Nearly 20 years ago Huntington Potter kicked up a storm of controversy with the idea that Down syndrome and Alzheimer’s were the same disease. Now the evidence is in: He was right.

And that’s not all. Down syndrome, artery-clogging cardiovascular disease, and possibly even diabetes, appear to share a common disease mechanism with Alzheimer’s disease, Dr. Potter and colleagues at the Florida Alzheimer’s Disease Research Center, USF Health Byrd Alzheimer’s Institute, recently reported.

The researchers’ two papers – one in Molecular Biology of the Cell and the other in PLoS ONE — implicate the Alzheimer’s-associated protein beta amyloid (amyloid protein), which damages the microtubule transport system responsible for moving chromosomes, proteins and other cargo around inside cells. Both studies were done in mice and humans cell cultures modeling Alzheimer’s disease. Together, the laboratory discoveries suggest that protecting the microtubule network from this amyloid damage might be an effective way to prevent or even reverse Alzheimer’s disease and associated disorders.

The first paper, by Antoneta Granic and colleagues published online Dec. 23 in Molecular Biology of the Cell, provides the mechanism behind previous work by Dr. Potter’s laboratory showing that all Alzheimer’s disease patients harbor some cells with three copies of chromosome 21, known as trisomy 21, instead of the usual two. Trisomy 21 is a characteristic shared by all the cells in people with the birth defect Down syndrome as well. This earlier work demonstrated that Alzheimer’s disease could be considered a late onset form of Down syndrome.

By age 30 to 40, all people with Down syndrome develop the same brain pathology seen in Alzheimer’s disease, including a nerve-killing buildup of sticky amyloid protein clumps. This contributes to accelerated nerve cell loss and dementia.

With the study reported in MBC, Dr. Potter and his colleagues now show that the Alzheimer’s-associated amyloid protein is the culprit that interferes with the microtubule transport system inside cells. The microtubules are responsible for segregating newly duplicated chromosomes as cells divide.

“Beta amyloid basically creates potholes in the protein highways that move cargo, including chromosomes, around inside cells,” said Dr. Potter, who holds the Eric Pfeiffer Endowed Chair for Research on Alzheimer’s Disease.

When the microtubule network is disrupted, chromosomes can be incorrectly transported as cells divide and the result is new cells with the wrong number of chromosomes and an abnormal assortment of genes. For example, Down syndrome cells contain three copies of the beta amyloid gene on chromosome 21 – leading to more accumulation of the “bad” amyloid protein over a lifetime, Dr. Potter says. “Alzheimer’s disease probably is caused in part from the continuous development of new trisomy 21 nerve cells, which amplify the disease process by producing extra beta amyloid.”

The second paper by lead author Jose Abisambra and colleagues, published Dec. 31 in the online journal PLoS ONE, describes another consequence of the damaged microtubule network caused by the amyloid protein.

Many Alzheimer’s disease patients also commonly develop vascular diseases and diabetes. Whether this coincidence is bad luck or due to shared disease processes is intensely debated. Research teams have investigated the role that low-density lipoprotein (LDL), the bad cholesterol that causes atherosclerosis, cardiovascular disease and stroke, may play in the development of Alzheimer’s with mixed results. However, the USF group focused on the amyloid protein’s potential effects on LDL metabolism. The receptor needed to detect and use LDL is among the proteins transported by the microtubules.

As previously reported by their colleagues in the MBC paper, the second USF team found that the amyloid protein inflicts damage to the microtubule network. As a consequence, the receptor needed to pull LDL circulating throughout the bloodstream into the body’s cells has trouble getting to the cell surface to retrieve this bad cholesterol. This interference with LDL metabolism may allow bad cholesterol to build up in into plaques that choke off blood supply to the brain and heart in people with Alzheimer’s, Dr. Potter said.

Similarly, other key proteins – including insulin receptors and receptors for brain signaling molecules — are also likely locked inside cells when the transport system is damaged by amyloid or other factors. “The insulin receptors are needed to get blood sugar inside the cell where it can be used for energy. The nerve cell signaling receptors help promote memory and learning,” Dr. Potter said. “So, if these receptors are unable to function properly, it may lead to diabetes and problems with learning and memory.”

“We’re beginning to understand how conditions like cardiovascular disease and diabetes may manifest some of the same underlying disease processes as Alzheimer’s disease,” he said, “rather than being independent diseases that just happen to develop in the same patient.”

Journal articles cited:

1. “Alzheimer Ab Peptide Induces Chromosome Mis-segregation and Aneuploidy, including Trisomy 21; Requirement for Tau and APP,” Antoneta Granic, Jaya Padmanabhan, Michelle Norden, and Huntington Potter. Molecular Biology of the Cell, Dec. 23, 2009.

2. “LDLR Expression and Localization Are Altered in Mouse and Human Cell Culture Models of Alzheimer’s Disease,” Jose Abisambra, Tina Fiorella, Jaya Padmanabhan, Peter Neame, Inge Wefes, and Huntington Potter, PLoS ONE, Volume 5, Issue 1. (January 2010).

Source: University of South Florida Health

Published in the journal Environmental Health Perspectives, The study revealed that people with higher concentrations of PFOA in their blood have higher rates of thyroid disease. The researchers analysed samples from the US Centers for Disease Control and Prevention’s nationally representative National Health and Nutrition Examination Survey (NHANES).

Tamara Galloway, a professor Ecotoxicology at the University of Exeter and the study’s senior author, says: “Our results highlight a real need for further research into the human health effects of low-level exposures to environmental chemicals like PFOA that are ubiquitous in the environment and in people’s homes. We need to know what they are doing.”

“There have long been suspicions that PFOA concentrations might be linked to changes in thyroid hormone levels,” adds study author, David Melzer, a professor of Epidemiology and Public Health at the Peninsula Medical School. “Our analysis shows that in the ‘ordinary’ adult population there is a solid statistical link between higher concentrations of PFOA in blood and thyroid disease.”

PFOA is a very stable man-made chemical that excels at repelling heat, water, grease, and stains. It is used during the process of making common household and industrial items including nonstick pots and pans, flame-resistant and waterproof clothing, wire coatings, and chemical-resistant tubing. PFOA can also be formed by the break-down of certain other highly fluorinated chemicals used in oil and grease-resistant coatings on fast-food containers and wrappers and in stain-resistant carpets, fabrics, and paints.

The study included 3966 adults aged 20 and older whose blood serum was sampled between 1999 and 2006 for PFOA and other perfluoroalkyl acid (PFAA) compounds, including perfluoroctane sulphonate (PFOS). The researchers found that the individuals with the highest 25% of PFOA concentrations (above 5.7ng/ml) were more than twice as likely to report current thyroid disease than individuals with the lowest 50% of PFOA concentrations (below 4.0ng/ml). The most specific analysis included 163 women and 46 men who reported having current thyroid disease and who were taking thyroid medication at the time the blood samples were taken. The models used in the analysis were adjusted for potential confounding factors, such as age, gender, ethnicity, smoking, and body mass index.

Previous animal studies carried out by other scientists have shown that the compounds can affect the function of the mammalian thyroid hormone system. This is essential for maintaining heart rate, regulating body temperature and supporting many other body functions, including metabolism, reproduction, digestion and mental health.

The findings are important because research has shown that PFAAs are found in water, air and soil throughout the world, even in remote polar regions. PFOA and PFOS have also been detected in the blood of people from across the globe, as well as in wildlife including birds, fish, and polar bears.

The main source of human exposure to PFOA and PFOS remains uncertain but is believed to be through diet. However, people may also be exposed through the PFAAs used in consumer goods such as textiles, footwear, furniture, and carpets, which can contaminate indoor air and dust.

Although more research is needed to understand the mechanism by which PFOA and PFOS may affect human thyroid functioning, it is plausible that the compounds could disrupt binding of thyroid hormones in the blood or alter their metabolism in the liver. However, this new evidence does not rule out the possibility that having thyroid disease changes the way the body handles PFOA and/or PFOS. The presence of the compounds might also prove to be simply a marker for some other factor associated with thyroid disease.

Thyroid diseases, particularly hypothyroidism, are much more common in women than men. However, in terms of the link between PFOA and thyroid disease, the researchers found no evidence of a statistically different effect between the sexes. The researchers also found a link between thyroid disease and higher concentrations of PFOS in men, but not in women.

Although previous studies of people living in communities near where PFOA and PFOS are manufactured did not find an association between exposure to these chemicals and thyroid hormone functioning, the largest study of such exposed communities is currently underway. (The ‘C8’ study of communities near DuPont’s Washington Works plant, including Marietta, OH, and Parkersburg, WV, both in the US).

In addition to Galloway and Melzer, the paper’s authors include Neil Rice of the Peninsula Medical School’s Epidemiology and Public Health Group; Michael H Depledge of the Peninsula Medical School’s European Centre for the Environment and Human Health; and William E Henley of the School of Mathematics and Statistics of the University of Plymouth . They used the U.S. NHANES dataset because it is the only large-scale data available on PFOA and PFOS in a ‘general’ population anywhere in the world.

Source: The Peninsula College of Medicine and Dentistry

That’s according to a new study by Texas AgriLife Research food scientists, who examined the five varieties most common in the U.S.: Kent, Francine, Ataulfo, Tommy/Atkins and Haden. Though the mango is an ancient fruit heavily consumed in many parts of the world, little has been known about its health aspects. The National Mango Board commissioned a variety of studies with several U.S. researchers to help determine its nutritional value.

“If you look at what people currently perceive as a superfood, people think of high antioxidant capacity, and mango is not quite there,” said Dr. Susanne Talcott, who with her husband, Dr. Steve Talcott, conducted the study on cancer cells. “In comparison with antioxidants in blueberry, acai and pomegranate, it’s not even close.”

But the team checked mango against cancer cells anyway, and found it prevented or stopped cancer growth in certain breast and colon cell lines, Susanne Talcott noted.

“It has about four to five times less antioxidant capacity than an average wine grape, and it still holds up fairly well in anticancer activity. If you look at it from the physiological and nutritional standpoint, taking everything together, it would be a high-ranking super food,” she said. “It would be good to include mangoes as part of the regular diet.”

The Talcotts tested mango polyphenol extracts in vitro on colon, breast, lung, leukemia and prostate cancers. Polyphenols are natural substances in plants and are associated with a variety of compounds known to promote good health.

Mango showed some impact on lung, leukemia and prostate cancers but was most effective on the most common breast and colon cancers.

“What we found is that not all cell lines are sensitive to the same extent to an anticancer agent,” she said. “But the breast and colon cancer lines underwent apotosis, or programmed cell death. Additionally, we found that when we tested normal colon cells side by side with the colon cancer cells, that the mango polyphenolics did not harm the normal cells.”

The duo did further tests on the colon cancer lines because a mango contains both small molecules that are readily absorbed and larger molecules that would not be absorbed and thus remain present in a colon.

“We found the normal cells weren’t killed, so mango is not expected to be damaging in the body,” she said. “That is a general observation for any natural agent, that they target cancer cells and leave the healthy cells alone, in reasonable concentrations at least.”

The Talcotts evaluated polyphenolics, and more specifically gallotannins, as being the class of bioactive compounds (responsible for preventing or stopping cancer cells). Tannins are polyphenols that are often bitter or drying and found in such common foods as grape seed, wine and tea.

The study found that the cell cycle, which is the division cells go through, was interrupted. This is crucial information, Suzanne Talcott said, because it indicates a possible mechanism for how the cancer cells are prevented or stopped.

“For cells that may be on the verge of mutating or being damaged, mango polyphenolics prevent this kind of damage,” she said.

The Talcotts hope to do a small clinical trial with individuals who have increased inflammation in their intestines with a higher risk for cancer.

“From there, if there is any proven efficacy, then we would do a larger trial to see if there is any clinical relevance,” she said.

According to the National Mango Board, based in Winter Park, Fla., most mangoes consumed in the U.S. are produced in Mexico, Ecuador, Peru, Brazil, Guatemala and Haiti. Mangoes are native to southeast Asia and India and are produced in tropical climates. They were introduced to the U.S. in the late 1800s, and a few commercial acres still exist in California and Florida.

Source: Texas A&M AgriLife Communications

Mangoes are certainly delicious and an easy way to add to your daily fruit intake. The information above is just a little too “seen it all before” to become excited about. Most claims assigning so-called “super food” status should be taken with a grain of salt. They are usually marketing dressed up in so-called science. Nevertheless, enjoy your mangoes.

The Vitamin D Newsletter

 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.  

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

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

In this edition Dr Jenny Tylee provides a brief and simple introduction to meditation. Effective meditation provides innumerable health benefits and should be a skill learned by everyone.

Brief discussion related to tinnitus is provided in answer to a reader’s question.