNS therapy. In
addition, they may experience a number of QOL improvements, some of which
exceed those classically observed following placement of a VNS device.
Kevin J. Tracey
A neurosurgeon and inventor, Kevin Tracey, is the man behind
the inflammatory reflex. The inflammatory reflex is a neural
circuit that regulates the immune response to injury and invasion. All reflexes
have an afferent and efferent arc. The Inflammatory reflex has a
sensory, afferent arc, which is activated by cytokines, and a motor, or
efferent arc, which transmits action potentials in the vagus nerve to suppress
cytokine production. Increased signaling in the efferent arc inhibits
inflammation and prevents organ damage.
We will be looking at his research and the Cholinergic anti-inflammatory
pathway, in later posts
Inflammation is clearly a factor in at least some cases of ASDs. Clearly a CRP would be a useful addition to the basic tests done at diagnosis - in the UK a panel is done, but it has many clear drawbacks. If there is inflammation, the body will raise its serum ferritin. I know of no research - you may - where iron levels in ASDs have been cheacked alongside inflammatory markers. If the body is keeping iron levels low in its attempt to reduce chronic inflammation then (a) serum ferritin will tell us little or nothing about the iron status of the child and (b) the child may well struggle as it grows, with the huge demands on iron supply growth brings. Iron depletion may well be part of the cascade effect from inflammation which has serious effects on mood, behaviour, memory etc. It might also be expected to have an impact on thyroid function, heart rhythmn and a host more areas which would trigger further cascades.
ReplyDeleteOne important point - the touch sensitive, highly pain sensitive, anxiou ASD subgroup would be under represented in any research involving scans or blood takes - indeed, in almost all research. I've never seen that fact commented on anywhere.
If you have already looked at this, please let me know! Last of all, are you a scientist or do you have any qualifications?
Here is a very useful paper on various markers of inflammation
Deletehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2991432/
it is by Paul Ashwood, who is British living in California. I am sorry but I do not think there is a mention of iron.
As someone who has had to restrain his child with ASD while blood samples are taken, I can only agree with you. It is possible, but highly unpleasant for parents. X rays no problem. EEG, MRI never tried. There is a video on my blog of an EEG being done on an autistic boy, the parents are amazed how smoothly it goes.
I have lots of qualifications, but not in medicine. I have Masters degrees from Imperial College and INSEAD.
I have been contemplating doing some kind of a bowel cleanse with my son, who is 24. His stomach is bloated and though others think it is some kind of belly fat, the rest of him is thin and this seemed to develop in a very short period of time sometime last year.
ReplyDeleteHe has never had any kind of scope procedure and has a long history of constipation, which at this point I address with cape aloe, and that seems to stimulate a bowel movement at least every other day.
Dr Hulda Clark has a cleanse which is herbal and appeals to me.
Might there be better ones people have tried?
Thanks
Nancy
Hi Peter, here's an interesting link on B12 levels and Crohn's disease.
ReplyDeletehttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9771213/
I'm curious on how FRAA affect the gut too. Probably not in a good way.
-Stephen
Furthermore, it appears gut bacteria plays an important part in folate metabolism and immune cells creation.
DeleteA Role for Folate in Microbiome-Linked Control of Autoimmunity
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8159645/
Hi Peter, We have an 8 year old kid who is autistic. We were to meet with Dr. Krigsman because his neurologist suspected Chron's. Just as he suspected, my child appears to have IBD based on Prometheus precis blood work. We will get the all scopes done for him to confirm it. I wanted to find out how this relates to his behavior. If we get IBD under remission, do you know of any behavioral improvements that we may notice. Thank you!
ReplyDeleteHi, yes, there certainly can be a connection between active IBD and behavior in autism.
DeleteIf your child does have active Crohn's disease or another form of IBD, intestinal inflammation can affect much more than the gut. Pain, bloating, diarrhea or constipation, poor sleep, fatigue, reduced appetite and nutritional deficiencies can all have quite noticeable effects on behavior. A child who cannot easily communicate abdominal pain may instead show increased irritability, anxiety, agitation, repetitive behavior, withdrawal, sleep disturbance or other changes that can look like a worsening of autism.
There is also increasing evidence for communication between the gut and brain through immune, metabolic, neural and microbial pathways. So it is biologically possible that significant intestinal inflammation could have effects on brain function in addition to the more obvious effects of being unwell.
The interesting question is therefore what happens when the IBD goes into remission. I would look particularly for changes in things such as:
• irritability and emotional regulation
• sleep quality
• anxiety or agitation
• attention and ability to engage
• social engagement and willingness to interact
However, I would not necessarily expect the core features of autism to disappear when the IBD is treated. It may be more realistic to think of this as removing an additional source of physiological stress that can make an autistic child's baseline difficulties considerably worse.
Many of Dr Krigsman’s patients end up taking Humira. This is an expensive drug that blocks TNF-α, one of the major inflammatory signaling molecules involved in inflammatory bowel disease. Some people with autism respond remarkably well behaviorally to this drug.
Thank you Peter. My son has vitiligo as well. I just checked that TNF-alpha biologics paradoxically can flare up vitiligo. He also has elevated Thyroid Peroxidase (TPO) and is FRAT positive. It appears that he has many autoimmune issues. I am worried that if we don't use the right immunosuppressant, some of his autoimmune will be under control while something else flares up. Any suggestion on who is a good doctor/immunologist who may analyze through bloodwork on the issues in the inflammation pathway and figure out for example if TNF-alpha is right or JAK inhibitors are right for him. Is there any literature that I can read to understand the sensitivities/effects of various pathways on different autoimmune diseases. Thank you!
DeleteThe combination of IBD, vitiligo and elevated TPO antibodies is quite interesting. I would not necessarily regard these as three completely unrelated problems. In some autistic children, the pattern of comorbidities can provide clues about an underlying immune dysregulation.
ReplyDeleteI would also not assume that TNF-α is necessarily the key pathway. TNF may be important, particularly if the IBD is active, but other inflammatory pathways could be involved, including IL-1, IL-6, IL-17, interferon or JAK/STAT signalling. It could also be an interaction between several pathways.
There is another question I would be particularly interested in: does his behavior fluctuate when his GI or other inflammatory symptoms flare? For example, do you see changes in irritability, hyperactivity, anxiety, sleep, repetitive behaviors, social engagement or other aspects of his usual autistic presentation when he is physically unwell? If there is a clear relationship, I would consider that an important clinical observation.
You may want to consider consulting Dr. Harumi Jyonouchi, a pediatric immunologist at Rutgers/Saint Peter's in New Jersey. Her research has focused specifically on immune dysregulation in autism, including autistic children with gastrointestinal problems and changes in behavioral symptoms following immune insults. She has also emphasized that autism is biologically heterogeneous and that immune abnormalities may define subgroups rather than there being one immune mechanism affecting everyone.
That is why I think she could be particularly useful in your son's case. A gastroenterologist may quite reasonably concentrate on diagnosing and treating the IBD, potentially including an anti-TNF drug such as Humira if that is appropriate for the Crohn's disease. But given the additional vitiligo and thyroid autoimmunity, I would also want someone to look at the whole immune phenotype rather than assuming that TNF is automatically the answer.
There have been some remarkable reports of behavioral improvements in autistic individuals following anti-inflammatory treatment, including anti-TNF treatment, but this does not mean that TNF causes autism. One possibility is that inflammation acts as a modifier that exacerbates an existing autistic phenotype in susceptible individuals.
So I would be interested in establishing what happens to his behavior as the IBD is brought under control, while also having someone like Dr. Jyonouchi consider whether the combination of IBD, vitiligo and thyroid autoimmunity points toward a broader immune mechanism.
I think that could potentially tell you much more than simply asking which cytokine is elevated in a blood test.