Super skinny is a poor role model and another
driver of autism risk via ensuing endocrine problems
While some types of autism cannot easily be prevented, those that relate to the lifestyle of future parents clearly can be reduced.
Rather than just be shocked about an “autism epidemic”, with ever increasing prevalence, why not start doing something about it? People are staying at home to reduce the incidence of Covid-19; the risk of autism can also be reduced.
Today’s post is about the young females who, under peer pressure and Instagram pressure, choose to starve themselves in the pursuit of looking “good”.
School lunches are a daily subject of conversation in our house, since I always ask Monty, now aged 16 with autism, what he had for lunch at school. Monty’s assistant tells me that even though the lunches at school are not bad, he is one of the few to eat them all. The boys generally just eat the meat and potatoes and do not touch the fruit, vegetables and of course not any salad. The girls eat next to nothing. Why do the already skinny girls at school eat nothing? It's cool to be super skinny and the popular role model is Billie Eilish. So, the girls want to be skinny and feel depressed.
In schools in rich Western countries, the perceived eating problem is usually too much, rather than too little. When I drop off Monty, aged 16 with autism, at school all I see is skinny kids. Some do a lot of sport and athletic should not be confused with anorexic.
Anorexia is nearly always an issue in young females, rather than males. It is also very common in females with Asperger’s type autism, who are naturally prone to obsessions.
For most people the skinny look is just a passing issue, does it do any long-term harm? Apparently, it does.
This post was prompted by reading about a “celebrity” mother with all 3 kids diagnosed with autism. She is clearly an Instagram type, even in middle age.
She looks healthy (thin), had her children young, she is not one of those high IQ types of autism parent; the Dad is not a maths professor. Why are all the kids diagnosed with autism? Fortunately for her, it is not severe autism; the children can talk, her six year old son is asking about corona virus and they play together for Instagram. They are fussy eaters and do not like loud noises.
Being a former model and now a “celebrity”, it should not be a surprise that she reveals having had anorexia for ten years, then was diagnosed with PCOS, had the consequential fertility problems, but wanted a large family. Now she has 3 children with autism; she seems not to have made the connection between PCOS and autism. (Clearly endocrine dysfunction may not be the only contributing factor)
The Mum is an Ambassador for the UK’s National Autism Society (NAS). I think the most useful role she could perform would be to go into schools and tell skinny girls to eat more, rather than keep pushing her look good (i.e. skinny) and exercise more image on social media. Perhaps the NAS needs to learn more about autism.
Orthorexia is another common eating disorder. It is characterized by a fixation to eat only healthy foods, or to avoid entire food groups. It is often accompanied by exercise addiction, where exercise is foremost in life, rather than including exercise in a balanced lifestyle.
I am quite sure you could make an algorithm to identify people with Orthorexia or Anorexia, with or without exercise addiction, based on their Instagram posts. Perhaps they should get sent a warning of likely endocrine disorders later in life, including fertility problems and a substantially higher risk of having children with autism. Perhaps, “You too could become an Ambassador for the UK’s National Autistic Society”, might shock some skinny girls into eating more. These are likely the very same "cool" girls who make their female classmates with Asperger's type autism feel socially excluded.
Instagram use is linked to increased symptoms of orthorexia nervosa
PCOS
Not everyone with PCOS has polycystic ovaries (PCO), nor does everyone with ovarian cysts have PCOS.
Women diagnosed with PCOS have increased risk of having a child with autism.
Women diagnosed with PCOS have an increased chance of being autistic themselves. This not surprising since elevated male hormones in women is associated with autism, as in Turner Syndrome, where one of the X chromosomes is missing, or partially missing.
People with Turner syndrome have a lifelong endocrine disorder, that was not of their making; they are almost always infertile.
People with anorexia have given themselves endocrine problems that may lead to a diagnosis of PCOS.
PCOS is associated both with being overweight and with being malnourished/anorexic.
There are different criteria used to diagnose PCOS, but it affects about 5-10% of females.
Anorexia and Endocrine Disorder
For the easy to read version, here is a good article: -
Overweight and obese patients are not the only patient group that needs lifestyle modification
Warren said that the incidence of fractures in this population when they are younger is up to eight times that of the normal population. “There is a high incidence of vegetarianism along with anorexia nervosa that may also contribute to osteoporosis because of fat avoidance and low protein, calcium and vitamin D intake,” Warren said. This problem is best treated nutritionally. With a return to a normal weight significant increases in bone density are seen and fractures will also stop, she said.
In addition, a lack of estrogen may also contribute to this extensive bone loss. Hormone replacement or oral contraceptives can be used as a secondary measure but appear to help only if that patient is eating well and near a normal weight.
Another common problem in women with anorexia nervosa is infertility. Many patients with eating disorders will not ovulate. Warren said that although patients may present with a fertility problem, endocrinologists should be sure that any underlying nutritional problem is resolved before a patient is encouraged to conceive. “You can help patients to conceive using drugs, but it is really not recommended until they have a normal BMI,” she said. “There is a higher incidence of miscarriage in these patients and higher incidence of low-weight babies due to intrauterine growth retardation.”
If the return to a normal weight does not solve the fertility problems, endocrinologists should also consider a premorbid hormonal imbalance. Warren said that some patients who have had anorexia nervosa may also have an anovulatory disorder like polycystic ovary syndrome. “Patients are overweight and then lose too much weight,” she said. “As they gain back weight, they return to their premorbid anovulatory state and although they may be making estrogen, they are not ovulating on a regular basis.”
Patients with anorexia nervosa may also present with symptoms that appear to be endocrine disorders but may in fact be a result of altered nutritional intake.
“Sometimes patients have low thyroxine and triiodothyronine,” Warren said. “They present with pseudo-hypothyroidism. It may be very mild, but endocrinologists have to be aware that this syndrome may present and it is not really hypothyroidism. It is just a reaction to severe nutritional deprivation.”
In addition, because patients with eating disorders may be compulsive water drinkers, they may also develop hyponatremia. “You have to look very carefully at how much [water] they are drinking,” she said.
Anorexia nervosa is a psychiatric disorder characterized by altered body image, persistent food restriction and low body weight, and is associated with global endocrine dysregulation in both adolescent girls and women. Dysfunction of the hypothalamic-pituitary axis includes hypogonadotrophic hypogonadism with relative oestrogen and androgen deficiency, growth hormone resistance, hypercortisolaemia, non-thyroidal illness syndrome, hyponatraemia, and hypooxytocinaemia. Serum levels of leptin, an anorexigenic adipokine, are suppressed and levels of ghrelin, an orexigenic gut peptide, are elevated in women with anorexia nervosa; however, levels of peptide YY, an anorexigenic gut peptide, are paradoxically elevated. Although most, but not all, of these endocrine disturbances are adaptive to the low energy state of chronic starvation and reverse with treatment of the eating disorder, many contribute to impaired skeletal integrity, as well as neuropsychiatric comorbidities, in individuals with anorexia nervosa. Although 5–15% of those affected by anorexia nervosa are men, only limited data exists regarding the endocrine impact of the disease in adolescent boys and men. Further research is needed to understand the endocrine determinants of bone loss and neuropsychiatric comorbidities in anorexia nervosa in both women and men, as well as to formulate optimal treatment strategies.
Autism four times likelier when mother's thyroid is weakened
Pregnant women who don't make nearly enough thyroid hormone are nearly 4 times likelier to produce autistic children than healthy women, report scientists from the Houston Methodist Neurological Institute and Erasmus Medical Centre in an upcoming Annals of Neurology.
Polycystic ovary syndrome and autism: A test of the prenatal sex steroid theory
Elevated levels of prenatal testosterone may increase the risk for autism spectrum conditions (autism). Given that polycystic ovary syndrome (PCOS) is also associated with elevated prenatal testosterone and its precursor sex steroids, a hypothesis from the prenatal sex steroid theory is that women with PCOS should have elevated autistic traits and a higher rate of autism among their children. Using electronic health records obtained from the Clinical Practice Research Datalink (CPRD) in the UK between 1990 and 2014, we conducted three matched case-control studies. Studies 1 and 2 examined the risk of PCOS in women with autism (= 971) and the risk of autism in women with PCOS ( n = 26,263), respectively, compared with matched controls. Study 3 examined the odds ratio (OR) of autism in first-born children of women with PCOS ( n = 8588), matched to 41,127 controls. In Studies 1 and 2 we found increased prevalence of PCOS in women with autism (2.3% vs. 1.1%; unadjusted OR: 2.01, 95% CI: 1.22–3.30) and elevated rates of autism in women with PCOS (0.17% vs. 0.09%, unadjusted OR: 1.94 CI: 1.37–2.76). In Study 3 we found the odds of having a child with autism were significantly increased, even after adjustment for maternal psychiatric diagnoses, obstetric complications, and maternal metabolic conditions (unadjusted OR: 1.60, 95% CI: 1.28–2.00; adjusted OR: 1.35, 95% CI: 1.06–1.73). These studies provide further evidence that women with PCOS and their children have a greater risk of autism.
Maternal polycystic ovarian syndrome in autism spectrum disorder: a systematic review and meta-analysis.
There is evidence showing a positive correlation between prenatal androgens and their effect on the development of central nervous system and the autistic spectrum disorder (ASD) phenotype in offspring of mothers with polycystic ovary syndrome (PCOS). We applied a systematic review to investigate whether women with PCOS have increased odds of having a child with ASD, while, secondarily, if these women themselves are at high risk of having the disease. Major databases from inception until 14th October 2018 were searched. The primary outcome measure was the odds of an ASD diagnosis in children of mothers with diagnosed PCOS, while the secondary outcome was the odds of ASD diagnosis in women with PCOS. Scheduled subgroup analyses were according to the time of birth and maternal age.Ten studies were eligible for inclusion, including a total of 33,887 ASD children and 321,661 non-ASD children. Diagnosed PCOS was associated with a 1.66 times increase in the odds of ASD in the offspring [95% CI: 1.51, 1.83, p = 1.99 × 10-25, 7 studies, I2 = 0%, τ2 = 0]. Women with PCOS were 1.78 times more likely to be diagnosed with ASD (95% CI: 1.10, 2.87, p = 0.0179, 5 studies, I2 = 85.4%, τ2 = 0.2432). Additional analyses did not change the initial result. The overall quality of the evidence was high. The pooled effects size displayed low heterogeneity for the primary outcome. While the heterogeneity in the secondary outcome appears to attenuate when only high quality studies are synthesized, still the result exhibits significant heterogeneity. Τhe available data allowed a subgroup analysis only for classification system for PCOS diagnosis and showed a significant increase of ASD diagnosis in the offspring of women with Read Code and ICD diagnosed PCOS. In conclusion, the available evidence suggests that women with PCOS have increased odds of having a child with ASD, an effect size estimate based on a large number of patients from studies of good quality. Regarding the evidence on the prevalence of ASD in PCOS women, results suggest that women with PCOS are more likely to be diagnosed with ASD.
As I have pointed out in earlier posts there is an association between parents who experience fertility problems and those who have children with autism. PCOS is only one risk factor, auto-immune conditions affect both fertility and autism risk. This was noted by one American fertility clinic, which decided to create a prevent autism website.
As specialists in reproductive immunology, we treat numerous patients who have suffered previous miscarriages and other pregnancy complications. Many of these women have had at least one child on the autism spectrum.
The most common question we encounter from our patients is, "Are the two outcomes connected?" Our patients want to know if diagnosis and treatment for the immune-related causes of miscarriage may also lessen the chance of a having a second child diagnosed with Autism Spectrum Disorder (ASD).
The Centers for Disease Control & Prevention (CDC) recently reported that about 1 in 68 children are diagnosed with autism. Accordingly, there are millions of couples asking the question, "Can we reduce our chances of a second child with ASD?"
In an effort to discover the answers my patients and countless other families are seeking, we have created this informational website. Our practice is currently investigating the following:
· Can autism be prevented by treating immune-related issues during pregnancy?
· Can we identify those babies that are most susceptible to these inflammatory responses from women with known or as yet unknown underlying autoimmune issues?
What We Know So Far
For some time now, we have noticed a trend among patients: Mothers with autoimmune disorders who experience an inflammatory flare during the second trimester appear to have an increased risk of having a child on the autistic spectrum. The correlation seems stronger in mothers who have had previous miscarriages and / or a previous child with ASD. Recent studies have also noticed the connection, citing data gathered from the CDC.
Because the second trimester is when critical brain development takes place, it seems logical to conclude that any hindrance to fetal growth at this time, including a trigger of the baby's autoimmune issues due to an overactive immunological response from the mother, could potentially be detrimental to the cognitive progression of the child.
Autism rates are on the rise, and it is our belief and experience that this is due to the many "triggers" present in our diets, as well as the medications that our "at-risk population of women" (women with underlying or known autoimmune syndromes) are exposed to.
Conclusion
If girls need a role model, best not to choose a skinny one. What about one that smiles (sorry, Billie Eilish) and eats.
Athletic good looks are not the same as being malnourished.
Undereating can be as harmful as over-eating and can cause permanent damage.
Autism is multifactorial, which means a long list of different things, either by themselves, or in combination can cause it. Since the severity of symptoms needed to warrant a diagnosis of autism has fallen dramatically over the years, issues like PCOS are likely behind many people’s autism diagnosis. Some cases of PCOS are likely genetic, but some are self-induced and so preventable.
Not all people with an endocrine disorder will get a PCOS diagnosis.
All endocrine disorders in mothers are linked to autism. For example, Type 1 diabetes (T1D), Type 2 diabetes (T2D) and Gestational Diabetes (GDM) all increase autism odds.
· 4.4 for exposure to T1D
· 3.6 for T2D
· 2.9 for GDM by 26 weeks
· 2.1 for GDM after 26 weeks
· 1.8 for no diabetes
If you are worried about an “autism epidemic” do something about it. Encourage healthy eating and a healthy body image; some may need to revise what they think of as healthy. Models and pop stars are generally a bad example.
There are numerous other preventable factors that increase autism prevalence/severity, some come from the mother, some from the father and some from the environment. (Recreational drug use, alcohol consumption, lack of exposure to the expected bacteria from pets and other domesticated animals etc).
This post was really about elevated male hormones in females affecting their offspring, but of interest is that obesity in fathers (and as we already knew, in mothers) appears to have a major impact on autism incidence.
Obesity among fathers appears to have a greater effect on severe autism incidence than obesity in mothers. "Normal" BMI is often quoted as being 18-25.
Parental body mass index also seems to affect different severity of autism to different degrees. I did rather suggest this when I wrote about PCOS above, meaning since autism is multifactorial, if you have no genetic predispositions to autism, being super skinny is adding just one set of risks. You are adding one bale of straw to the camel's back, so to speak.
Here is the effect of body mass index of both parents on the risk of offspring later being diagnosed with Asperger's type autism. OR = Odds Ratio, so greater than one is increased risk and less than one is reduced risk.
Here (above) the skinny mother increases the odds ratio that her children will have mild autism, but this is not severe non-verbal autism. The same risk increase effect applies to skinny fathers.
The effect is not the same when you look at who later gets diagnosed with Autistic Disorder (Severe Autism)
In the above chart, being an anorexic mother has almost no effect on the odds that her child will have severe autism. Having a skinny father is associated with a reduced chance of severe autism.
The real takeaway point from the study is don't forget about Paternal Obesity, it is not just about the mother.
There are numerous other preventable factors that increase autism prevalence/severity, some come from the mother, some from the father and some from the environment. (Recreational drug use, alcohol consumption, lack of exposure to the expected bacteria from pets and other domesticated animals etc).
This post was really about elevated male hormones in females affecting their offspring, but of interest is that obesity in fathers (and as we already knew, in mothers) appears to have a major impact on autism incidence.
Obesity among fathers appears to have a greater effect on severe autism incidence than obesity in mothers. "Normal" BMI is often quoted as being 18-25.
Parental body mass index also seems to affect different severity of autism to different degrees. I did rather suggest this when I wrote about PCOS above, meaning since autism is multifactorial, if you have no genetic predispositions to autism, being super skinny is adding just one set of risks. You are adding one bale of straw to the camel's back, so to speak.
Here is the effect of body mass index of both parents on the risk of offspring later being diagnosed with Asperger's type autism. OR = Odds Ratio, so greater than one is increased risk and less than one is reduced risk.
Asperger's
Here (above) the skinny mother increases the odds ratio that her children will have mild autism, but this is not severe non-verbal autism. The same risk increase effect applies to skinny fathers.
The effect is not the same when you look at who later gets diagnosed with Autistic Disorder (Severe Autism)
Autistic Disorder (Severe autism)
In the above chart, being an anorexic mother has almost no effect on the odds that her child will have severe autism. Having a skinny father is associated with a reduced chance of severe autism.
The real takeaway point from the study is don't forget about Paternal Obesity, it is not just about the mother.
Source: Parental Obesity and Risk of Autism Spectrum Disorder
"Paternal obesity is an independent risk factor for ASDs in children. The associations should be investigated further in genetic and epigenetic studies."
Yep, here I am. Self-diagnosed Asperger, insulin resistance diagnosis aged 21 (after having 8 years of having my period either 12 months every day, or completely off 12 months and terrible misinformed hormonal therapies), started Metformin, ditched it after 18 months in favor of balanced diet. Pcos present. Lost the 10kg excess weight, was at 62kg when I got pregnant after 6 months of trying, so skinny pcos asperger mom, mild autism kid, dad and kid are mthfr, got bitten by a tick during pregnancy. C section, Longacef immediately after for probably false E.coli swab of uterus. Perfect storm.
ReplyDeleteHere is some new research that maybe would be an interesting autism avenue to explore:
ReplyDeletehttps://phys.org/news/2020-04-physical-spurs-gene-reveals.html
Basically, the researchers found that physical force such as the stretching of cells or else mechanical vibrations can modulate gene expression directly. Some genes are effected and others are not and Histone 3 was the primary histone that silenced the gene expression effect of genes it was bound to. In other words, if this histone was not bound to a particular gene, then its activity could be upregulated by mechanical forces.
How you would selectively apply this with respect to autism, I really don't know but simply putting someone with autism on a vibrating plate for 20 minutes a day at the suggested frequencies and see what happens. Some people do this already because they believe it keeps them healthier and who knows maybe in light of this research they are right.
It also makes you wonder whether certain forms of stimming may be related to this effect. This is kind of far out there kind of thinking so don't take any of this too seriously with respect to autism, but it would be very interesting to explore, though it would probably have to be a network of parents as budgets for science will soon be slashed back to the middle ages in light of the economic devastation from poor decision making by world leaders in handling the coronavirus crisis. I saw recently that Sweden seems to be doing very little with regards to social distancing other than to recommend high risk groups stay home. It will be interesting to see how they fare with respect to the United States and other western countries which I believe have made the biggest strategic policy error in the history of mankind that may leave us in the dustbin of history in the not too distant future.
Peter, a question I don’t think you’ve addressed so far: how did you know when to raise the bumetanide dosage? when your child was gaining weight, when he was showing less attention or just after a specific amount of time? and in what increments did you do the increase?
ReplyDeletetpes, I think you should use the largest dose that does not cause troubling side effects and still shows a benefit. The benefit is cognitive and very visible.
DeleteI do not think people with mild autism can have a severe chloride imbalance. So for an Aspie, if there is a bumetanide effect, I doubt a dose of more than 1mg a day is ever needed.
In someone with severe autism and particularly in someone whose autism gets worse in times of inflammation (from allergy, virus or anything else) then a higher dose may give a further benefit. The side effects relate mainly to loss of fluids and so electrolytes. With extra fluid and extra potassium, most people can tolerate higher doses of bumetanide, but care has to be taken.
Clearly an adult with severe autism will need a higher dose than a toddler; but in very young children bumetanide should give some permanent effects, because the brain will develop more normally when the E/I imbalance is corrected.
One parent reports their child has no diuresis from bumetanide and so uses a higher bumetanide dose.
Measuring potassium levels in blood is necessary.
I think any level of ASD can and should be treated, even up to Aspergers. I have seen a lot of people online that have been diagnosed with mild forms of ASD but still suffer a lot and are not as functional as they would like and they can't catch up with life.
ReplyDeleteI have a friend that we talk a lot these days and his experience is no better. In fact, he is experiencing debilitating symptoms . Diagnosed with very mild ASD but still with a ton of "comorbidities". Given the clear evidence that brain disorders from Sz, MDD to autism are interlinked and overlap biologicaly and symptomaticaly there is a very good reason for the treatment of all ASD, no matter how mild it is.
This research should give us some hope in treating autism as it shows that injured neurons can go back to an embryonic state and then resprout axons so as to repair injured areas of the brain:
ReplyDeletePress Release:
https://www.sciencedaily.com/releases/2020/04/200415133654.htm
Paper:
https://www.nature.com/articles/s41586-020-2200-5
This paper shows that corticospinal neurons (the most myelinated and longest neurons in the brain) when injured will revert back to an embyronic state via an epigenetic mechanism, whereby they can then resprout axons and thereby repair damaged projections to the spinal cord.
This makes you wonder with respect to autism and post-mortem findings showing cortical neurons being immature in the autism brain in a manner suggesting arrested development. Perhaps another possibility might be that cortical neurons are being constantly injured somehow (oxidative stress maybe?) and that they are constantly being put into reboot mode and never allowed to fully mature and have their connections pruned.
I have no evidence of course, but the idea came to my head when reading this paper and makes you wonder if persistent brain damage from various stresses might be what holds back development and that treating those stresses without a break might lead to a better outcome as if those stresses were allowed to come back, you might get this situation where cortical neurons (and perhaps others in the brain) get stressed/injured to the point they keep going back to an embryonic stage.
Just an idea, but it might explain some forms of autistic regression.
Hello Peter, I read your blog everyday. About a year and a half ago your blog started to appear in my searches, I wish I paid more attention, it seemed complicated to me to understand all the information and well, it still is but I understand a bit more, your blog is helping me a lot. My son has been on bumetanide for a month but the first two weeks he only took .5 mg. He's been on 1mg for 2 weeks now and at the time when he started with 1mg he was in a very bad mood, now he seems better, I think it had something to do with his potassium levels, because he had a cramp, and we had no bannanas for two or three days, he drinks a lot of water so I don't worry a lot that he will be dehydrated. He talks more, but I haven't noticed any other improvements, he is stimming a lot and has OCD issues. I think he needs more time and also he gets very sick in winter, the doctor told me he has allergies, he also has GI issues, so maybe that's interfering with his response to bumetanide.
ReplyDeleteIt's hard for me to read about brain damage and inflammation in autism, I wish I could do every test and treatment but it's impossible for me. My next step is buying NAC Sustain, and for his allergies and gut problems I don't know where to start, months ago I thought that by giving him yakult he would be better, but now I know it's something more complex.
I read your post and I have PCOS, insulin resistancy, hypertension, hirutism, and a pituitary microadenoma. I had subacute bacterial meningitis when I was 24, I was then diagnosed with Bipolar disorder (though I think I have many autistic traits), and was given psychotropics without the doctor looking at my hormone imbalances, the meningitis after effects or my noticeable socialization problems, without investigating if it they would be detrimental for me, and withdrawal was very hard. I've never received enough information from any doctor, and the same is for the autism diagnosis of my son, in five minutes the doctor just told me he had autism and that maybe he was going to need medication, he didn't order any tests.
I have been reading your article about regressive autism and I found an article about the relation of PCOS and Mitochondrial Dysfunction. I'm not sure if he has this kind of autism, he did start to stim more after the MMR vaccine . If there are many different triggers and causes for autism, and as a result different treatments for it, would it be helpful to know what may have possibly caused it to find the accurate treatment? Could a treatment that works for me, work for him?
Thank you, sorry for the long post!
This is the article I found: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6698037/
Lisa, a treatment that works for you may well work for him. For example some people with bipolar benefit from Verapamil and some people with Irritable Bowel Syndrome benefit from Verapamil. Some people with allergy benefit from Verapamil. Unfortunately testing does not yet exist to reliably tell you what drugs will help. There is a lot of trial and error.
DeleteHaving disturbed hormones will have many effects and if this is combined with other factors may create a very specific case, which is why people need personalized medicine.
Thank you for your response Peter, I read about your son and it gives me hope, I won't give up until I find what can help my son have a better life, though it is hard to be patient. Can you tell me if he says more words, does this mean that he is responding well to bumetanide?, how much time do you recommend for the trial? Do I give him something for his GI problems before trialing with NAC? I really am excited to try NAC, I hope he responds well to it. Sorry, I should've asked these things first.
DeleteI just read about Verapamil and it also is for hypertension, and seems to benefit IR, it seems a better option than Losartan because of Covid, and it's easy to find it in Mexico
Lisa, if he talks more I think you are seeing a benefit from bumetanide. The researchers suggest a two month trial.
DeleteAllergy and GI inflammation will work to counter the effect of bumetanide, since inflammation increases the ratio NKCC1/KCC2.
The best interventions are usually the cheapest. Verapamil is very cheap. Our reader Maja has found Pentoxifylline works well with bumetanide; it is anti-inflammatory so will lower NKCC1/KCC2. It was used in autism trials decades ago and is used in the used by DAN/MAPS doctors. It should be cheap.
Trying to solve the GI problems would be a good idea as soon as possible. They will affect both his mood and biology. Some GI therapies are cheap and some expensive, price does not correlate with effect. It is very hard to find what works; one reader even found that Memantine solved the GI problems.
Ok, thank you for the information Peter! Have a nice day.
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