Dr. G’s comments:

Why are our tissues so calcified when we age? What has vitamin D got to do with it???

I have lectured on this for over 35 years now and we all suffer a tendency toward secondary hyperparathyroidism. This is because our SAD diet supplies on average 1400 mg of phosphorus and only 800 mg of calcium. This stresses our endocrine system and we get secondary hyperparathyroidism, as a result that leads to weak bones and hard calcified arteries. See text and CALCIPHYLAXIS by Hans Selye published by Univ of Chicago Press.

What this article shows you is that higher levels of vitamin D clearly help overcome this serious but nearly epidemic Endocrine condition. Vitamin D then can lead to less bone pathology and if bones are better mineralized, less of the calcium will wind up in blood vessels and you can achieve better blood vessel elasticity.

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com

Link: http://www.nhiondemand.com/hsjarticle.aspx?id=987&utm_source=NHI+OnDemand+Newsletter+List&utm_campaign=49b87e5f60-HSJ_Jan18_2011&utm_medium=email

Excerpt:

“Hyperthyroidism” is when the thyroid gland is overactive instead of underactive. It secretes too much thyroid hormone. In this case, more of a good thing is definitely not better. Excess thyroid hormone can cause rapid heartbeat. Body temperature is elevated. The hyperthyroid individual may experience extreme weight loss, in spite of a huge appetite, because they burn up calories too fast. Hyperthyroidism can make a person nervous, emotionally unstable, and unable to sleep.

This PROTOCOL will dramatically improve almost any skin condition for any patient. Always think systemically; always deal with foods that are sensitizing the patient and toxins and infections that are not necessarily just skin infections.

Please get an atomizer from Longevity Plus and fill it 50/50 with Quinton Marine Plasma Hypertonic and ACS 200 and spray often. Alternate that with sprays from ACZ Nano, which if not responding we can make stronger by putting one ZeoGold cap in 2 ounces of good water, let it hydrate and draw off the top 10 cc or two tsp. Use that to “spike” the ACZ Nano after 10 cc have been used or put in water and drank but that way we have POWERFUL HEALING from the stronger Zeolite form in ZeoGold that I find even helps cancer lesions on the skin. 

When using Quinton always take at least 3-4 of the Isotonic orally to maximize effect but spraying it is amazing particularly with the help of the other suggestions. Get two atomizers to use up the 10 cc or simply drink the residual contents.

Longevity Plus also has the strongest topical Aloe Vera used in nursing homes by Carrasyn. Use that lightly on the skin, as it will dry and form a thin film helping the other spray applications become longer acting.

Always top off the program with MY INFECTION PROGRAM. Orally use 5 days of high dose Vit A, 300-500,000 units each day, and always use high dose Vit D, 5000 a day, and Immuni-T2, three bid, and use the ACS 200 orally, 1 ounce to start then 25 sprays tid, which is 1/2 ounce daily, for days or weeks depending on condition. 

But EVERYONE has to learn my FIGHT program and the oral program here will help skin recover by lowering total body burden of pathogens but all skin is an accessory detox organ so soak in tub with Beyond Clean (EDTA) and follow instructions on the jar to alternate with Epsom then vinegar, etc.

Always use my Power Drink (MACA, Beyond Fiber, BIOEN’R-G’Y C and Organic Green) with Beyond Chelation-Improved and ZeoGold, as I can show you that even lifetime disfiguring psoriasis or other impossible eczema etc will always respond to my FIGHT program. Always increase Omega 3 to 4 caps daily for a month in addition to the one cap in each BC-I packet but the primrose in those is essential too. The diet is tough, stop sensitizing foods; listen to my webinars on FOOD and FIGHT and SILVER to learn more. 
.
Sincerely,

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com

Nod (nucleotide-binding oligomerization domain) 1 and Nod2 are intracellular PRMs (pattern-recognition molecules) of the NLR (Nod-like receptor) family. These proteins are implicated in the detection of bacterial peptidoglycan and regulate pro-inflammatory pathways in response to bacteria by inducing signalling pathways such as NF-kappaB (nuclear factor kappaB) and MAPKs (mitogen-activated protein kinases). The Nod proteins act independently of the TLR (Toll-like receptor) cascade, but potently synergize with the latter to trigger innate immune responses to microbes. Most importantly, mutations in Nod2 have been shown to confer susceptibility to several chronic inflammatory disorders, including Crohn’s disease, Blau syndrome and early-onset sarcoidosis, underscoring the role of Nod2 in inflammatory homoeostasis. This review summarizes the most recent findings in the field of Nod1 and Nod2 research.

Abstract

The innate immune system comprises several classes of pattern recognition receptors, including Toll-like receptors (TLRs), NOD-like receptors (NLRs), and RIG-1-like receptors (RLRs). TLRs recognize microbes on the cell surface and in endosomes, whereas NLRs and RLRs detect microbial components in the cytosol. Here we discuss the recent understanding in NLRs. Two NLRs, NOD1 and NOD2, sense the cytosolic presence of the peptidoglycan fragments meso-DAP and muramyl dipeptide, respectively, and drive the activation of mitogen-activated protein kinase (MAPK) and the transcription factor NF-kappaB. A different set of NLRs induces caspase-1 activation through the assembly of large protein complexes named inflammasomes. Genetic variations in several NLR members are associated with the development of inflammatory disorders. Further understanding of NLRs should provide new insights into the mechanisms of host defense and the pathogenesis of inflammatory diseases.

 ========================================

Curr Opin Immunol. 2008 Aug;20(4):377-82. Epub 2008 Jul 2.

NOD-like receptors (NLRs): bona fide intracellular microbial sensors.

Shaw MH, Reimer T, Kim YG, Nuñez G.

Department of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI 48109, USA.

Abstract

The nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) (nucleotide-binding domain leucine-rich repeat containing) family of proteins has been demonstrated to function as regulators of innate immune response against microbial pathogens. Stimulation of NOD1 and NOD2, two prototypic NLRs, results in the activation of MAPK and NF-kappaB. On the other hand, a different set of NLRs induces caspase-1 activation through the assembly of an inflammasome. This review discusses recent findings regarding the signaling pathways utilized by NLR proteins in the control of caspase-1 and NF-kappaB activation, as well as the nonredundant role of NLRs in pathogen clearance. The review also covers advances regarding the cellular localization of these proteins and the implications this may have on pathogen sensing and signal transduction.

========================================

Cell Host Microbe. 2008 Mar 13;3(3):146-57.

Caspase-12 modulates NOD signaling and regulates antimicrobial peptide production and mucosal immunity.

LeBlanc PM, Yeretssian G, Rutherford N, Doiron K, Nadiri A, Zhu L, Green DR,Gruenheid S, Saleh M.

Department of Medicine, Division of Critical Care, and Centre for Study of Host Resistance, McGill University, Montreal H3A 1A1, Canada.

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com

From: John Cannell, M.D.
The Vitamin D Newsletter
January 30, 2010.

Dear Dr. Cannell:
At age 2.5 years, between December 2007 and January 2008, my son experienced a fairly dramatic onset of symptoms that led to his diagnosis of autism. His symptoms (many of which we did not even know the terminology for at the time they first occurred) included:
–The inability to sleep at night, we would put him to bed at 8:00 or 8:30 p.m. following his normal bedtime routine
–Development of anxiety and refusal to leave the house even to do preferred activities
–Obsessive-repetitive questions and monologuing/run-on speech
–Sensory issues (refusal to wear jeans or any fabrics other than fleece, screaming hysterically at bath time, complaining and covering eyes in sunlight, covering ears for everyday noises that had not bothered him before (toilets flushing, pulling pots and pans from cupboards, etc.)
–Toe-walking
–Flapping and self-stimulating behaviors (repeatedly tapping his cheeks and eyes with all ten fingers, continually twisting up his fingers in pretzel-like configurations, holding objects in his peripheral range of vision and straining to see them from the corner of his eyes)
–Development of an unusual pattern of stuttering/vocal tic at the end of words,he would repeat the last sound/syllable,”I don’t want to go to the store-or-or-or-or-or-or. It won’t be fun-n-n-n-n-n-n-n.” He would make sounds even in his sleep “n-n-n-n-n-n” or “s-s-s-s-s-s-s”
–Loss of muscle tone (stopped walking up and down stairs and began crawling/sliding instead, decline in balance and motor skills)
–loss of handedness (began switching left to right hand, after seeming predominantly left-handed)
–Marked increase in hyperactivity
–Frequent spacing out/unresponsive episodes

Our son and his twin sister were born at 36 weeks, 5 days on March 17, 2005 after four months of bed-rest. As early as their 8 week appointment, I mentioned to our pediatrician that we had concerns about our son’s eye contact and social responsiveness (in comparison to his sister). I felt that I was having more difficulty bonding with him. We were told “don’t worry, but don’t wait” and were referred to our state’s Early On intervention program. At the end of June a physical therapist and speech pathologist from our intermediate school district came to our home to evaluate our then 3 month old son and told me that he was doing just fine and that I was worrying too much. I agreed that by the time they saw him he had begun smiling and making better eye contact.
We didn’t worry again about our son until fall 2006. He had walked just before his first birthday, but by 18 months+ he still seemed clumsy and prone to falling compared to his sister. We took him back to the intermediate school district for evaluation and were told that all of his development seemed to be in the normal range and that we shouldn’t worry. We were advised that we could take him to music and gym classes to work on his coordination and told that we could pay for private physical therapy if we elected. We followed all of the recommendations.

For a year, we didn’t notice any other changes until the sudden onset of symptoms listed above when he was 2.5 years. With the sudden onset of symptoms above, we took our son to see a number of specialists during the winter of 2008 including a neurologist (who diagnosed him with Asperger Syndrome), a psychologist (who diagnosed with autism), and a second psychologist who specialized in the treatment of autism (who diagnosed him with Pervasive Developmental Disorder Not-Otherwise-Specified). All three diagnoses are on the autism spectrum. He also began seeing an occupational therapist, a speech therapist, a behavioral specialist, and a DAN! (Defeat Autism Now!) doctor for dietary interventions. We saw a dramatic improvement by April/May of that year. Nearly all the symptoms on the list above had resolved. We assumed the improvements were due to diet but he started to go into the sun around that time. Our son slept well and spent many peaceful, happy and anxiety-free months during the spring and summer after turning three.

In mid-November 2008, I sent the following e-mail to the DAN doctor who had been helping us with our son.

“You saw our son Jonathan Switzer a few times regarding his autism diagnosis and diet issues, etc. He had a regressive period last winter from about December through April when his autism was diagnosed, then did pretty well all summer. Nursery school started off okay, too, but now he seems to be having another regression. 

Main symptoms:
–Great difficulty getting to sleep (fidgets for 2 plus hours most nights while he had been falling asleep easily for several months prior to that)
–Marked increase in anxiety (again refusing to leave the house even to do things he loves, frequently shaking/clenching and telling us “I’m scared)
–Onset of OCD-like behaviors (afraid to get hands dirty, get extremely upset if he gets even tiny drips of water on himself)
–Increase in self-stimulatory behaviors (flapping, fidgeting, noise-making)
–Frequent crying jags and telling us he’s just giving up on everything

We have had other parents tell us that their kids on the spectrum have a worsening of symptoms during the winter months and we feel like we are observing this same pattern. We’ve done some reading about light therapy for depression/anxiety and to help correct disturbed sleep patterns and would like to give it a try for Jonathan.

Wondering if you have ever prescribed a light therapy box for pediatric patients before. Our insurance told us they will cover it with a diagnosis of Seasonal Affective Disorder, but I don’t even know if that is something that can be diagnosed in children. Guess we’re willing to try anything at this point. Do you know much about this type of therapy?”
Neither the DAN Doctor nor our pediatrician would write a prescription for a therapy light, so we purchased one on our own and found it made no discernible impact on his symptoms.
By December, our son’s symptoms had worsened further and we decided to put him in a very expensive and intensive autism treatment program through our local hospital. He made slow progress during his participation in the program from January through April. He was also involved in speech and occupational therapy during the winter months. At his IEPC meeting at school in March, we were encouraged to put him in the district’s program for children with developmental delays. We instead elected to register him for regular pre-school for the following year.

During that winter, I was crying to some friends about my son and describing his seemingly seasonal pattern of symptoms. We had just seen a second neurologist searching for help, and I was extremely frustrated when, after listening to my son’s symptoms and history, he told me bluntly, “There is nothing seasonal about autism,” then suggested that we put our son on an anti-depressant. We refused the medication. One of the friends I was crying to is a research librarian and the other is a medical researcher. After our conversation, they located and e-mailed me a few journal articles they thought might help, one of the articles was by Dr. Cannell and discussed his vitamin D theory of autism. Reading the article was one of those “Aha!” moments and I felt hopeful that Dr. Cannell was on to something.

By June our son was released from both speech therapy and occupational therapy and we were told that he no longer showed any delays for his age. When he had begun occupational therapy in January, the OT had been astonished at our son’s lack of muscle tone. She recommended that he also receive Physical Therapy services, so we went on a long waiting list. Our initial OT was in a car accident, and in May we were transferred to a new OT. When the new OT first saw our son, she said could not believe he was the same child described in the notes. By May the low muscle tone, hyperactivity and distractibility noted in his file, were no longer evident. His turn came up for physical therapy and we were told he no longer needed it.

Our son has always spent a lot of time outdoors in the summer, without sunblock. He had a happy and relaxing summer. As fall/back-to-school approached, I began to fear the onset of another regression and again read the article by Dr. Cannell my friend had sent. I visited his website and decided we would try a vitamin D supplement. Our pediatrician did not encourage any dose higher than 400 i.u. (that found in a typical multivitamin) but did write a script to have his 25-hydroxy level tested. In August his level was 37, so we started him on 5,000 iu daily and had his level retested on October 21st. By October his level was 96. The pediatrician was concerned that this was too high and told us he should not have more than 400 iu per day.

Knowing that Nov-March are typically his worst months, we reduced the dosage down only to 3,000 iu from October through mid-December. At an appointment in December our son was doing wonderfully (none of his usual fall/winter symptoms yet evident) and the pediatrician told us 3,000 iu was too much and that we should be giving no more than 400 iu. In mid-December we reduced the dose to 1,500 iu. By the beginning of January we noted a marked loss of eye contact. We also noted that our son was again interchanging his right hand for writing and eating (after using his left hand exclusively for 8+ months). We increased his vitamin D level to 4,000 iu daily in early January. On January 11 we had his 25-Hydroxy level checked on January 11 and found that it was 89. By the end of January, we and his grandparents noted improvement in his eye contact.

In January 2010 we attended his preschool conferences. The teacher had marked cards with the following code (1=age appropriate, 2=developing, 3=area of concern). Our son received 1s in all areas with the exception of hopping on one foot and balance beam where he received 2s. We were told that he is on par with or ahead of his peers in all areas (academic, fine motor, etc.), and that his teacher had noted no unusual symptoms or concerns.

During the fall/winter 2009-2010 our son has been free from nearly all of the most troubling symptoms that plagued him the previous two winters. The following example may demonstrate the improvement in his daily life since last winter.

One of our son’s low points was a Christmas party we attended in December 2008. Before leaving the house to attend the party our son screamed and yelled about having to take a bath and because we would not let him wear sweatpants to the party. He then begged us not to make him leave the house. During the 40 minute trip to the party our son asked us repetitive questions and talked incessantly. Upon arriving at the party, he immediately walked into an unoccupied room adjacent to the room where the party was occurring, and put his face into the corner. Despite much coaxing by my husband and me, he refused to come out of the corner.

After approximately 45 minutes of standing in the corner we managed to get him out through the promise of some food rewards. He proceeded to walk around and around the perimeter of the living room where all of the other kids were playing. He rubbed himself along the walls and covered his ears as he walked. He finally settled into playing alone in a corner of the room. All of the kids at the party participated in a book exchange. Our son refused to come to the area where the other kids were gathered. We coaxed him over only to have him throw the book he received and refuse to thank the parent who had purchased it for him. He spent much of the evening in time-outs for that and other inappropriate behavior.

In June of 2008, after playing in the sun for several months, we met for a picnic with the same group of friends at a local park. Our son ran up to the other children and joined right in playing bulldozers in the sand with them. He behaved and interacted in a completely appropriate and typical way during the picnic which lasted several hours.

This year (2009) we attended the same Christmas party at the same house. Our son got ready and left for the party without anxiety or incident. He chatted normally during the drive to the party. He walked into the house, said, “Hey, check out my new train,” to some of the kids already playing and settled in to playing happily with the other kids. During the book exchange, he received a book, smiled and gave a big hug to the person who gave it to him.

In December of 2008, I took a leave from my job so I could get my son to the intensive behavioral treatment program he was in and to all of his other therapy appointments. I dedicated 40-60 hours per week to my son’s various appointments and home therapy program.

This winter (January 2010), a former colleague asked me what Jonathan’s current therapy program consists of. I told her I spend about 30 seconds each day opening the jar of vitamins and giving him his chewable vitamin D. In my opinion, the 3 minutes or so I spend each week giving him his vitamin D have been much more effective, and much less expensive, than any other treatment we have pursued. 
Thank you.
Jeannette, Wisconsin

Dear Jeanette:
You’re welcome. Several things need comment. First, the symptoms are typical of autism. Second, the seasonality of symptoms suggest a vitamin D deficient disease. Third, the treatment in the spring of 2008 seemed effective but, in hindsight, it was simply due to spring sun exposure. Fourth, as you may now know, light boxes for seasonal affective disorder make no vitamin D. Fifth, your pediatrician knows little about Vitamin D other than what committees tell him; your decision to ignore his advice probably saved your son’s brain from further injury, as autism is a progressive inflammatory destruction of brain tissue. Sixth, the fact that you needed bed rest and gave birth prematurely suggests you were Vitamin D deficient during your pregnancy.

Seventh, his twin sister has never had autism, despite the same intrauterine environment. This is consistent with my theory, that autism is caused from a quantitative, not qualitative, variation is one of the enzymes that metabolize Vitamin D. That is, there are no structural differences in these enzymes in autism, only a genetically determined difference in the amount present. These enzymes are responsive to estrogen; estrogen protects the brain from being damaged by low Vitamin D, probably by increasing the amount of activated Vitamin D present, explaining why boys are four times more likely to have the disease.
The report that your son deteriorated when his dose was reduced from 3,000 to 1,500 IU suggests autistic children need adult doses of Vitamin D. When you reduced the dose from 3,000 to 1,500 IU/day he worsened although his level on 1,500 IU/day was probably still greater than 50 ng/ml. This makes me think that dosage needs to be stable and suggests that Professor Reinhold Vieth’s theory of a detrimental seasonal resetting of the intercellular metabolism of Vitamin D may even be true at levels above 50 ng/ml, where the body is storing the parent compound, cholecalciferol, in muscle and fat.

His current dose of 4,000 IU per day is perfectly safe and will give him a level of 80-100 ng/ml, inside the reference ranges of American laboratories. Toxicity (asymptomatic high blood calcium) begins somewhere above 200 ng/ml. Generally speaking, autistic children should take 2,000 IU per every 25 pounds of body weight for six weeks, then have a 25(OH)D blood test and adjust the dosage to get into the high end of the reference range, 80-100 ng/ml.

Although I first published the Vitamin D theory of autism theory 3 years ago, few autistic children are currently treated for their Vitamin D deficiency. This is due to several reasons. One, those who think, correctly, that autism is a genetic disease, stop thinking after that, reasoning that genetic diseases are untreatable. Such thinkers do not understand epigenetics (upon the genome). Vitamin D is probably the heart of epigenetics, as nothing works upon the genome like vitamin D.

Secondly, the “all autism is caused from vaccinations” crowd cannot accept the Vitamin D possibility as it threatens their core beliefs. They simply cannot change their minds.
Finally, as you now know, organized medicine would say you should stop the vitamin D and watch your son deteriorate, which is why slavery to evidence based medicine is fine for scientists and unethical for practitioners.

John Cannell, MD
Executive Director
Vitamin D Council

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
The Vitamin D Newsletter
Another Autism Case Report
by John Cannell, M.D.
vitamindcouncil@vitamindcouncil.org

January 30, 2010.
(This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you would like to subscribe please go to the Vitamin D Council’s website. http://www.vitamindcouncil.org/)
This month, I dedicate the entire newsletter to a mother’s lengthy case report of her autistic son. Other than name and place of residence, the letter was not edited.
Dear Dr. Cannell:
At age 2.5 years, between December 2007 and January 2008, my son experienced a fairly dramatic onset of symptoms that led to his diagnosis of autism. His symptoms (many of which we did not even know the terminology for at the time they first occurred) included:
–The inability to sleep at night, we would put him to bed at 8:00 or 8:30 p.m. following his normal bedtime routine
–Development of anxiety and refusal to leave the house even to do preferred activities
–Obsessive-repetitive questions and monologuing/run-on speech
–Sensory issues (refusal to wear jeans or any fabrics other than fleece, screaming hysterically at bath time, complaining and covering eyes in sunlight, covering ears for everyday noises that had not bothered him before (toilets flushing, pulling pots and pans from cupboards, etc.)
–Toe-walking
–Flapping and self-stimulating behaviors (repeatedly tapping his cheeks and eyes with all ten fingers, continually twisting up his fingers in pretzel-like configurations, holding objects in his peripheral range of vision and straining to see them from the corner of his eyes)
–Development of an unusual pattern of stuttering/vocal tic at the end of words,he would repeat the last sound/syllable,”I don’t want to go to the store-or-or-or-or-or-or. It won’t be fun-n-n-n-n-n-n-n.” He would make sounds even in his sleep “n-n-n-n-n-n” or “s-s-s-s-s-s-s”
–Loss of muscle tone (stopped walking up and down stairs and began crawling/sliding instead, decline in balance and motor skills)
–loss of handedness (began switching left to right hand, after seeming predominantly left-handed)
–Marked increase in hyperactivity
–Frequent spacing out/unresponsive episodes
Our son and his twin sister were born at 36 weeks, 5 days on March 17, 2005 after four months of bed-rest. As early as their 8 week appointment, I mentioned to our pediatrician that we had concerns about our son’s eye contact and social responsiveness (in comparison to his sister). I felt that I was having more difficulty bonding with him. We were told “don’t worry, but don’t wait” and were referred to our state’s Early On intervention program. At the end of June a physical therapist and speech pathologist from our intermediate school district came to our home to evaluate our then 3 month old son and told me that he was doing just fine and that I was worrying too much. I agreed that by the time they saw him he had begun smiling and making better eye contact.
We didn’t worry again about our son until fall 2006. He had walked just before his first birthday, but by 18 months+ he still seemed clumsy and prone to falling compared to his sister. We took him back to the intermediate school district for evaluation and were told that all of his development seemed to be in the normal range and that we shouldn’t worry. We were advised that we could take him to music and gym classes to work on his coordination and told that we could pay for private physical therapy if we elected. We followed all of the recommendations.
For a year, we didn’t notice any other changes until the sudden onset of symptoms listed above when he was 2.5 years. With the sudden onset of symptoms above, we took our son to see a number of specialists during the winter of 2008 including a neurologist (who diagnosed him with Asperger Syndrome), a psychologist (who diagnosed with autism), and a second psychologist who specialized in the treatment of autism (who diagnosed him with Pervasive Developmental Disorder Not-Otherwise-Specified). All three diagnoses are on the autism spectrum. He also began seeing an occupational therapist, a speech therapist, a behavioral specialist, and a DAN! (Defeat Autism Now!) doctor for dietary interventions. We saw a dramatic improvement by April/May of that year. Nearly all the symptoms on the list above had resolved. We assumed the improvements were due to diet but he started to go into the sun around that time. Our son slept well and spent many peaceful, happy and anxiety-free months during the spring and summer after turning three.
In mid-November 2008, I sent the following e-mail to the DAN doctor who had been helping us with our son.
“You saw our son Jonathan Switzer a few times regarding his autism diagnosis and diet issues, etc. He had a regressive period last winter from about December through April when his autism was diagnosed, then did pretty well all summer. Nursery school started off okay, too, but now he seems to be having another regression.
Main symptoms:
–Great difficulty getting to sleep (fidgets for 2 plus hours most nights while he had been falling asleep easily for several months prior to that)
–Marked increase in anxiety (again refusing to leave the house even to do things he loves, frequently shaking/clenching and telling us “I’m scared)
–Onset of OCD-like behaviors (afraid to get hands dirty, get extremely upset if he gets even tiny drips of water on himself)
–Increase in self-stimulatory behaviors (flapping, fidgeting, noise-making)
–Frequent crying jags and telling us he’s just giving up on everything
We have had other parents tell us that their kids on the spectrum have a worsening of symptoms during the winter months and we feel like we are observing this same pattern. We’ve done some reading about light therapy for depression/anxiety and to help correct disturbed sleep patterns and would like to give it a try for Jonathan.
Wondering if you have ever prescribed a light therapy box for pediatric patients before. Our insurance told us they will cover it with a diagnosis of Seasonal Affective Disorder, but I don’t even know if that is something that can be diagnosed in children. Guess we’re willing to try anything at this point. Do you know much about this type of therapy?”
Neither the DAN Doctor nor our pediatrician would write a prescription for a therapy light, so we purchased one on our own and found it made no discernible impact on his symptoms.
By December, our son’s symptoms had worsened further and we decided to put him in a very expensive and intensive autism treatment program through our local hospital. He made slow progress during his participation in the program from January through April. He was also involved in speech and occupational therapy during the winter months. At his IEPC meeting at school in March, we were encouraged to put him in the district’s program for children with developmental delays. We instead elected to register him for regular pre-school for the following year.
During that winter, I was crying to some friends about my son and describing his seemingly seasonal pattern of symptoms. We had just seen a second neurologist searching for help, and I was extremely frustrated when, after listening to my son’s symptoms and history, he told me bluntly, “There is nothing seasonal about autism,” then suggested that we put our son on an anti-depressant. We refused the medication. One of the friends I was crying to is a research librarian and the other is a medical researcher. After our conversation, they located and e-mailed me a few journal articles they thought might help, one of the articles was by Dr. Cannell and discussed his vitamin D theory of autism. Reading the article was one of those “Aha!” moments and I felt hopeful that Dr. Cannell was on to something.
By June our son was released from both speech therapy and occupational therapy and we were told that he no longer showed any delays for his age. When he had begun occupational therapy in January, the OT had been astonished at our son’s lack of muscle tone. She recommended that he also receive Physical Therapy services, so we went on a long waiting list. Our initial OT was in a car accident, and in May we were transferred to a new OT. When the new OT first saw our son, she said could not believe he was the same child described in the notes. By May the low muscle tone, hyperactivity and distractibility noted in his file, were no longer evident. His turn came up for physical therapy and we were told he no longer needed it.
Our son has always spent a lot of time outdoors in the summer, without sunblock. He had a happy and relaxing summer. As fall/back-to-school approached, I began to fear the onset of another regression and again read the article by Dr. Cannell my friend had sent. I visited his website and decided we would try a vitamin D supplement. Our pediatrician did not encourage any dose higher than 400 i.u. (that found in a typical multivitamin) but did write a script to have his 25-hydroxy level tested. In August his level was 37, so we started him on 5,000 iu daily and had his level retested on October 21st. By October his level was 96. The pediatrician was concerned that this was too high and told us he should not have more than 400 iu per day.
Knowing that Nov-March are typically his worst months, we reduced the dosage down only to 3,000 iu from October through mid-December. At an appointment in December our son was doing wonderfully (none of his usual fall/winter symptoms yet evident) and the pediatrician told us 3,000 iu was too much and that we should be giving no more than 400 iu. In mid-December we reduced the dose to 1,500 iu. By the beginning of January we noted a marked loss of eye contact. We also noted that our son was again interchanging his right hand for writing and eating (after using his left hand exclusively for 8+ months). We increased his vitamin D level to 4,000 iu daily in early January. On January 11 we had his 25-Hydroxy level checked on January 11 and found that it was 89. By the end of January, we and his grandparents noted improvement in his eye contact.
In January 2010 we attended his preschool conferences. The teacher had marked cards with the following code (1=age appropriate, 2=developing, 3=area of concern). Our son received 1s in all areas with the exception of hopping on one foot and balance beam where he received 2s. We were told that he is on par with or ahead of his peers in all areas (academic, fine motor, etc.), and that his teacher had noted no unusual symptoms or concerns.
During the fall/winter 2009-2010 our son has been free from nearly all of the most troubling symptoms that plagued him the previous two winters. The following example may demonstrate the improvement in his daily life since last winter.
One of our son’s low points was a Christmas party we attended in December 2008. Before leaving the house to attend the party our son screamed and yelled about having to take a bath and because we would not let him wear sweatpants to the party. He then begged us not to make him leave the house. During the 40 minute trip to the party our son asked us repetitive questions and talked incessantly. Upon arriving at the party, he immediately walked into an unoccupied room adjacent to the room where the party was occurring, and put his face into the corner. Despite much coaxing by my husband and me, he refused to come out of the corner.
After approximately 45 minutes of standing in the corner we managed to get him out through the promise of some food rewards. He proceeded to walk around and around the perimeter of the living room where all of the other kids were playing. He rubbed himself along the walls and covered his ears as he walked. He finally settled into playing alone in a corner of the room. All of the kids at the party participated in a book exchange. Our son refused to come to the area where the other kids were gathered. We coaxed him over only to have him throw the book he received and refuse to thank the parent who had purchased it for him. He spent much of the evening in time-outs for that and other inappropriate behavior.
In June of 2008, after playing in the sun for several months, we met for a picnic with the same group of friends at a local park. Our son ran up to the other children and joined right in playing bulldozers in the sand with them. He behaved and interacted in a completely appropriate and typical way during the picnic which lasted several hours.
This year (2009) we attended the same Christmas party at the same house. Our son got ready and left for the party without anxiety or incident. He chatted normally during the drive to the party. He walked into the house, said, “Hey, check out my new train,” to some of the kids already playing and settled in to playing happily with the other kids. During the book exchange, he received a book, smiled and gave a big hug to the person who gave it to him.
In December of 2008, I took a leave from my job so I could get my son to the intensive behavioral treatment program he was in and to all of his other therapy appointments. I dedicated 40-60 hours per week to my son’s various appointments and home therapy program.
This winter (January 2010), a former colleague asked me what Jonathan’s current therapy program consists of. I told her I spend about 30 seconds each day opening the jar of vitamins and giving him his chewable vitamin D. In my opinion, the 3 minutes or so I spend each week giving him his vitamin D have been much more effective, and much less expensive, than any other treatment we have pursued.
Thank you.
Jeannette, Wisconsin
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Dear Jeanette:
You’re welcome. Several things need comment. First, the symptoms are typical of autism. Second, the seasonality of symptoms suggest a vitamin D deficient disease. Third, the treatment in the spring of 2008 seemed effective but, in hindsight, it was simply due to spring sun exposure. Fourth, as you may now know, light boxes for seasonal affective disorder make no vitamin D. Fifth, your pediatrician knows little about Vitamin D other than what committees tell him; your decision to ignore his advice probably saved your son’s brain from further injury, as autism is a progressive inflammatory destruction of brain tissue. Sixth, the fact that you needed bed rest and gave birth prematurely suggests you were Vitamin D deficient during your pregnancy.
Seventh, his twin sister has never had autism, despite the same intrauterine environment. This is consistent with my theory, that autism is caused from a quantitative, not qualitative, variation is one of the enzymes that metabolize Vitamin D. That is, there are no structural differences in these enzymes in autism, only a genetically determined difference in the amount present. These enzymes are responsive to estrogen; estrogen protects the brain from being damaged by low Vitamin D, probably by increasing the amount of activated Vitamin D present, explaining why boys are four times more likely to have the disease.
The report that your son deteriorated when his dose was reduced from 3,000 to 1,500 IU suggests autistic children need adult doses of Vitamin D. When you reduced the dose from 3,000 to 1,500 IU/day he worsened although his level on 1,500 IU/day was probably still greater than 50 ng/ml. This makes me think that dosage needs to be stable and suggests that Professor Reinhold Vieth’s theory of a detrimental seasonal resetting of the intercellular metabolism of Vitamin D may even be true at levels above 50 ng/ml, where the body is storing the parent compound, cholecalciferol, in muscle and fat.
His current dose of 4,000 IU per day is perfectly safe and will give him a level of 80-100 ng/ml, inside the reference ranges of American laboratories. Toxicity (asymptomatic high blood calcium) begins somewhere above 200 ng/ml. Generally speaking, autistic children should take 2,000 IU per every 25 pounds of body weight for six weeks, then have a 25(OH)D blood test and adjust the dosage to get into the high end of the reference range, 80-100 ng/ml.
Although I first published the Vitamin D theory of autism theory 3 years ago, few autistic children are currently treated for their Vitamin D deficiency. This is due to several reasons. One, those who think, correctly, that autism is a genetic disease, stop thinking after that, reasoning that genetic diseases are untreatable. Such thinkers do not understand epigenetics (upon the genome). Vitamin D is probably the heart of epigenetics, as nothing works upon the genome like vitamin D.
Secondly, the “all autism is caused from vaccinations” crowd cannot accept the Vitamin D possibility as it threatens their core beliefs. They simply cannot change their minds.
Finally, as you now know, organized medicine would say you should stop the vitamin D and watch your son deteriorate, which is why slavery to evidence based medicine is fine for scientists and unethical for practitioners.
John Cannell, MD
Executive Director
Vitamin D Council
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This is very interesting research that would cause you to want to take exposure to flu more seriously!  First, let’s stay healthy so we do not get flu or colds with all that I discuss from Immuni-T 2 and 3 to long term detoxification, as in FIGHT program. Then since for many that is too rigorous a requirement, so let’s have an EMERGENCY SUPPORT PACKAGE in the homes of anyone that realizes who important this new research is!  Have BioE’nR-G’y C, ACS 200, and high dose D AND A available to immediately begin at the first sign of active infections.

What if their vaccines turn out to be as wrong for stopping H1N1, as MMR has been shown to be for compromised children? After MMR in autistic kids the live virus from the vaccination later has been shown to be growing in the CSF of these children.  Will the current testing of the new swine flu vaccines even attempt to look for how many receiving the vaccines actually wind up being infected with the virus instead of being protected against the virus, as they are not able to launch an immune response to the vaccine?

It appears that the virus accesses the neuron through the axons in the GI tract and lung. This sets the stage then for loss of Dopamine secreting cells over time.

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com
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Recent studies have suggested that the currently circulating strain of avian influenza has similar pathology to the 1918 flu. Though the subtypes of the viruses are different (Spanish flu shares the H1N1 subtype with the current H1N1 swine flu, whereas avian influenza has an H5N1 subtype), both viruses appear to enter the central nervous system (CNS) and can cause encephalitis, or inflammation of the brain.

Highly pathogenic H5N1 influenza virus can enter the central nervous system and induce neuroinflammation and neurodegeneration
http://www.pnas.org/content/early/2009/08/07/0900096106.abstract

1.       Haeman Janga,b,
2.       David Boltzc,
3.       Katharine Sturm-Ramirezc,1,
4.       Kennie R. Shepherda,2,
5.       Yun Jiaoa,
6.       Robert Websterc and
7.       Richard J. Smeynea,3

+Author Affiliations
1.       Departments of aDevelopmental Neurobiology and
2.       cInfectious Diseases/Virology, St. Jude Children’s Research Hospital,
262 Danny Thomas Place, Memphis, TN 38105-3678; and
3.       bIntegrated Program in Biomedical Sciences, University of Tennessee
Health Science Center, Memphis, TN 38163
1.      1Present address: Fogarty International Center, National Institutes
of   Health, 16 Center Drive, Room 202, Bethesda, MD 20892.
2.      2Present address: Department of Environmental and Occupational
Health, Rollins School of Public Health and Center for
neurodegenerative Disease, Emory University, Whitehead Biomedical
Research Building, 5th Floor, Room 575.1, Atlanta, GA, 30322.

Abstract
One of the greatest influenza pandemic threats at this time is posed by the highly pathogenic H5N1 avian influenza viruses. To date, 61% of the 433 known human cases of H5N1 infection have proved fatal. Animals infected by H5N1 viruses have demonstrated acute neurological signs ranging from mild encephalitis to motor disturbances to coma. However, no studies have examined the longer-term neurologic consequences of H5N1 infection among surviving hosts. Using the C57BL/6J mouse, a mouse strain that can be infected by the A/Vietnam/1203/04 H5N1 virus without adaptation, we show that this virus travels from the peripheral nervous system into the CNS to higher levels of the neuroaxis. In regions infected by H5N1 virus, we observe activation of microglia and alpha-synuclein phosphorylation and aggregation that persists long after resolution of the infection. We also observe a significant loss of dopaminergic neurons in the substantia nigra pars compacta 60 days after infection. Our results suggest that a pandemic H5N1 pathogen, or other neurotropic influenza virus, could initiate CNS dis