CAR INSURANCE QUOTES COLORADO

Car Insurance Quotes Colorado
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We know you are wont to living at elevated altitudes, American state residents, however that does not mean your automobile insurance premiums ought to be thus high they are snowcapped.

In fact, Esurance offers a number of the foremost competitive motorcar insurance rates in Colorado, beside 24/7 client service and versatile on-line policy management.

Break the ice and obtain to grasp United States by beginning a free Colorado automobile insurance quote. you will gain instant access to our interactive on-line tools that build the automobile insurance method clear, more cost-effective, and simple to grasp.

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Good news, Coloradans: we have a good array of discounts to assist bring your motorcar insurance premiums nearer to water level. Here's a sampling of our money-saving discounts:

Anti-Theft Device discount
Claim-Free discount
Defensive Driver discount
Fast 5� discount
Good Student discount
DriveSense� discount
Homeowners discount
Multi-Car discount
Paid-in-Full discount
Safety Device discount
Multi-Policy discount
Discounts ar subject to eligibility. If you are a current client with questions on your Colorado motorcar discounts, offer United States a move into 1-800-ESURANCE (1-800-378-7262).

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Required coverages
Colorado needs its drivers to hold insurance with a minimum of the subsequent limits:

$25,000 bodily injury liability coverage per person
$50,000 bodily injury liability coverage per accident
$15,000 property harm liability coverage per accident
You'll typically see these numbers written as 25/50/15. you'll opt for higher limits to possess additional coverage once you customise your policy.

Optional coverages
These extra coverages give you with the additional peace of mind and security you would like, whereas providing you with magnified monetary protection within the event of a claim:

CarMatch Rental Coverage�
Collision coverage
Comprehensive coverage
Custom components and instrumentality coverage
Loan/lease gap coverage
Medical and ceremonial occasion service coverage
Towing and labor coverage
Uninsured driver bodily injury coverage
Uninsured driver property harm coverage
Plus, CoverageMyWay�, solely from Esurance, provides coverage choices to assist confirm you simply procure what's right for you. It's only one manner we attempt to form automobile insurance quicker, simpler, and more cost-effective.

how we have a tendency to calculate your colorado premium
Colorado automobile insurance corporations (like Esurance) will use the subsequent factors to see your automobile insurance rates:

The coverages, limits, and deductibles that you simply opt for for your policy
Accidents and violations inside the past three to five years
Marital standing, gender, age, and variety of years commissioned
ZIP Code wherever the vehicle is garaged or position
Your vehicle's year, make, model, and condition
Prior insurance history, as well as variety of years insured unceasingly
insurance facts and data
Proof of insurance in Colorado
We're all human: typically we have a tendency to forget to throw our updated ID cards within the glove box. however if you get force over, you are not out of luck: Colorado permits drivers to supply electronic proof of automobile insurance on their smartphones and different devices as applicable proof of coverage.

Even higher, if you are associate Esurance client, you'll access our free mobile app 24/7 for your ID cards, policy documents, and more.

Failure to supply proof of coverage upon request may result in an exceedingly 4-point penalty on your driving record, moreover as a fine.

Uninsured drivers in Colorado
A report from the Insurance analysis Council found that fifteen p.c of Colorado drivers were uninsured in 2009, that was higher than the national average of thirteen.8 percent.

While uninsured and underinsured motorists coverage is nonmandatory in your state, it provides monetary protection if you are ever in associate accident caused by associate uninsured or underinsured driver, and it additionally protects you within the event of a hit-and-run accident.


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Leukemia, IL-6 IL-10 and an Autism Flare-up


   
Leukemia/Leukaemia  is cancer that begins in the bone marrow and result in high numbers of abnormal white blood cells.

I received a comment on this blog a long time ago from a parent whose child had initially responded well to some of the autism therapies suggested on this blog. Later on all the therapies stopped working.  That child also has leukemia.

We now know this is a common event when you start treating autism, some comorbidity arises that blocks the effects of those therapies.  In my son�s case it is a simple pollen allergy, but it can be all kinds of inflammatory conditions such as colitis, IBS, IBD, GERD, celiac disease, juvenile arthritis, mastocytosis etc.  This list goes on, but now I know why it includes leukemia.

I do not consider epilepsy, or indeed cognitive dysfunction, as comorbidities.  Epilepsy is periodic extreme neuronal hyper-excitability, whereas in much autism there is chronic neuronal hyper-excitability.  Not surprisingly, chronic neuronal hyper-excitability can develop to periodic extreme neuronal hyper-excitability.  So I see epilepsy as a natural progression from childhood autism, but one that perhaps could and should be prevented.

Earlier on writing this blog I thought that genetics and cancer pathways would be beyond its scope, but in apparent absence of anyone much else publicizing the connections with autism I revised my view.

It has been known since 1930 that leukemia is comorbid with Down Syndrome (DS).  DS is caused by caused by the presence of all, or part of a third copy of chromosome 21 this leads to over expression of 300+ genes.  DS is usually easy to diagnose based on physical appearance .  The gene over-expression frequently leads to autistic behaviors and somewhat less frequently to various types of leukemia and in later years early onset Alzheimer�s.  The good news is that DS  children with acute myeloid leukemia (AML), and in particular the acute megakaryocytic leukemia (AMkL) subtype, have exceptionally high cure rates.

The particular gene that is over-expressed in DS and can cause leukemia is called HMGN1.

DS is increasingly rare in Europe, but quite common in the US due to differences in parental choice regarding the termination of pregnancies identified as high risk of Down Syndrome.

I think it only fair to consider leukemia as a possible comorbidity of autism, since may people with DS do indeed exhibit autistic behaviors.

There is no quality data to say how common leukemia is in non-DS autism.
 

Leukemia and Cytokines IL-6 and IL-10

I do consider the pro-inflammatory cytokine IL-6 to be public enemy number one of autism, while the anti-inflammatory cytokine is a potential friend.

There are different types of Leukemia, but it appears that IL-6 and IL-10 play a key role and at least in acute myeloid leukemia can predict the outcome.  Generally speaking leukemia is associated with elevated IL-6 and in particular when there is a relapse.

Acute myeloid leukemia (AML) blast cells frequently produce interleukin-6 (IL-6) 



Cytokine profiles in acute myeloid leukemia patients at diagnosis: survival is inversely correlated with IL-6 and directly correlated with IL-10 levels

An aberrant production of the pro-inflammatory cytokines IL-6 and TNF-a and the anti-inflammatory cytokine IL-10 is observed in AML patients. Low levels of IL-6 and high levels of IL-10 represent favorable prognostic factors for survival in AML patients. These results support the idea that cytokine deregulation may be useful as a marker for predicting clinical evolution in AML patients.

So we can infer that a leukemia relapse will likely lead to a worsening of autism driven by an elevation in the level of the pro-inflammatory cytokine IL-6.  This would account for why the autism drugs �stopped working� in the case of our reader.

We could then ponder that a therapy that reduces IL-6 and increases IL-10 might help keep some types of leukemia in remission.

This is altering the Th1/Th2 balance which was the target of our reader Alli from Switzerland who did decide to spend many hours reading the oncology research to understand all those cellular signaling pathways.

For those interested in why DS increases the risk of leukemia, scientists at the Dana-Farber Institute in Boston have figured this out, at least in the case of one common form of Leukemia.





If only some more of the clever people studied autism.






Performances

Nearly all parents like to see their children performing on stage.  

This week I attended two very different performances.

The first was a play organized by my son Monty�s piano teacher; we came along to show support.  She organizes numerous events for children with special needs, she includes people with Asperger�s and all kinds of autism; some have an assistant on stage to support them and some do not.  One was in a wheelchair. She also includes some typical kids in the more demanding roles.  

As expected there were big smiles all around, happy performers and happy friends and family in the audience.  They have several repeat performances.

A couple of days later was another performance, this time Monty�s big brother was performing at the school poetry night.  Here again, the students were performing in front of the assembled parents.  As usual it was poems in a wide variety of languages, from Russian to Indonesian to Swedish.  Some students were showing off by reciting in their third or fourth language.

On the one hand the two performances were very different, because of the different level of ability, but in other ways it shows how everyone enjoys the chance to perform with their friends.

I don�t see Monty enjoying reciting poetry up on the stage, but he would happily play his piano.

Big brother clearly enjoyed reciting his poem in German and next year he will probably choose Russian. While little brother will likely always struggle with spoken language, big brother now speaks five languages.  But he probably would not enjoy having to play the piano up there on stage.

Each to his own and as the student presenter of the poetry night commented, �it beats sitting at home�.






Agenesis of the Corpus Callosum


Today�s post is about another supposedly rare cause of autism called Agenesis of the Corpus Callosum (ACC).

As regular readers of this blog will have noted, extremely rare causes of autism, taken as a group are not so rare after all.  In fact it seems that autism is just a very large collection of somewhat rare biological conditions. 
Of the very few "Autism Dads" I have had a face to face conversation with, one has a child with ACC and another has a son with the even rarer Sotos syndrome. Sotos syndrome is characterized by gigantism, mild ID/MR and often autism. Mutations in the NSD1 gene cause Sotos syndrome

ACC is physical malformation of the brain that shows up clearly on MRI scans and potentially shows up on the mother�s regular ultrasound scans. 

The corpus callosum is a wide, flat bundle of fibers about 10 cm long that connects the left and right sides of the brain.  It facilitates communication between the two sides of the brain.
Agenesis of the corpus callosum (ACC) is a birth defect in which there is a complete or partial absence of the corpus callosum.

ACC leads to behaviors compatible with a diagnosis of autism or Asperger�s in about half of cases.

Symptoms of ACC  vary greatly among individuals, as they do in all types of autism.  Seizures are common, some people have poor motor coordination, and some people are non-verbal.

It is suggested by many that a diagnosis of ACC is not compatible with a diagnosis of autism; this just shows a lack of understanding.
Autism is just a description of behaviors, ACC is a biological diagnosis, like Fragile X syndrome or Down Syndrome.  So if a person has autistic behaviors caused by ACC, it is still autism, it is just autism with an explanation of its origin.

The most famous person with ACC was Kim Peek who was the inspiration for the character played by Dustin Hoffman in the well-known film Rain Man.

In addition to having the physical ACC malformation it has been suggested that the cause of ACC in his case was likely FG Syndrome.

Most mutations that cause FG syndrome can be found in the MED12 gene. However, mutations have also been found in FMR1, FLNA, UPF3B, CASK, MECP2, and ATRX genes. Mutations on these different genes lead to the different types of FG syndrome, all with similar characteristics.  Congenital heart defects are common and Peek died of a heart attack aged 58, outlived by his father.  


Agenesis of the Corpus Callosum and broader Autism

Undoubtedly there are people diagnosed with autism, who have undiagnosed ACC, since they never had an MRI scan.  Just like there are many people with autism who have an undiagnosed, but treatable, Chiari �brain hernia�.

It also appears that having a smaller corpus callosum, but falling short of what would be diagnosed as ACC by the MRI scan, is a feature of some people�s autism. You could consider it as partial ACC, like we had partial biotin/biotinidase deficiency.

A very recent paper from the 2016 Society for Neuroscience annual meeting suggested one reason why autism is more prevalent in males.  The study looked at infecting pregnant rats with group B streptococcus to activate the mothers immune system.  Inflammation was then triggered in the fetal side of the placenta, but only in male fetuses.
The males go on to develop brain and behavioral features reminiscent of autism.
Female fetuses were somehow protected and developed normally.  Hopefully Barons Cohen will read this and stop looking for undiagnosed females with autism. There are many good reasons why autism is less prevalent in females, and they are not just �better at hiding it�, as the so-called expert claims. 



What is interesting is that in the male pups with �autism� they had an unusually thin corpus callosum. It turns out that such minor malformations occur in broader human autism. 



The largest of the white matter tracts is known as the corpus callosum, which allows communication between the two hemispheres (halves) of the brain.
"The size of the corpus callosum was smaller in the group with autism, suggesting that inter-regional brain cabling is disrupted in autism," Dr. Just said.

In essence, the extent to which the two key brain areas (prefrontal and parietal) of the autistic participants worked in synchrony was correlated with the size of the corpus callosum. The smaller the corpus callosum, the less likely the two areas were to function in synchrony. In the normal participants, however, the size of the corpus callosum did not appear to be correlated with the ability of the two areas to work in synchrony.

"This finding provides strong evidence that autism is a disorder involving the biological connections and the coordination of processing between brain areas," Dr. Just said.




CONCLUSIONS:

These longitudinal results suggest atypical early childhood development of the corpus callosum microstructure in autism that transitions into sustained group differences in adolescence and adulthood. This pattern of results provides longitudinal evidence consistent with a growing number of published studies and hypotheses regarding abnormal brain connectivity across the life span in autism.




The study suggests that white matter abnormalities manifest early in autism, says Thomas Frazier, director of Center for Autism at the Cleveland Clinic in Ohio. �It also serves as a nice demonstration that brain abnormalities in autism will become clearest and most helpful for pointing to etiology when we look at them developmentally, longitudinally, rather than at a single age," he says.



The findings do not imply that corpus callosum abnormalities cause autism, cautions Ralph-Axel M�ller, professor of psychology at San Diego State University, who was not involved with the work. Rather, any irregularities in the corpus callosum may stem from other abnormalities in the brain that have been associated with autism, M�ller says.



Still, changes in the corpus callosum may help to explain why autism symptoms worsen in some individuals and improve in others, Travers says. "Is there some aspect of white matter micro-structure occurring early in the developmental pathology that locks in persistent autism across the lifespan? What are the mechanisms? Can they be unlocked?� she says. �These will be important questions for future research.�



  

Conclusion

It is estimated that at one in 4,000 individuals has a disorder of the corpus callosum. I suspect it is more, but you would need to routinely give MRI scans to people diagnosed with autism to find out.

It is clear that milder disorders of the corpus callosum may be a feature of many people�s autism and those changes over time in the corpus callosum may help to explain why autism symptoms worsen in some individuals and improve in others.






Preventing Auto-Immune Disease and some Autism

Today�s post is another one filling in some gaps in this blog.

I think it is common sense to say that preventing a problem from developing is much wiser than trying to solve it later on.  This is a recurring issue in both life and medicine.

In the research we now see preventative measures developed to reduce the risk of cancer, we also see how some interventions are only effective when started very early.

In the case of autism we have seen than often it is caused by a myriad of factors that by themselves might have been harmless but when taken together are the multiples hits that caused the brain to develop differently.

Much research looks individually at these factors that increase the risk of autism.  In the wider media much disdain is directed to these findings as if each factor is THE cause of autism and how can so many things cause autism.  But by understanding these factors you can then set about countering them.

I did create my simplified schematic to explain classic autism a while back.  It is not perfect but it does illustrate much of what is going on.




I do get occasional questions about reducing the risk of autism.  For example, Monty now aged 13 with ASD, has a big brother and he wants to know.  Our reader, Kritika from India, has also raised this issue.  If you have autism in your family you may well decide you would like to minimize the risk of more cases.

In practical terms, you cannot change your genes or those inherited epigenetic markers.  Maybe this will change in future.  But there are things you can do.

We know that oxidative stress is a driver of much disease including autism.  This can be minimized by lifestyle changes and indeed with a little pharmacological help.

I was interested to see a study that used NAC to treat mothers who suffer unexplained pregnancy loss, the antioxidant showed a significant increase in the take-home baby rate�.  I was really just looking for safety information.


Pregnancy could be associated with a state of oxidative stress that could initiate and propagate a cascade of changes that may lead to pregnancy wastage. This process of oxidative stress may be suppressed by the antioxidant effect of N-acetyl cysteine (NAC). The current study aimed to evaluate the effect of NAC therapy in patients diagnosed with unexplained recurrent pregnancy loss (RPL). The study was a prospective controlled study performed in the Women's Health Centre, Assiut University, Egypt. A group of 80 patients with history of recurrent unexplained pregnancy loss were treated with NAC 0.6 g + folic acid 500 microg/day and compared with an aged-matched group of 86 patients treated with folic acid 500 microg/day alone. NAC + folic acid compared with folic acid alone caused a significantly increased rate of continuation of a living pregnancy up to and beyond 20 weeks [P < 0.002, relative risk (RR) 2.9, 95% confidence interval (CI) 1.5-5.6]. NAC + folic acid was associated with a significant increase in the take-home baby rate as compared with folic acid alone (P < 0.047, RR 1.98, 95% CI 1.3-4.0). In conclusion, NAC is a well-tolerated drug that could be a potentially effective treatment in patients with unexplained RPL.


This then made be recall a US fertility clinic, that our reader Roger once mentioned in a comment.




�At Braverman Reproductive Immunology, we believe Autism Spectrum Disorder (ASD) and various pregnancy and infertility complications (listed below) appear to have the same cause. In fact, we have found that a large number of patients who present to our center with the below complications already have a child with ASD.
This discovery started us on the journey to see if ASD itself could be prevented while treating other associated conditions. We believe treatment for these common issues will not only prevent the pregnancy complications listed below, but may also prevent ASD in the group of patients that have already had a child with ASD.�

Dr Braverman does not mention oxidative stress, but perhaps he should.

So step one would be to reduce oxidative stress during pregnancy, via lifestyle changes and taking antioxidants.

Step two would be to avoid inflammation, Dr Braverman refers to the link to auto-immune disease and miscarriage/autism.

We know that maternal inflammation is one of the easiest ways to cause autism in mouse models (the MIA model - Maternal Immune Activation).
  
We have some research to show that the risk of auto-immune disease can indeed be reduced and indeed that the risk of progression from minor to more major auto-immune disease can also be minimized.

We even have a tiny study showing that immuno-modulatory therapy using a probiotic during pregnancy can reduce incidence of ADHD and autism. For me ADHD is just a case of autism-lite.


A possible link between early probiotic intervention and the risk of neuropsychiatric disorders later in childhood: a randomized trial


Background:

Recent experimental evidence suggests that gut microbiota may alter function within the nervous system providing new insight on the mechanism of neuropsychiatric disorders.

Methods:

Seventy-five infants who were randomized to receive Lactobacillus rhamnosus GG (ATCC 53103) or placebo during the first 6 mo of life were followed-up for 13 y. Gut microbiota was assessed at the age of 3?wk, 3, 6, 12, 18, 24 mo, and 13 y using fluorescein in situ hybridization (FISH) and qPCR, and indirectly by determining the blood group secretor type at the age of 13 y. The diagnoses of attention deficit hyperactivity disorder (ADHD) and Asperger syndrome (AS) by a child neurologist or psychiatrist were based on ICD-10 diagnostic criteria.

Results:

At the age of 13 y, ADHD or AS was diagnosed in 6/35 (17.1%) children in the placebo and none in the probiotic group (P = 0.008). The mean (SD) numbers of Bifidobacterium species bacteria in feces during the first 6 mo of life was lower in affected children 8.26 (1.24) log cells/g than in healthy children 9.12 (0.64) log cells/g; P = 0.03.

Conclusion:

Probiotic supplementation early in life may reduce the risk of neuropsychiatric disorder development later in childhood possible by mechanisms not limited to gut microbiota composition.


The issue, as with NAC during pregnancy, is whether immuno-modulatory therapy is safe.

The study on ADHD and autism was actually a study looking at whether a certain probiotic if given during pregnancy could reduce eczema later on in the child.

  
We also have the studied effect of having a pet dog at home.

House dust exposure mediates gut microbiome Lactobacillus enrichmentand airway immune defense against allergens and virus infection

 

Early-life exposure to dogs is protective against allergic disease development, and dog ownership is associated with a distinct milieu of house dust microbial exposures. Here, we show that mice exposed to dog-associated house dust are protected against airway allergen challenge. These animals exhibit reduced Th2 cytokine production, fewer activated T cells, and a distinct gut microbiome composition, highly enriched for Lactobacillus johnsonii, which itself can confer airway protection when orally supplemented as a single species. This study supports the possibility that host�environment interactions that govern allergic or infectious airway disease may be mediated, at least in part, by the impact of environmental exposures on the gastrointestinal microbiome composition and, by extension, its impact on the host immune response.



One of my views is that by early treatment of autism you may indeed reduce the risk of epilepsy.  The key here is �reduce the risk�, it does not mean there is no risk.  There are likely hundreds of causes of epilepsy, but if you can reduce the incidence by 30+% that would look like a big success to me.

I recall another study that looked at treating people with eczema to see if you could reduce the chance of progression to asthma.  Using Ketotifen the trial showed that it was indeed possible.

Prevention of asthma by ketotifen in infants with atopic dermatitis. 

To evaluate the prophylactic effect of ketotifen against the onset of asthma we selected 121 infants with atopic dermatitis, without any history suggestive of asthma (cough and/or wheezing). Sixty-one children received ketotifen twice daily. Those who weighed less than 14 kg received 0.8 mg; 14 kg or more, 1.2 mg. Sixty children, a placebo syrup indistinguishable from the active syrup. Both groups were followed for 1 year, with bimonthly evaluations. The criteria for onset of asthma were two different episodes of wheezing treated with bronchodilator drugs. Both groups were comparable regarding age, sex, weight, onset, and duration of atopic dermatitis and age at the onset of asthma. During the 1 year study, asthma was observed in eight children of the ketotifen group (13.1%) and in 25 children of the placebo group (41.6%) (P less than .001). Side effects were negligible and routine laboratory tests disclosed no significant alterations. Ketotifen is a very useful drug for prevention of asthma in children with atopic dermatitis and total IgE more than 50 IU/mL.


Somali Autism Clusters

This then takes me back to that issue I looked at long ago, which was the reason for the Somali immigrants to Sweden and US having so many children with autism.  This even got termed the Swedish Disease by the migrants, they claimed to have never seen autism back home in Somalia.

Then we have the hygiene hypothesis which in effect says that, within limits, a little dirt is good for you.



Hormonal Dysfunction

We know that gestational diabetes increases the risk of autism and we also known that the mother being hypothyroid increases the risk.  In some cases the hormone dysfunction is a consequence of the auto-immune dysfunction.

We also know the female hormone progesterone is extremely neuro-protective.  The level of this hormone is supposed to rise during pregnancy.




  
In past times hormones were given to some pregnant mothers, but this went out of fashion.  Perhaps this should be revisited?

Then we have the surge of the hormone oxytocin that the baby is supposed to receive at birth.  This surge may be relevant to the GABA switch when shortly after birth this neurotransmitter is supposed to switch from excitatory to inhibitory as the neurons mature. If the baby is born by Caesarian there will be no oxytocin surge for the baby.   



Preventing Regressive Autism Secondary to Mitochondrial Disease (AMD)

It is on open secret that doctors at Johns Hopkins have identified a variant of regressive autism called Autism secondary to Mitochondrial Disease (AMD).

It remains unclear how rare this is and absolutely nobody serious is going to research this, if they ever want to receive a research grant in the future.

We saw that in people with a genetic predisposition to mitochondrial dysfunction, an immune over-reaction to an insult like multiple vaccinations can trigger mitochondrial disease.  This will present itself as autism and quite possibly severe autism in a previously unaffected child.

Those doctors treating AMD use mild immuno-suppressing drugs before any future vaccinations.

How do you minimize the chance of AMD? 

The first thing is to never use paracetamol/acetaminophen in a baby or child, particularly just after vaccination.  This drug may kill the pain but it depletes GSH the body�s main antioxidant, just when it needs it most.   Use something like Ibuprofen.

Vaccines are given in multiples so as to save time and money and I suppose improve compliance. You might expect giving them one-by-one would actually make them more effective as well minimizing any collateral damage to a small percentage of kids.




Conclusion

As I keep reminding readers, I am not a doctor, but it would be nice if a few more doctors other than Braverman took preventing autism seriously.

I would like to know if progesterone is an effective therapy in the MIA model of autism.  In this model they trigger the mother�s immune system during pregnancy which leads to offspring with autism.  What would be the effect of giving progesterone?  Would it protect the pups?

Are progesterone levels reduced in mice that will become autistic?

So I suppose I would trial NAC and progesterone in the mother mouse.

For everyone else it is case of choosing whether or not to make lifestyle changes to reduce oxidative stress.  Improving gut bacteria can be done via probiotics, eating more (slightly dirty) fruit and vegetables, having a pet dog, spending some time in the nature.  

As for vaccine risk, however small it might indeed be, there will never be a serious investigation of this, for understandable reasons. 







Broccoli Powder without the Taste





In this blog I make a point of not promoting non-generic products, except when they have some special features.  This was the case with sustained release NAC, which does seem to be a much better product than the gelatin capsules.

In the case of broccoli powder and Sulforaphane, there was some testing done that showed most products sold in the US do not actually produce any Sulforaphane.  Small doses of broccoli powder do indeed seem to have a positive effect in some people�s autism and even on insulin sensitivity in people with diabetes.  We assume this is down to sulforaphane, but even that is not certain, there are other interesting substances in broccoli

In the Johns Hopkins research on sulforaphane they use a deep frozen product made in the lab that is not commercially available.  The research was initially in cancer, but does now extend to autism.

We saw in earlier posts that that some broccoli powders have retained the necessary enzymes needed to produce Sulforaphane in your body. You can always add back the enzyme that got destroyed in processing, using Daikon radish, which is similar to what happens in Johns Hopkins lab process.

One producer, whose product I have not used, has come out with a new product that will be interesting to people whose child does not swallow pills and hates the taste of broccoli.

The producer keeps writing to me to tell me that their product produces the most sulforaphane.  What would be nice would be independent testing of several products currently on the market.




            �Delicious tasting, all natural blend of three of Nature�s most highly-prized plant foods; Pomegranate Juice, Coconut Water and 100% Whole Nutraceutical Grade Broccoli Sprouts�



Their broccoli powder is called EnduraCell and the more child friendly drink is called PomGenex.

You can buy their products in Australia and from their US distributor.


Anyone trying it is very welcome to leave their feedback here.








Ketones and Autism Part 4 � Inflammation, Activated Microglia, CtBP, the NLRP3 Inflammasome and IL-1�

This series of posts on ketones and the ketogenic diet (KD) is nearly finished and I am glad that I made favourable comments about the KD ea...