Alex and Autism: His Perfect Storm

As promised, a little about Alex’s hellishly awful start to life.  Looking back – which I really, really try not to do, as it only causes me pain (but I’ve had some emails of readers asking so here goes) – it does seem as though everything that could have gone wrong did.  I liken it to a snowball rolling downhill.  I have to believe that the severity of his autism and long history of physical illness were the result of insult after insult.

Autism is probably never caused by just one thing.  But in Alex’s case it was…kind of everything.

I already had a long history of immune issues myself and then got the flu (perhaps forming the original little snowball) in my 7th month of pregnancy.  Undoubtedly, I was told to take acetaminophen to keep the fever down. (snowball rolling…)

Alex developed a fever at about 24 hours old, just after we were released from the hospital.  As per normal protocol, he was re-hospitalized and put on an IV of antibiotics, while tests were run (mainly looking for meningitis).  For 5 days, antibiotics were pumped into him, 24 hours a day. (snowball rolling…)

To boot, as Dr. Parker points out in the previous post, he was likely given acetaminophen every 4 hours during those days in the hospital.  (snowball rolling…)

He stopped breast feeding and I was told that if I didn’t put him on a bottle, we’d be kept in the hospital longer, as he was becoming jaundiced.  Not knowing any better, I of course complied (snowball rolling…)…as long as he could get soy formula, since I have always had horrendous lactose intolerance.  (Alex was probably doomed to autism by the time he was 3 days old.) (snowball rolling…)

While his development was normal, and he certainly was not autistic, there were bad signs early on.  He projectile vomited with almost every bottle.  He screamed way more than normal in those early months. He didn’t hold his head up until 4 months, at least.[i]  He never, ever, EVER slept normally.  He had an insanely violent startle reflex and a proverbial pin dropping on the other side of the apartment had him jerking awake even after only a few minutes sleep – and staying awake for the next 18 hours.  I had to carry him everywhere, all the time, that Baby Bjorn strapped to my chest day and night.

A typical day in his first year of life…

I still remember only too well, when Alex was probably about 4 months old, being so tired I thought I was going to die.  I thought to myself, I’ll just hold him in my arms and lie down to sleep a little…and when I did, he promptly vomited formula all over me and the bed.  I cried and cried as I now had to not only not sleep, but clean the mess up.

However, while he had these physical signs and symptoms, there were no real signs of autism 15 months old.  Prior to that, he was social, had normal eye contact, met all developmental milestones on time, etc.   He and I both came down with a stomach bug.  It last 24 hours for me; it last 3 weeks for him. And when it finally was gone, so was Alex.  He abruptly stopped playing with me, stopped responding to his name…just left me.

So very little has helped Alex over the years.  He is, without a doubt, one of the worst non-responders I have ever come across.  I can count on 1 hand the things that have had any kind of positive impact on him.  The two biggest hits were, without anything else coming close, the Specific Carbohydrate Diet and helminths, both of which have profound effects on the composition of the biome, as you know.

So, yes…there is reason behind my madness.

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[i] http://abcnews.go.com/Health/head-lag-babies-sign-autism/story?id=16353502

 

GUEST POST: BY DR. WILLIAM PARKER, The Autism/Acetaminophen Link – Summary of Research

I am leaving for Russia in a little more than a week, to talk about the therapeutic use of helminths in autism at the Autism Challenges and Solutions Conference, in Moscow.  Also speaking there is Dr. William Parker, one of the foremost researchers into the immunological effects of helminths.  I have talked about William many times on this blog.  As you know, I’ve been a fan since first reading his work back in 2010.  William is covering the microbiome/autism connection at the conference so our talks are synergistic, and he actually speaks just prior to me.  He’s promised me a great introduction.  I’ll let you all know how he does!

Anyway, William called me a couple of  nights ago to catch up and chat about our upcoming trip – but we ended up spending a good portion of an hour talking about his latest research, on the toxic effects of acetaminophen.

William asked me to share his summary of that research (see below), which was conducted with colleagues from both Duke and Harvard, and was published last month.  This is simply too important for you not to know, especially if you are thinking of having a baby or have a young child.  Please! – pass this on to anyone you know who may benefit!

I told William this depresses the hell out of me (Alex undoubtedly had a load given him when he was re-hospitalized at 36 hours old – more about that in a future post)…but he told me that now that they are isolating the exact mechanism by which acetaminophen does harm, it’s more likely they can come up with treatments in the future.  Well…I can only live in hope.

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By William Parker, PhD

Department of Surgery

Duke University Medical Center

Durham, NC 27710

Mounting data pointing at the potential for acetaminophen exposure during early childhood to induce autism in children. A review from scientists and clinicians at Duke and Harvard.

A summary of the evidence presented in the review recently published in the Journals of International Medical Research (http://journals.sagepub.com/doi/pdf/10.1177/0300060517693423) is presented here. Citations for this information can be found in the review, which is open access and contains 195 references.

  1. The review cites eight peer-reviewed studies (there are more*) which now demonstrate that acetaminophen exposure is neurotoxic to the developing brain of humans. Seven of these studies evaluated the effect on children following exposure in utero. Effects of exposure evaluated by various groups included lowered IQ, autism, and behavioral problems. The only study to evaluate the effect of exposure after birth found more than a 60-fold greater risk (literally) of developing autism following exposure after birth than studies looking at the risk of exposure before birth.
  2. A very wide range of factors, all of which are associated with inflammation and oxidative stress, are in turn associated with an increased risk of autism. Thus, it appears that whatever is inducing the epidemic of autism probably acts in concert with inflammation and oxidative stress. This conclusion is consistent with the hypothesis that acetaminophen exposure to infants and children after birth is a leading cause of autism.
  3. Laboratory animals develop permanent brain damage characterized by problems with social function when they are exposed to acetaminophen during an early period of brain development that corresponds to human infancy.
  4. Margaret McCarthy, chair of Pharmacology at the University of Maryland, has elucidated the mechanism by which acetaminophen damages the developing brain, and has explained why acetaminophen is more dangerous to males than to females. This potentially accounts for the increased propensity for males to acquire autism compared to females.
  5. Acetaminophen substantially alters brain chemistry, and temporarily impairs awareness of social issues in adult humans. Although the drug could naively be considered to be anti-inflammatory, exposure to the drug actually causes inflammation, even in healthy adults, and depletes metabolic components needed to deal with inflammation. Further, the drug is immunosuppressive, blocking an important immune function (the febrile response).
  6. No study has ever shown acetaminophen to be safe for the developing brain of a human or a laboratory animal. A major manufacturer of acetaminophen in the US acknowledges that the drug was never proven safe for brain development when used during pregnancy or in childhood. All safety tests that have been conducted were performed with the assumption that any side effects would be acute in nature (e.g., bleeding or organ damage soon after administration of the drug).
  7. A very wide range of circumstantial evidence** points toward the potential for acetaminophen to be at the root of many if not most cases of autism:

(a)   The epidemiology of autism matches the historic use of acetaminophen, with both rising sharply in the early 1980s following the identification of Reye Syndrome as a possible side effect of aspirin use in children.

(b)   The qualitative nature of autism apparently shifted from infantile to regressive at the same time that acetaminophen use in infants and children became more popular, in the early to mid-1980s. Other than post-birth acetaminophen exposure as a major inducer of autism, no other plausible explanation for this observation is known to exist.

(c)   A wide range of inflammatory conditions that affect the potential to tolerate oxidative stress are associated with autism. It is expected that these conditions will adversely affect metabolism of acetaminophen. A notable exception is cystic fibrosis, a condition of oxidative stress not known to be associated with autism. Cystic fibrosis is also unusual as a condition of oxidative stress that actually enhances rather than impairs metabolism of acetaminophen. Other than post-birth acetaminophen exposure as a major inducer of autism, no other plausible explanation for this observation is known to exist.

(d)  The number of possible environmental suspects for the induction of autism at a level that would account for the epidemic is dwindling, leaving acetaminophen use in infants and small children as one of the few remaining suspects. A good suspect is one which is newly (since 1980) and widely introduced into the population, and which should be associated with a profoundly large (10-fold or greater) increase in risk of autism. Most suspects tested to date have shown moderate and sometimes variable (dependent on the population studied) associations with autism.

(e)   Genetic variants associated with autism, many associated with oxidative stress, likely influence the metabolism of acetaminophen.

(f)   Circumcision has been identified as a significant risk factor for autism, and the only reasonable explanation put forth for this observation is that acetaminophen use during the procedure is probably inducing autism.

(g)  History demonstrates to us that it is a mistake to ignore the observations of parents when it pertains to autism. Many parents who have historically blamed vaccines for their child’s autism may have actually observed the effects of acetaminophen. In the 1990s, vaccination was advertised as the number one indication for use of acetaminophen. Other than post-birth acetaminophen exposure as a major inducer of autism, no other plausible explanation for this observation is known to exist.

(h)  The idea that acetaminophen use, particularly in infants and small children, is responsible for many if not most cases of autism is an attractive hypothesis, as it satisfies Occam’s Razor in being a simple explanation that explains a wide range of observations.

Conclusions of the review:

  1. There are several unknowns: We have almost no idea just how much benefit that acetaminophen actually provides. (That was never tested.) Perhaps it can be easily replaced by non-pharmaceutical means of reducing fevers, and perhaps not. Second, we don’t know exactly how much neurological damage acetaminophen causes when administered to infants and children.
  2. Despite unknowns, given the preponderance of evidence described above, we conclude that parents and doctors should know all available facts so that they can make informed decisions about use of acetaminophen.
  3. An incisive study needs to be done as quickly as possible, with all available resources at its disposal. Despite the fact that acetaminophen is the most popular drug used in infants, children, and pregnant women, neither the benefits nor the risks of using the drug in those populations have been thoroughly evaluated.
  4. The cost of an incisive study would cost less than the cost of raising and caring for three individuals with autism. Just three.

* Our review cites 8 papers, but there are others, and more on the way.

  • Skovlund and colleagues found that acetaminophen use but not opioid use during pregnancy is associated with a reduction in communication skills. (https://www.ncbi.nlm.nih.gov/pubmed/28168770)
  • A study by Liew et al (Epidemiology 2016; 27: 912–918) showing lower IQ associated with acetaminophen use during pregnancy is cited in our review but not counted as one of the 8 studies listed as showing neurotoxic effects of acetaminophen during development.
  • Vlenterie and colleagues found communication problems and delayed motor milestone attainment associated with acetaminophen use during pregnancy. (https://www.ncbi.nlm.nih.gov/pubmed/27585674)

** Additional circumstantial evidence exists, but was not cited in our review. For example, the unexplained and unusually high prevalence of autism in South Korea (https://www.ncbi.nlm.nih.gov/pubmed/21558103) just happens to occur in a country where children’s acetaminophen capsules were inadvertently overloaded with active ingredient (http://www.saul.com/sites/default/files/3591_WCW062513tcgmp.pdf).

The Oral Microbiome and…Cancer risk?!

There was an interesting article[i] on Live Science last week, about the link between the kinds of bacteria in your mouth and your risk of certain cancers, as presented by a an New York University researcher, Jiyoung Ahn, at a talk she gave on April 2nd to the American Association for Cancer Research.

According to Dr. Ahn, the ability to use DNA sequencing to truly discern the bacteria of the human biome only came about in the last 5 years.  This ability has led scientists to be able to make links they never could have in the past.

Ahn’s research has shown that people with higher levels of the bacteria Porphyromonas gingivalis have a 60% higher risk of developing pancreatic cancer!  Another kind of bacteria, Aggregatibacter actinomycetemcomitans was linked to more than double the risk.  Astounding!

Pancreatic cancer is one of the deadliest there is.  Can you imagine being able to recognize this risk early on, and use biome restoration to avert development?  How many lives might be saved?

Apparently, there are also differences in the oral microbiomes of people who go on to develop esophageal cancer.  Those who develop it have lower levels of Proteobacteria.

What has yet to be determined is cause and effect.  That is, are these differences the cause of the cancer?  Or, are both the microbiome changes and the cancer the result of some other factor?  For example, smoking and alcohol can change the oral microbiome and both are risk factors for both esophageal and pancreatic cancers. Smokers have lower levels of Proteobacteria in their mouths and people who drink more than two alcoholic beverages per day have lower levels of good bacteria, like Lactobacillus.

Can oral probiotics or fermented foods make a difference in the oral microbiome?  Can we make a probiotic mouthwash or how about toothpaste?!  We know that the presence of helminths positively affects the microbiome up through the esophagus (more on this in this blog post) but how about into the mouth?  What about prebiotics?  I really look forward to reading more about this subject in the future.

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[i] http://www.livescience.com/58512-oral-microbiome-cancer-risk.html

Yet Another Brood, re: IBD…Or…Another Big Judy Eye Roll

Ok, so…remember how I’ve told you that I was a brooder?  And that I didn’t let go of things once I’m angry or upset?  And, um, remember that I have been kinda fuming over that post[i] from a few weeks ago by Dr. Mercola?…the one I kinda promised to not talk about any more?

Well, I lied.  I have to talk about it one more time.  And once I show you WHY I need to harp on about it again, you will totally agree with me that this is worth yet another mention.

I’m sure by now, having read about it on this blog like 2000 times, you remember one Dr. Mercola’s reasons for why we should all avoid repopulating our biomes with helminths:

“Although worm therapy may be touted as the best new therapy for inflammation, there are already many proven ways to treat inflammatory bowel disease and some of the other illnesses and disorders very effectively without resorting to deliberately introducing parasites into your system.”

Now let me tell you about an article I spotted this week on IBD News Today, entitled, FDA Reports Crohn’s Disease Side Effects Have Increased, Analysis Finds.[ii]  The article explains that “Drugs used to treat Crohn’s disease and other autoimmune disorders are among those with the greatest number of reported side effects filed with the U.S. Food and Drug Administration…”

It goes on to explain that, “Drugs which suppress the immune system to fight inflammation can cause serious and sometimes lethal infections including tuberculosis, and have been linked with blood disorders, including lymphoma, a blood cancer.”

The article looks at the drug, Humira, in detail. This FDA approved  medication, one of Dr. Mercola’s “proven ways to treat IBD,” apparently has been linked to “more than 200,000 reports of adverse events, including 4,200 deaths…Humira can also cause hepatitis B infection, allergic reactions, nervous system problems, blood problems, certain immune reactions including lupus-like syndrome, liver problems, and new or worsening heart failure or psoriasis.”

Er…call me crazy but…how exactly is this better than taking a therapeutic dose of helminths?

Is it me?

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[i] http://articles.mercola.com/sites/articles/archive/2017/03/13/helminth-therapy.aspx

[ii] https://ibdnewstoday.com/2017/04/03/fda-reports-of-crohns-disease-treatment-side-effects-have-increased/

Another Look at the Microbiota/Macrobiota Connection

I am preparing slides for a talk I’m giving on helminths at an autism conference in Moscow at the end of the month.  I’m struggling more than I usually do because there is an overwhelming amount of information to try to fit into a 1 hour talk…and it seems new research on the biome comes out daily now.  So while I am trying to cut the number of slides down, I find some other crucial piece of information I feel like I absolutely must include.  I mean…how can I NOT include information from the paper I just finished reading this morning, Helminth Colonization is Associated with Increased Diversity of the Gut Microbiota[i]?!

Once I give you some of the highlights, you’ll understand my quandary.   This group of researchers, who include Dr. P’ng Loke, whose work I have mentioned before, compared the microbiota of people – some with helminths, some without – from a rural area of Malaysia. They hypothesized “…that helminth infected individuals may have increased microbial diversity relative to uninfected individuals.”  The feces of 36 of the 51 individuals in the study demonstrated the presence of helminths.  Their results “…showed that the helminth-positive subjects had significantly greater species richness (total number of species present) than the helminth-negative subjects…These results suggest that helminth colonization significantly affects the gut microbiota and may increase the species diversity of the bacterial communities.”

There were several other really interesting findings:

  1. The researchers also compared the microbiota of these Malaysians to those of people in New York City and found that there was a “…much larger difference than the difference between helminth infected and non-infected people in Malaysia.”   They attribute this to helminth exposure, and point out that even the Malaysians who were not currently infected may have been in the past… explaining perhaps why the differences between the two groups of Malaysians was far less dramatic those found between the New York City residents and the Malaysians.
  2. They also noted that the intestinal microbiota evolves to “…resemble an adult-like configuration within the first three years of life.” We know though that diet, later-in-life helminth exposure, prebiotics, stress levels, etc. can change the microbiota but perhaps only with continual exposure.  That is, I wonder if someone in New York starts taking helminths, will her microbiota look more like one of these Malaysian infected individuals?  And if she stops exposing herself to helminths, will her microbiota go back to baseline or will it look more like the other Malaysians who had likely been infected in the past?
  3. Helminths co-evolved with the microbiota and significant interactions therefore exist. For example, one species of helminth, Trichuris muris, only hatches in the presence of commensal bacterial species.
  4. Some of the differences between the Malaysians and the Americans may be diet related. The microbiota found in the New York City residents is associated with diets heavy in animal proteins and saturated fats, whereas the microbiota of the Malaysians is associated with simple sugar and high fiber diets (plant-based foods).

In their final discussion, the researchers state that the increase in microbiota diversity “…among helminth-infected individuals could be important because higher microbiota diversity has been associated with better health.”

So as I said at the start, how can I not put all this information into my lecture?  I will just have to talk fast and hope the translator can keep up!

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[i] Lee, SC, Tang, MS, Lim, YA, Choy, SH, Kurtz, ZD, Cox, LM, Gundra, UM, Cho, I, Bonneau, R, Blaser, MJ, Chua, KH, Loke, P. Helminth colonization is associated with increased diversity of the gut microbiota. PLoS Neglected Tropical Diseases. 2014. 8(5):e2880.

 

Autism, the Biome and Potential Treatments

Fist pump!  A paper that actually presents information that can help people who are sick!  Woopa!

As promised, here is a summary of that fantastic article[i] about autism and the biome that I discovered on Dr. MacFabe’s new website.  I’ve ranted enough over the last few months about ending suffering NOW for you to know that I am more than a little fed up with the lack of helpful science.  (Now that I think of it, I am definitely going to write a post soon about stupid science.  It will be hugely cathartic, spewing some vitriol!)

I’m a little less cranky than usual ’cause reading this paper was a little bit of a balm for my festering wound of anger.  (That same festering wound whose scab Dr. Mercola managed to pick off two weeks ago. (Yup.  Still brooding.))

The researchers start off by saying that “Many lines of research point to the importance of the development of the enteric microbiome during the first 3 years of life as being critical in the establishment of a healthy immune system.”  So, what is disrupting the biome (and thus, the immune system) of children to the point where now 1 in 68 children are autistic in the USA (with equally grim numbers around the industrialized world)?

Three potential mechanisms driving the autism epidemic are proposed, and these are most certainly not mutually exclusive.

  1. Biome Depletion – “If there is disruption in any of these three areas [immune system, microbiome and macrobiome], the ecosystem becomes destabilized and can lead to proinflammatory, allergic, and/or autoimmune related conditions…alterations of the microbiome are a consequence of eradication of helminths, protozoans and other symbionts that co-evolved with humans to regulate, stabilize, and provide modulatory activity for our immune system…”
  2. Propionic Acid Theory – “ASD’s may be the result of disturbances in the enteric microbiome resulting in the increased production of the short chain fatty acid (SCFA) known as PPA….PPA as well as other SCFAs can alter diverse metabolic and immune pathways, gene expression and synaptic plasticity, in a manner that is consistent with findings of ASD.”  (See my post on Dr. MacFabe’s work for more on this.)
  3. Cell Danger Response Theory – “…refers to an adaptive response by the cell to a perceived threat. The potential pathological nature of this response occurs when CDR becomes chronic.”  Over time, this permanent “fight or flight” on the cellular level leads to changes in a host of physiological processes.  Interestingly, the “proposed triggers for the CDR in contemporary society include changes in human migratory patterns, diet, toxin exposures and cultural activity” which certainly overlap with the changes that have led to biome depletion….

Call me crazy, but I wouldn’t be surprised if all three of these were major factors.  After all, we know that the loss of helminths, for example, leads to alterations in the microbiome, which certainly could lead to an excess of PPA-producing bacteria.  And toxin exposure, like PPA getting into the blood stream, could lead to CDA.  And since there is growing laboratory evidence supporting all these mechanisms…yeah, I’m going for the whole poop show.

The paper then goes on to enumerate specific potential triggers for autism and – my favorite part – potential therapeutic interventions.  This is too lengthy to get into in detail for a blog post (and you can download the whole paper for free here  so don’t think I’m leaving you in the lurch!), but to give you a small taste with a few examples:

  1. Acetaminophen – avoid it whenever possible!  For more on this, see Dr. William Parker and colleagues’ paper on this, published this month, which you can read here.
  2. Folate metabolism – “treat with reduced folates (i.e. folinic acid) and avoid folic acid”
  3. Poor diet – “Eat foods high in microbiota accessible carbohydrates [prebiotics!] along with fruits and vegetables.”
  4. Helminths – “Re-introduction of helminths into the intestinal ecosystem is necessary to re-establish the balance of the ecosystem.”

The paper concludes on a positive note:

“The promising news is that there may be many disease modifying strategies that are at our disposal that could be implemented potentially reduce ASD symptomatology or prevent ASD altogether by targeting the enteric microbiome.”  Amen to that. As I have repeatedly stated in this blog, while we don’t yet know how to optimize all these things, and we are light years away from knowing all the answers, there is NO DOWNSIDE, ONLY POTENTIAL UPSIDE, TO DOING THESE THINGS NOW.  Remember my mantra:  If it can’t hurt, and it could help, do it.
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[i] Slattery, J, MacFabe, DF, Kahler, SG, Frye, RE. Enteric ecosystem disruption in autism spectrum disorder: can the microbiota and macrobiota be restored? Current Pharamceutical Design. 2016:22,6107-6121.

 

A Big Day for the Biome Buzz!

Ok…I am a little googly-eyed today.  Not a screaming and fainting at the sight of the Beatles kind of hysteria –a more a refined, intellectual, only-slightly-girly kind of fandom.  🙂

So here is my embarrassing confession for the day: only once in my life have I ever written fan-mail and that  was to Dr. William Parker, the researcher at Duke University who is studying (among other things) the immunological effects of helminths.  In October 2010, I came across William’s online article, Reconstituting the Depleted Biome to Prevent Immune Disorders[i] and thought, “This guy totally gets it!”  I couldn’t resist – I wrote to him telling him (in so many words) that he rocks on with his bad self.  (William has subsequently become a friend but no, I have never asked him if he read that letter! Ugh.)

However, back on January 19th I kind of wrote a sorta fan-letter blog post about Dr. Derrick MacFabe, a researcher at the Cumming School of Medicine in Canada.  As I told you, I have been a huge admirer of Dr. M’s research for many years.  In the dark and dismal world of autism research (which, as you readers know, I pretty much regard as an oxymoron), he has been one of the few shining lights.  So you can imagine how thrilled I was this morning to see his positive comment on the post this morning!  Holy cow!  Dr.  MacFabe actually read the Biome Buzz!

Dr. MacFabe heads up a multi-disciplinary research group that studies “…how metabolic products of the gut microbiome control brain function and behavior in autism, and also related neuropsychiatric conditions, such as obsessive compulsive, anxiety, movement, eating and learning disorders. We are particularly interested in the role of short fatty acid metabolites of gut bacteria and their role in autism and the development of novel clinical biomarkers and therapies to prevent, identify, screen and treat the disorder.”  The website he provides us in his comment contains copious amounts of research, and videos for you visual types.

I was skimming through Dr. M’s research on the website and came across a paper that I’ll write about in my next post:  Enteric ecosystem disruption in autism spectrum disorder: can the microbiota and macrobiota be restored?

“Many lines of scientific research suggest that Autism Spectrum Disorders (ASDs) may be associated with alterations in the enteric ecosystem, including alterations of the enteric macrobiome (i.e. helminths and fauna) and changes in predominant microbiome species, particularly a reduction in microbiome species diversity.”[ii]

Their conclusion:  “If these theoretical models prove to be valid, they may lead to the development of practical interventions which could decrease ASD prevalence and/or morbidity.”  Yes, for scientists this is all still theoretical.  For us in the real world – not so much.  Based upon 21 years of experience in the autism world, my observations of the kids I’ve worked with (including my own son) and my experience with the Specific Carbohydrate Diet, probiotics, prebiotics and helminths…there’s a 100% certainty that these interventions work. But obviously, we need to know a whole lot more.  Alex is a hell of a lot better but he’s still profoundly autistic and sick.  So I am very grateful (more than I can say) to have researchers like William and Dr. MacFabe out there.

Thanks again, Dr.  M.

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[i] https://evmedreview.com/reconstituting-the-depleted-biome-to-prevent-immune-disorders/

[ii] Slattery, J, MacFabe, DF, Kahler, SG, Frye, RE. Enteric ecosystem disruption in autism spectrum disorder: can the microbiota and macrobiota be restored?  Current Pharmaceutical Design. 2016;22(40)6107-6121.

New Research on the Microbiome and IBD

I recently spotted this article[i] on research coming out of the University of North Carolina:  “UNC cancer researchers find potential treatment for inflammatory bowel diseases.”  (Now, not that I am obsessing on Dr. Mercola’s article from last week or anything but I admit, this particular quote from one of the researchers did strike a nerve:  “At this point we have limited treatment options and no cure for people with inflammatory bowel disease.”…as opposed to Dr. Mercola’s dismissal of the use of therapeutic helminths because, “there are already many proven ways to treat inflammatory bowel disease… very effectively.”)

Humph.

Still brooding over here. (I did warn you in my last post that I was pit bull when it comes to not letting go of things!)
Back to this UNC paper[ii]: the researchers found that inflammation in the gut can go unchecked if an inflammation-inhibitor protein called NLRP12 is missing. (I’m not sure I fully understand why someone would be deficient in the protein, but it appears that it may be a genetic fragility.) This out-of-control inflammation, in turn, affects the balance of bacteria in the gut.  (Another example of how everything in the body is more than a two- way street. An increase in bad bacteria causes inflammation – and inflammation causes an increase in bad bacteria.)  The researchers found that certain types of pro-inflammatory bacteria were more abundant, along with lower levels of anti-inflammatory bacteria, when NLRP12 is absent.

The researchers call NLRP12 a “checkpoint” for the immune system.  What they suggest causes the devastation in IBD is not just the absence of the protein but also, its subsequent missing interaction with the gut flora.  Adding beneficial bacteria back into the gut can end this vicious cycle.  “We could potentially screen people for reduced expression of NLRP12, or who have this bacterial signature. Could this be a relatively simple fix for people who have this signature of the disease? At least, it appears to be the case in animals,” says one of the lead researchers.

You do have to wonder if this is not a factor in the development of autism, considering its relationship to gut pathologies (i.e. autistic enterocolitis) and altered gut flora?

Logically, then – genetic fragility of not – keeping your biome in good health (via diet, helminths, probiotics, prebiotics, minimal use of antibiotics, etc.) may ward off the development of IBD.

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[i] https://lifesciencedaily.com/academic-research/20640-unc-cancer-researchers-find-potential-treatment-inflammatory-bowel-diseases/

[ii] Chen, L, et. al. NLRP12 attenuates colon inflammation by maintaining colonic microbial diversity and promoting protective commensal bacterial growth. Nature Immunology. 2017:doi:10.1038/ni.2690.

March 22: A Day for More Brooding

I have always been a brooder.  My brain pretty much never shuts down anyway, and once I latch onto something that upsets me, I’m like a pit bull – I don’t let go.  So what am I still contemplating?  (Actually, better said…fuming over?)  Yes, it’s that post (1) by Dr. Mercola last week.  Specifically, this comment of his:  “Although worm therapy may be touted as the best new therapy for inflammation, there are already many proven ways to treat inflammatory bowel disease and some of the other illnesses and disorders very effectively without resorting to deliberately introducing parasites into your system.”

“Some of the other illnesses and disorders.” So, how about the others, like autism (and ALS, and Alzheimer’s and Parkinson’s…), for which there are NO accepted treatments?

Forgive me for more crankiness. Tomorrow is the 21st anniversary of my son’s diagnosis.  I remember nearly every minute of that terrible day.  What did the doctors at Mount Sinai Hospital here in New York tell me?  Firstly, that my beautiful baby had an incurable and devastating developmental disorder.  Secondly, that he may not be finished regressing and we may lose more skills (which indeed happened) and nothing could be done.  And third – that medical science had zero answers for me.

And 21 years later…medical science has zero answers for me.

Sure, it is at least now somewhat accepted that many children on the spectrum have GI involvement and yes, there’s some grasp of the fact that the gut biome is altered and the immune system is involved.  (But then again…at my first meeting with Dr. Sid Baker, 19 years ago, he already told me that autism is the result of abnormalities in the gut-brain-immune axis….)  However, in terms of accepted treatments for autism, there is still nothing.

Also, how about Dr. Mercola’s assertion that there are “…many proven ways to treat IBD some of the other illnesses and disorders very effectively”?! Many people do not respond to these treatments.  As one helminth user shared:

“I was diagnosed with Crohn’s disease aged 16, have had all major pharmaceutical treatments with little to no sustainable impact, and subsequently had a colostomy procedure in my mid-20s as a result. I was one of the first 20 patients in the world to receive helminthic therapy, and have found through weekly dosages …I have achieved remission with no lasting side-effects.  Auto-immune disorders affect your nervous system, and regardless of all the other horrible symptoms, leave you feeling constantly tense and anxious. To be able to be free from that sensation after 17 years or more is an emotion that cannot be fully understood, unless you have experienced it yourself.”

Like this gentleman Alex’s colitis did not respond to prednisone, 6MP, colazal, pentasa, Gastrocrom and/or Nexium.  It did respond to the “unproven” treatments of the Specific Carbohydrate Diet and helminths.  Alex is completely symptom free now, and off all special diets.

Those of us dealing with situations outside medical knowledge are simply not in a position to summarily dismiss anything that is not yet accepted by the medical establishment.  My conclusion is that holding to my mantra remains the best course of action: “When faced with prolonged scientific uncertainty, use your best judgement.”

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  1. http://articles.mercola.com/sites/articles/archive/2017/03/13/helminth-therapy.aspx

ALS, Icebuckets and the Gut Biome

Several years ago, my Dad had a co-worker die of ALS:  he was only 42 or so.  My Dad tried to talk him into trying helminths.  After all, what did he have to lose?  And there is some speculation there that ALS may have an autoimmune component.  But the man’s doctor objected:  after all, helminths might kill him.  Wait…WHAT?!  (You can’t make this stuff up.)

The poor man, father of two little girls, was dead in less than 2 years.

Every time I read articles about ALS, I think of my Dad’s friend.  I never met him personally, but my Dad was fond of him…and how can anyone not be affected by the tragic death of someone so young?

My big brother also has a very dear friend who developed ALS a couple of years ago.  I first met her 30 or more years ago.  I think about her every day and my heart literally aches every time.  She is so unbelievably sick now – it’s unbearable.  Back in January, I spotted an article[i] out of the University of Illinois, “Rebalancing gut microbiome lengthens survival in mouse model of ALS.”  Believe it or not, the research was actually paid for by the famous Ice Bucket Challenge.

“Sun and her colleagues studied transgenic mice that were engineered to carry human genes known to contribute to certain forms of ALS. The mice were found to have an abnormal microbiome, along with damaged junctions between the cells of the intestinal lining. Poorly functioning junctions can cause the tissue to become leaky, and have been found to be associated with the onset of ALS in humans.

When the researchers fed the ALS-prone mice butyrate in their water, starting when the mice were 35 to 42 days old, the mice showed a restored gut microbiome profile and improved gut integrity. Butyrate-treated mice also showed improved neuromuscular function and delayed onset of ALS symptoms. Treated mice showed symptoms at 150 days old compared to control mice at about 110 days. Treated mice also lived an average 38 days longer than mice not given butyrate.”

Butyrate is a natural byproduct of normal intestinal bacteria.  Feeding it to the mice restored the equilibrium to the intestinal bacteria and improved lesions in the gut wall.

By the way, I had already read previously that gut bacteria play a role in ALS (as well as Parkinson’s and Alzheimer’s, which you already know from previous posts).  Research out of the University of Louisville[ii] discovered that the misfolding of proteins in the brain that characterize these diseases can be initiated by proteins produced by gut bacteria.  One of the researchers concluded, “These new studies in two different animals show that proteins made by bacteria harbored in the gut may be an initiating factor in the disease process of Alzheimer’s disease, Parkinson’s disease and ALS.”

I know my brother sent the information on to his friend.  She can read, but she cannot talk – she has to use some kind of special computer. He visits her regularly – I hope he can convince her. My Dad will always regret that Rob could not be convinced.  Of course, I have absolutely no idea if working on her gut biome at this stage can help but…it can’t hurt either, can it?   And as I said a few weeks back, talking about my Grandmother and Alzheimer’s, let’s all “not go gentle into that good night…”

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[i] https://news.uic.edu/rebalancing-gut-microbiome-lengthens-survival-in-mouse-model-of-als

[ii] https://www.sciencedaily.com/releases/2016/10/161006092015.htm