Vitamin D most important early in life to prevent type 1 diabetes, says new research

http://www.vitamindcouncil.org/vitamin-d-news/14787/

Vitamin D most important early in life to prevent type 1 diabetes, says new research
Posted on September 18, 2013 by Vitamin D Council

A new meta-analysis published in the journal Nutrients has found that in effort to prevent type I diabetes, vitamin D intake may be most important early in life.

Type I diabetes (T1D) is an autoimmune disease acquired early in life, usually diagnosed during childhood or early adulthood. What happens is the body’s own immune system destroys insulin-producing beta cells, creating a state of insulin deficiency in the body.

Researchers believe vitamin D can help prevent T1D, but they’re still trying to figure out at what stage of development it’s most important. Some studies have shown that vitamin D has a protective association against T1D in offspring if the mother gets enough during pregnancy. And some studies show that if infants get enough vitamin D, they may reduce their risk of T1D later in life.

In the present study, researchers performed a meta-analysis, gathering all studies that examined vitamin D intake during pregnancy or early infancy and compared the intakes to risk of getting T1D later in life.

When all the studies were pooled together, they found that babies that received vitamin D supplements in infancy were 29% less likely to develop T1D later in life compared to the babies that didn’t get vitamin D supplements.

They also observed an effect in pregnant women, though the effect was more modest and not statistically significant. They observed a 5% reduction in risk in offspring getting T1D in the mothers who supplemented during pregnancy compared to those who didn’t. The mothers may not have gotten enough vitamin D in these studies to see a larger effect. The researchers also call for more studies on vitamin D intake during pregnancy and risk of offspring getting T1D, as there were relatively fewer studies of this type compared to supplementation in early infancy.

The researchers concluded, “Our findings suggest that vitamin D intake during early life is associated with a reduced risk of type 1 diabetes.”

Source
Dong JY et al. Vitamin D Intake and Risk of Type 1 Diabetes: A Meta-Analysis of Observational Studies. Nutrients, 2013.

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MTHFR Gene Mutation: Common in Autism, Autoimmune Diseases, Chronic fatigue, Fibromyalgia, PANDAS , Thyroid Disease

“Holy MTHFR!” from http://www.easytolovebut.com/?p=2782

Posted on December 12, 2012 by Laura Matheos

If I say MTHFR, then Methylenetetrahydrofolate Reductase are the two words that pop into your brain, right? No? Well, hopefully after reading this, you’ll see more than that swear word that caught your attention.
If I next mention bipolar struggles, rapid mood swings, depression, anxiety, heart disease, strokes, macular degeneration, miscarriages – and any of these issues hit home for you, then read on, because you might just want to know about MethyleneTetraHydroFolate Reductase – better known by its abbreviation – MTHFR.
MTHFR is a gene and like all genes, it acts as a light switch – turning on or turning off various body processes. In this case, MTHFR takes folate (vitamin B9) and methylates (converts) it into methylfolate (5-methylTHF). Hardly seems like a big deal, does it? Yet, if you belong to an autism, Pandas, Lyme or chronic fatigue group, you’ve probably noticed a big buzz around this thing called methylation. While the past decade has seen MTHFR studied in terms of cardiovascular disease and cancer, it turns out it might also be a very big deal for those raising kids with developmental, neurological or behavioral symptoms and for those fighting chronic infections.

Methylwhat?
A lot of parents raising kids with challenges are already overwhelmed – too overwhelmed to start stuffing their brains with hard to pronounce words describing hard to understand biochemistry. But you can think of methylation as a kind of metabolism. Imagine the insides of a clock with many cogs, each cog regulating specific chemical reactions. This is an over-simplified diagram of the methylation cycle:

The cogs in this picture turn in your body billions of times per second. But quick, before your eyes glaze over, find the MTHFR in the middle of the picture. Got it? The MTHFR gene sits at a critical point. If you have a glitch that keeps this gene from doing its job, the cogs on both sides of the picture are going to get mucked up. Instead of the light switch being on or off, it’s stuck in some sort of dimmer switch mode, functioning, but not nearly as well as it should be. The proper interaction of methylfolate and Methyl-B12 is what drives your body’s ability to fuel every cell in your body with energy (this is what’s going on in the green and red cogs). Methyl-B12 regulates certain T-cells that may play a role in some autoimmune diseases. Improper methylation can also raise your levels of homocysteine (look to the bottom of the red cog on your right).  This can greatly increase your risks for heart disease, stroke, macular degeneration, dementia and some cancers (e.g. lung, colon and leukemia). It also impedes your ability to manufacture glutathione (bottom right of diagram), the body’s master antioxidant (the “sanitation engineer”) that plays a critical role in autism treatments, chronic Lyme disease and some tic disorders. While there isn’t enough research to say for certain, some MTHFR literature discusses a possible role of MTHFR mutations and increased miscarriages. Insufficient levels of methylfolate are linked to neural tube defects, which is why pregnant women are told to take supplements of folic acid. But if your body has a faulty MTHFR gene and can’t properly convert folate into methylfolate, then this advice may not be having the intended benefits.

So you can see why this one little gene is a big deal. And you can find some pretty decent articles on the web on why treating an MTHFR mutation is so important for many health issues. But there’s one more important role that MTHFR plays. One that doesn’t get nearly enough ink. Look to the left of the MTHFR circle. See the blue cog labeled “BH4 cycle”? MTHFR plays a direct role in how well the BH4 cycle works – and the BH4 cycle controls those two neurotransmitters that are so essential to people with behavioral and emotional challenges – serotonin and dopamine. This has a huge potential impact for how some kids might be helped – kids whose parents are averse to psychotropic medications as well as kids for whom medications have been ineffective or caused serious side effects.

After months of studying everything I could get my hands on, I came to realize that given my long family history of heart disease and depression, this microscopic chemical conductor, aptly named MTHFR, might be the cause of a lot of suffering along my family tree.

Testing MTHFR is actually very simple. Most commercial labs in the U.S. can test for it.  Go to your local lab’s website, find their test menu (usually under the section for doctors) and search on “mthfr” or “methylfolate” or some similar phrase. This should bring you the test code number that you can ask your physician to order. The list price for my test was $150 but my insurance negotiated rate was $50 and since we’d met our annual deductible, my 20% portion of the bill was $10.

The results for one of my children came back normal. So the source of his hurdles lay elsewhere. MTHFR, no matter how important, is certainly not the single root of all evil. But my other child showed one mutation (called a polymorphism) on her MTHFR gene. At least 24 mutations have been identified on the MTHFR gene. Only two are well studied at this point – mutations labeled C677T and A1298T. My daughter had one mutation of C677T, making her heterozygous. (If she had two mutations of C677T, she’d be homozygous).
In the U.S., it’s estimated that roughly 45% of the population may have at least one mutation of MTHFR, though your heritage can increase or decrease your individual risk. While exact numbers are hard to verify, one mutation on C677T means you’re probably methylating (converting) folate into methylfolate at 40-60% efficiency. 

If you have two mutations, that number drops to approximately 10% efficiency.

In my personal experience, this is a pretty big deal when it comes to dealing with anxiety and depression. (I couldn’t find estimates for A1298C mutations and much less is written about this. It seems to play a greater role in gut health. For more details, you’ll need to watch Dr. Amy Yasko’s videos. It’s well beyond my ability to do justice to A1298C.)

By following the green cog counterclockwise to the blue cog, you can see the impact on serotonin and dopamine and why knowing about this gene can be important to those who struggle with mood and behavioral disorders.

So what to do about it?
Those who’ve studied methylation extensively have developed various protocols depending on what ailment they’ve focused on. But the common thread for those with a C677T mutation is that if your body can’t convert folate into methylfolate properly, then you can help your body around this hurdle by taking a supplement that already contains methylfolate (not regular folate) to make up for the shortage.  (Think of using instant mashed potatoes where the hard work has already been done for those of us who are cooking-challenged – except unlike potatoes, methylfolate from a store is just as good as “home-made”).

Because this is an emerging field of research, little guidance is out there regarding dosage and step by step how-to’s. There’s no vetted resource to tell you the proper dosage of 5-methylTHF to give an adult, let alone a child. I know one child who’s doing well at less than 100mcg/day (that’s micrograms) and a teen who’s on 10mg/day (that’s milligrams) of Deplin (a prescription form of methylfolate). This is an enormous range for dosage. Most sources I’ve come across discuss ranges of 100-400mcg for a child and 800mcg-1mg for an adult. But many factors are at play and it’s best to work with a physician if possible. Unfortunately, the whole field of epigenetics is so new that few clinicians have much experience in this area. So you may need to do a lot of research alongside an open-minded doctor. We started out slow – very slow, then gradually built up dosage under the guidance of my daughter’s doctor. Even with a doctor’s help, there was still an element of guesswork involved, in the same way doctors work with any patient to zero in on an ideal dosage for any medication.

Supplementing with methylfolate has made a huge difference for my daughter (and has also helped my own health). Over a few months, my daughter’s anxiety, mood cycling and sadness evaporated. So we kept tweaking. At the two month mark, we unwittingly went too high and endured a period of extreme anger, serious depression, food refusal, rapid mood swings, oppositional defiance and truly ugly times – the very things that drove us to our supplementation trial to begin with. Confused, I was ready to give up. But then, almost by accident, we stumbled onto the problem when I stopped the methylfolate in order to do a lab test. Within 24 hours of being methylfolate-free, my daughter’s issues melted away. Hmmm. She became pretty stable – for about a week. Had we been on the wrong path? Then things started to head south again. That feeling of panic returned to the pit of my stomach – that feeling just before you plunge over the peak of the rollercoaster track and you start screaming for your life.

So I re-started the methylfolate at a low dose – and things got good again. It felt like the sun had come back out from behind the clouds. So we built back up once more, not as high as before but just to the point where things got a little dicey again. When warning signs of a meltdown showed on the horizon, I used the advice from one of the MTHFR researchers and gave a small dose of niacinamide (vitamin B3), which has the effect of using up methyl groups (think of it as a sponge mopping up a spill). Within the hour, things were calm again – and stayed that way. Over the course of a few weeks, we zeroed in on the dose of methylfolate that seemed to work best. It will inevitably change as my daughter grows and when her body may need extra resources, like when she’s fighting an illness. It will always be a little bit of an experiment, in the same way that dosing of an SSRI or psychotropic medication is never carved in stone. After all, what fun would parenting be if you were allowed to figure things out and then get on with your life?

Our experiment has been going on for awhile now and I’m happy to report that things have stayed pretty stable. I did find that in addition to methylfolate, my daughter also needs methyl-B12, because both are necessary to keep the methylation cycle functioning properly. If you only take one without the other, you can develop what’s called a folate trap and you can end up thinking you’re on the wrong track when you’re really not. I’ve also tried to keep my daughter away from things fortified with regular folate – things like cereals and multi-vitamins. Her body just can’t handle the regular stuff and if she consumes too much, we end up paying for it with glimpses of the bad old days. Things we once used to help with anxiety have gone by the wayside. My own methylfolate supplement has lowered my blood pressure to the point where I may be able to stop taking prescription medication. I’ll never know if I’ve averted some other ailment, such as the macular degeneration that robbed my father of his eyesight or the strokes that crippled my grandmother or the congestive heart disease that killed my uncle. But I know that both my daughter and I have improved our own odds significantly. Best of all, as winter brings shorter days, it isn’t bringing the depression and sense of dread that has often come with it. Is this all because of a supplement? Hard to say. I’m sure having a happy child plays a role in many ways. But unless things take a dramatic change for the worse, I’m feeling like we’ve found a key piece of our behavioral and health puzzles.

MTHFR is by no means the Holy Grail. The entire field of epigenetics promises to bring even greater gifts and ideas and more than a few dead ends. But for now, this one little gene has proven to be one big deal in my family.

• Dr. Amy Yasko http://www.dramyyasko.com/ ,
• Rich Van Konynenburg  http://forums.phoenixrising.me/index.php?threads/documents-by-rich-van-konynenburg-parts-1-7.11488/ and
• Dr. Ben Lynch http://mthfr.net/
• Dr. Bill Walsh has also written extensively on the subject of methylation. His latest explanation of the role methylation plays in emotional health can be found in his book Nutrient Power http://www.walshresearch.mybigcommerce.com/nutrient-power-book/
• Many other informative discussions can also be found online.

Vitamin D beneficial against lung cancer, says new large cohort study

Vitamin D beneficial against lung cancer, says new large cohort study

http://www.vitamindcouncil.org/vitamin-d-news/vitamin-d-beneficial-against-lung-cancer-says-new-large-cohort-study/

Recent research published in the American Journal of Clinical Nutrition suggests that vitamin D may protect against lung cancer in never-smoking postmenopausal women.

Researchers took a look at the Women’s Health Initiative, a cohort of 128,779 postmenopausal women. Among the entire cohort, 1,771 had lung cancer between the years of 1993-2010.

They found that for those who took more than 800 IU of vitamin D per day had a 63% decreased risk of developing lung cancer among never-smokers compared to those who took less than 100 IU/day.

Furthermore, the researchers looked at a specific portion of participants among the cohort that enrolled in a trial of taking 1,000 mg/day of calcium and 400 IU/day of vitamin D or daily placebos. There were about 38,000 participants in this subset trial.

While there was no benefit against lung cancer in taking calcium plus vitamin D in initial analysis, when the researchers only looked at participants that took less than 1,000 IU/day of vitamin A (retinol form), they did indeed find benefit in calcium + vitamin D. There was a 31% decreased risk of developing lung cancer if you took calcium and vitamin D and kept your retinol intake down compared to taking placebo and keeping your retinol intake down.

What does this mean? Researchers believe that if you take too much vitamin A in retinol form, it may negate any benefit in taking vitamin D and calcium, particularly for lung cancer.

Source
Cheng TY et al. Vitamin D intake and lung cancer risk in the Women’s Health Initiative. Am J Clin Nutr, 2013

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Vitamin D: A role in eating disorders?

http://www.vitamindcouncil.org/blog/vitamin-d-a-role-in-eating-disorders/

Anorexia nervosa (AN) and bulimia nervosa are two common eating disorders.

AN is characterized by food restriction and irrational fear of gaining weight, as well as a distorted body self-image. Those suffering from AN often view themselves as “too fat” even if they are often emaciated. Recent studies show the onset age has recently decreased from an average of 15 years of age to 10 years of age. It occurs in ten times more females than males. The average caloric intake in AN is 500–800 calories per day, but extreme cases of complete self-starvation require intravenous feeding.

AN is a serious mental illness with a high incidence of comorbidity (especially autism and depression) and mortality similar to other serious psychiatric disorders. People suffering from AN have extremely high levels of ghrelin (the hunger hormone that signals a physiological desire for food) in their blood. The high levels of ghrelin suggest that their bodies are desperately trying to make them hungry; however, that hunger call is being ignored or suppressed.

AN is more prevalent in the upper social classes and it is thought to be rare in less-developed countries. It is more common at higher latitudes and some studies show emergency admissions for AN are seasonal.

Bulimia nervosa (BN) is an eating disorder characterized by binge eating and purging, or consuming a large amount of food in a short amount of time followed by an attempt to rid oneself of the food consumed (purging), typically by vomiting, taking a laxative, diuretic, or stimulant, and/or excessive exercise, because of an extensive concern for body weight.

Like most psychiatric disorders, there is a distinct seasonality of Google searches for eating disorders, searches peaking in the winter.

Recently, Doctor Karina Allen and colleagues, working under senior author Professor Andrew Whitehouse, all of the University of Western Australia, were the first to discover that low 25(OH)D levels during pregnancy increase the risk of eating disorders in their offspring in later adolescence.

Allen KL, Byrne SM, Kusel MM, Hart PH, Whitehouse AJ.  Maternal vitamin D levels during pregnancy and offspring eating disorder risk in adolescence. Int J Eat Disord. 2013 Jun 26.

The researchers looked at a cohort of 526 Caucasian mothers who had their 25(OH)D levels measured at 18 weeks of pregnancy and whose offspring were studied up to 20 years of age. The authors assessed eating disorder symptoms at ages 14, 17 and 20 years. Core analyses were limited to female offspring (n=308).

At 18 months gestation, quartile one’s 25(OH)D was between  6 –18 ng/ml;  quartile 2 between 18–24 ng/ml; quartile 3 between 24–29 ng/ml and quartile 4 between 29–62 ng/ml.

At 20 years of age, eating disorders had been diagnosed in 98 of the 526 offspring studied, making the prevalence rate 18% by age 20.

Maternal 25(OH)D concentrations in the lowest quartile of 25(OH)D were associated with a significant two-fold increase in eating disorder risk in women, relative to concentrations in the highest quartile of 25(OH)D. Female participants born in spring were also significantly more likely to experience an eating disorder by age 20 years than participants born in winter, but this association did not hold up under multivariate analysis. No relationships were found for males.

The authors concluded:

“This study has provided new data to link low gestational 25(OH)D to increased eating disorder risk in female offspring of Caucasian mothers. This association may account for the season of birth effects observed in eating disorder groups previously. Ongoing research is required to extend our findings and to clarify the role of vitamin D in the pathogenesis of eating disorders. We recommend that our findings are viewed as preliminary, and as a basis for further research in this area.”

Important Article: PANDAS: Linked with Strep Infections

PANDAS: Linked with Strep Infections
www.homeopathyforwomen.org/PANDAS.htm

Read Tourette Syndrome and PANDAS Recovery Story!
Read About Treating PANDAS with Homeopathy

by Kari J. Kindem, CFHom, Classical Homeopath, CEASE Practitioner
Based in San Jose, California, USA.

PANDAS -  Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections.
(also known as PANS: Pediatric Acute-onset Neuropsychiatric Syndrome)

I have seen in my practice that PANDAS can result in children who often get colds/sinus infections/sore throats/ear infections and similar acute illnesses that are treated with antibiotics or other suppressive medications.
A PANDAS diagnosis is associated with symptoms occurring rapidly after a strep throat or strep related acute, at any age prior to adolescence.

PANDAS onset is rapid and always related to an incident of strep infection. I have see these types of symptoms in children whose cases I have treated successfully with homeopathy, in any combination of following:
ADHD; angry outbursts; anorexia or very picky eating; anxiety; aversion to bathing or washing their hair; aversion to cutting nails or hair; child who can't fall asleep easily at night or alone; compulsive arm movements or hand motions; compulsive behaviors; compulsive eating; constipation that is severe; bedwetting; depression; excessive hand washing; eye blinking; eye rolling; fear of the dark or at night; germ phobias (fear of germs; handwriting difficulty or a sudden change in handwriting; head twitching or shaking; "high maintenance" personality; hyperactivity; inability to focus; jerking in limbs; muscles or body while awake or asleep; making odd mouth noises; moodiness or mood swings; night mares or night terrors; OCD - Obsessive Compulsive Disorder; silly behaviors that are excessive; sensitivity to bright lights; repetitive behaviors; tics; throat clearing;  twitching; rage episodes; sensory issues; separation anxiety; suicidal thoughts and  violent behaviors.

What is PANDAS?

This diagnosis was first identified in the late 1990's. Unfortunately, still many pediatric doctors have never heard of PANDAS, studied it, tested for it or even know about it.  It is more often that the parents who do internet research out of desperation, then bring their child to the doctor, asking for the blood testing and a diagnosis - not the other way around.

The National Institutes of Mental Health (NIMH) Investigators discovered that the OCD, tics, and other symptoms usually occurred in the aftermath of a strong stimulant to the immune system, such as a viral infection or bacterial infection.  The research indicated that there are a subset of children with rapid onset of obsessive-compulsive disorder (OCD) and/or tic disorders and these symptoms are caused by group A beta-hemolytic streptococcal (GABHS) infections.

With PANDAS, children can have dramatic and sudden OCD exacerbations and tic disorders following streptococcus infections. The abnormal behaviors come on suddenly and are overt and easily recognized. PANDAS has been associated with a wider range of related behaviors. Affected children can have any combination of the following symptoms:  ADHD type symptoms, OCD, anorexia, anxiety, germ phobias, rage hyperactivity and depression symptoms.

PANDAS is not the only immune system disease that may initially cause OCD to appear suddenly.  Other disorders may need to be ruled out. They include: Lyme Disease, Thyroid Disease, Celiac Disease, Lupus, Sydenham Chorea, Kawasaki’s Disease, and acute Rheumatic Fever.

Below is the medical symptom criteria for PANDAS.
Additional symptoms, such as severely restricted food intake, may also occur such as in anorexia.

Symptoms include sudden onset of OCD and/or Tics along with a least two other following systems.

·        Sensory sensitivities

·        Separation anxiety

·        Sleep difficulties

·        Personality changes

·        Urinary frequency

·        Tics - repetitive vocalizations or body movements or abnormal movements; Tourette Syndrome

·        Irritability or aggression

·        Inability to concentrate or ADHD

·        Deterioration of learning abilities

·        Developmental or age regression

Download Symptom Scale for Parents for PANDAS - PANS (PDF)

Diagnostic Criteria for PANDAS:

·        Presence of obsessive-compulsive disorder and/or a tic disorder

·        Pediatric onset of symptoms from age 3 years to puberty

·        Episodic course of symptom severity

·        Association with group A Beta-hemolytic streptococcal infection (a positive throat culture for strep or history of Scarlet Fever)

·        Association with neurological abnormalities such as hyperactivity, or adventitious movements, such as rapid, jerky movements.

Lab and Blood Testing For PANDAS 

• Strep Throat Culture:
  Getting a rapid throat swab and 48-hour strep culture is a good first step. A throat culture for GABHS – Group A beta-hemolytic streptococcus (Streptococcus pyogenes, or GAS) should be taken even if the child has no complaints of a sore throat. Even if the quick in-office strep test is negative, it can often be seen the longer 48 hour throat culture come back positive on more than one occasion. In order to have a reliable throat culture, the swab must reach the top back part of the throat which typically is slightly uncomfortable and makes the child gag. A throat culture swab that only touches the back of the tongue will give a falsely negative result, as will one that is just touched to the sides of the throat. Poorly done throat cultures are a common cause of false negative results. Rapid strep tests can also give falsely negative results, as they miss about 10-15% of cases of strep throat. If the rapid strep test is negative, an overnight culture should be done to make sure that there aren’t strep bacteria present.

• Blood Tests:
  In addition to diagnose PANDAS, the doctor should order specific blood tests to look for immunologic evidence of a recent strep infection.  As blood strep titers can stay elevated for many months, often a repeat test may be needed a few weeks later.  If the titer is continuing to rise then this is strong support for the illness being due to strep. If it is declining, then this may serve as a reference point for future blood work if at another point in time there is a suspicion of a recurrent strep infection.
   
• About The ASO Titer - Blood Test for Strep
  Antistreptolysin O, commonly called that ASO titer test can help distinguish beta-hemolytic Group A Streptococcal rheumatic fever from acute rheumatic diseases. ASO is an antibody found in human blood produced upon an infection by Group A Streptococcus bacteria.  In an infected individual, the Group A Streptococci produced Streptolysin O acts as a protein antigen and causes the patient’s immune system to mount a defensive response with Antistreptolysin O antibodies. A rise in ASO titer level begins about 1 week after infection and peaks 2-3 weeks later. In the absence of complications or re-infection, the ASO titer will usually fall to pre-infection levels within 6-12 months. Approximately 80-85% of the patients who demonstrate a Group A Streptococcal infection will also demonstrate an elevated ASO titer.

Group A Streptococcus has caused more widespread diseases than any other group of bacteria. Upon initial infection by Group A Streptococcus, a patient may present with a sore throat and general malaise.  However, there also exists a correlation between the initial illness and development of post-streptococcal syndromes. Of these, acute rheumatic fever and acute glomerulonephritis are the most debilitating. To determine if a streptococcal infection was the root cause, an Antistreptolysin O test is performed.  A marked rise in titer or a persistently elevated titer indicates that a Streptococcus infection or post-streptococcal sequelae are present. Both clinical and laboratory findings should be correlated in reaching a diagnosis.

o   A normal ASO reference range for adults with most labs is <100 Todd units or a 1:99 dilution.
The majority of physicians will order a differential diagnosis panel to be run on a sample consisting of ASO titer, C-Reactive Protein (CRP) and Rheumatoid Factor (Rf). Eighty percent of Group A Streptococcal infected patients also have elevated CRP levels greater than 1.2 mg/dL.
 

o   A negative test result means you have likely not had a recent strep infection.
The healthcare provider may repeat the test again in 2 - 4 weeks. Sometimes a test that was first negative will come back positive. Normal value ranges may vary slightly among different laboratories. Talk to your doctor about the meaning of your specific test results.
 

o   An abnormal or positive test means you recently had a strep infection, even if you had no symptoms.
The ASO test may stay positive (sometimes called detectable) for 2 to 4 months afterward you are first infected.
 

·        False positive ASO titers can happen.
This can be caused by increased levels of serum beta-lipoprotein produced in liver disease and by contamination of the serum with Bacillus cereus and Pseudomonas. ASO titers are elevated in 85% of patients with rheumatic fever but may not be elevated in cases involving skin or renal sequelae.

Anti-streptococcal titers can also be used to diagnose a strep throat, but require that two separate blood tests are done several weeks apart and timed just right to show a “rising titer.” Strep infections trigger the production of anti-streptococcal antibodies, which are measured by the titers. When the child is initially infected with the strep bacteria, his titers will be low, but should increase over the next 4-6 weeks as more anti-streptococcal antibodies are produced. If the child’s blood is tested too late, the titers may already be elevated, but it won’t be possible to know if these “high titers” are related to the current difficulties, or if they’re left over from a previous strep infection, since titers can remain elevated for several months or longer. Thus, a single “high anti-streptococcal antibody titer” isn’t sufficient to prove that a strep infection was the trigger for the child’s symptoms.

ASO rises approximately 1-4 weeks from colonization and Anti-DNAseB rises between 6-8 weeks from colonization. Even then ASO and Anti-DNAse B together fail to show a rise in 31% of children with strep colonization. Titers have to be measured at two points (typically a week apart.  ASO is typically measured at 4 and 5 weeks from the date of suspected infection and Anti-DNAseB measured at 6 weeks and 8 weeks from the suspected event. The two data points are needed to look for a rise. Absolute values are not as important as the rise/fall of the titer. For this reason it is important that both samples are done by the same lab. In the absence of having two titers, many labs use a measure known as the "upper-limit-of-normal". This value is helpful if the measured value is significantly higher than the upper limit. If it is lower than the ULN, then typically two samples are needed to look at the slope/trend.

A strep ASO and D-Nase Titer test is beneficial in helping to establish the strep connection. Ask the doctor/laboratory to give you a numeric result – not just positive or negative. Anything above the labs normal range should be quantified with a specific numerical value. Many times the titers will be only moderately elevated – and at times not elevated or extremely elevated. This is the variable nature of the strep bacteria.  Since each lab measures titers in different ways, it is important to know the range used by the laboratory where the test was done – just ask where they draw the line between negative or positive titers.

• About the D-Nase Test (also known as Antideoxyribonuclease B titer; ADN-B test)
  This is the short name for "deoxyribonuclease (DNase) test" and it detects the degradation of DNA by bacterial species that produce DNase.  The purpose is to see if the microbe can use DNA as a source of carbon and energy for growth. Use of DNA is accomplished by an enzyme called DNase.  Anti-DNase B is a blood test to look for antibodies to a substance produced by Group A Streptococcus, the bacteria that cause strep throat. A blood sample is needed and no special preparation is necessary.  This test is most often done to tell if you have previously had a strep infection and if you might have rheumatic fever or kidney problems (glomerulonephritis) due to that infection. When used together with the ASO titer test, more than 90% of past streptococcal infections can be correctly identified.

A negative test is normal. This means:

• Adults: less than 85 units/mL
• School-age children: less than 170 units/mL
• o   Preschool children: less than 60 units/mL
  Normal value ranges may vary slightly among different laboratories. Talk to your doctor about the meaning of your specific test results.  The examples above show the common measurements for results for these tests. Some laboratories use different measurements or may test different specimens.  Increased levels of DNase B levels may indicate rheumatic fever or post-streptococcal glomerulonephritis after strep throat or strep-related skin infection. 

• The Cunningham Panel of Tests
  A series of 5 tests to help determine the “likelihood of the patient’s condition being auto-immune in nature”, including possible PANDAS, is commercially available by Moleculera Labs. This test is derived from the research done by Dr. M. Cunningham.  Currently the panel is comprised of five different tests ($925 if no insurance, $425 deposit with the test with insurance). Four of these tests measure the level of circulating antibodies directed against different neurologic receptors or antigens, and one assay which measures the immune stimulating intensity of the patient’s serum against neuronal cells. The collective results of the panel of 5 tests will provide an assessment as to the anti-neuronal and autoimmune state of the patient at the time of testing.  The physician is provided a composite report containing the 5 assay results, each compared to normal controls.  The collective results can aid the physician in determining a proper diagnosis and support the appropriate treatment decision.  Currently, the Cunningham Panel does not include testing for streptococcal or anti-streptococcal antibody titers in PANDAS.  Their goal at this time is to assist the physician and family by determining if there are elevated anti-neuronal antibodies and neuronal cell activating antibodies currently circulating in the blood, rather than attempting to identify the infection related to the autoimmune condition. PANS is also associated with other infections. Therefore, in the future we may add additional tests to the Cunningham Panel that would assist in identifying these infectious agents.