Major Study Finds Pregnancy Issue Actually Linked to Autism, And It’s Not Vaccines

It’s a common but erroneous belief among anti-vaxxers that if a pregnant woman gets jabbed, she puts her unborn child at risk of autism.

This couldn’t be further from the truth. Instead, a growing body of research suggests that when a mother goes unvaccinated, that is when she truly leaves her child vulnerable.

A new study of nearly 1.8 million children in Sweden has found that the risks for autism and depression are significantly higher if your mother was hospitalised with an infection during pregnancy.

The results build on a nascent but burgeoning idea that specific infections, when contracted during pregnancy, can harm a developing brain, boosting the risk of psychiatric disorders coming on later in life, including conditions such as bipolar disorder, schizophreniadepression, and autism.

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This new study, however, paints a much broader stroke. Instead of revealing one or two bad infections, the authors found that the results remained the same whether or not the hospitalisation was due to severe infections – like influenza, meningitis and pneumonia – or much more mild UTIs.

In other words, it isn’t necessarily a specific virus, but infection in general that appears to be causing these problems, and it seems to be the case even when the affliction can’t reach the fetal brain.

“The results indicate that safeguarding against and preventing infection during pregnancy as far as possible by, for instance, following flu vaccination recommendations, may be called for,” says Verena Sengpiel, an expert in obstetrics and gynaecology at the University of Gothenburg.

Drawing on data from the Medical Birth Register for almost 1.8 million children, born in Sweden between 1973 and 2014, the authors tallied how many of their mothers had been hospitalised with an infection during their respective pregnancies.

The researchers then tracked these children and their mental health through the inpatient register until 2014, when the oldest ones were turning 41.

Statistical analysis of the data revealed a worrying link between a child’s mental health and their mother’s immune system.

While the study did not find an increased risk of schizophrenia or bipolar disorder, the authors did find that when a pregnant woman goes to the hospital for an infection, her child is more likely to seek hospital treatment for depression and autism later on in life.

In fact, among these children, the increased risk was 79 percent for autism and 24 percent for depression.

“Overall, we found evidence that exposure to maternal infection during fetal life increased the risk of autism and possibly of depression in the child,” the authors write.

“Although the individual risk appears to be small, the population effects are potentially large.”

As fascinating as it is, the study is only observational, so it can’t tell us exactly how a maternal infection would impact a child’s developing brain.

Nevertheless, recent studies on animal models have suggested that these infections might be causing an inflammatory reaction in the nervous system, altering gene expression in the brain and changing its architecture.

The thing is, many of these studies also note there are a multitude of genetic factors at play, so the answer to this puzzle could be highly complex.

“Our results cannot exclude the possibility of increased risk for psychopathologic conditions as a result of a dual “hit”: an inflammatory fetal brain injury on a background of genetic susceptibility,” the authors of the new study write.

More research will be needed before we can say for sure what is going on. In the meantime, however, the best thing a pregnant mother can do is stay healthy and adhere to the best medical advice out there. Getting all your vaccinations is a good start.

Source: JAMA Psychiatry.

Aluminum, Fluoride and Glyphosate — A Toxic Trifecta Implicated in Autism and Alzheimer’s Disease Research

Aluminum is a known neurotoxin, and according to Professor Christopher Exley of Keele University, aluminum-containing products are likely fueling the rise in Alzheimer’s disease. In an article published in the journal Frontiers in Neurology, he writes: “We are all accumulating a known neurotoxin in our brain from our conception to our death. The presence of aluminium in the human brain should be a red flag alerting us all to the potential dangers of the aluminium age. How do we know that Alzheimer’s disease is not the manifestation of chronic aluminium toxicity in humans?”

People with aluminum toxicity display many of the same symptoms as those with dementia, Parkinson’s, ADHD, autism, and other neurological diseases, and mounting evidence suggests aluminum may play a significant role in the development of those (and other) diseases.

By taking steps to protect yourself, you can minimize your exposure while maximizing your body’s ability to rid itself of this toxic metal, which will move you toward a long and healthy life well into your senior years. Other toxins to beware of also include fluoride and glyphosate; all of these are toxic in their own right, but research suggests they may be even more hazardous in combination.

You May Be Exposed to More Aluminum Than You Think

Aluminum can be found in a wide range of consumer products, including:

  • Foods such as baking powder, self-rising flour, salt, baby formula, coffee creamers, baked goods, and processed foods, coloring, and caking agents.
  • Drugs, such as antacids, analgesics, anti-diarrheals, and others; additives such as magnesium stearate.
  • Vaccines, including Hepatitis A and B, Hib, DTaP (diphtheria, tetanus, pertussis), pneumococcal vaccine, Gardasil (HPV), and others — many of which also contain also contain glyphosate.
  • Cosmetics and personal care products such as antiperspirants, deodorants (including salt crystals, made of alum), lotions, sunscreens, and shampoos.
  • Aluminum products, including foil, cans, juice pouches, tins, and water bottles.

According to the CDC, the average adult in the US consumes about seven to nine mg of aluminum per day in food, plus a lesser amount from air and water.

Approximately one percent of the aluminum you ingest orally gets absorbed into your body, the rest is moved out by your digestive tract — providing it’s functioning at its optimum. The remaining aluminum is then deposited not only in brain tissue, but also in your nerves, bone, liver, heart, spleen, and muscle.

While one percent may sound like a tiny amount, your overall toxic load will depend on the total amount of toxins you’re exposed to over time. Your diet and digestive health, as well as ongoing toxic exposures, will also determine how much your body is actually able to eliminate and how much builds up in the body.

Occupational Exposure to Aluminum Raises Your Risk for Alzheimer’s

One published case study found high levels of aluminum in the brain of a man who was exposed to aluminum at work for eight years. He later died from Alzheimer’s disease. According to the authors, it’s the first case showing a direct link between Alzheimer’s disease and elevated brain aluminum following occupational exposure.

Another study suggested that aluminum from food and drinking water may be contributing to rising Alzheimer’s rates, noting that:

“In recent years, interest in the potential role of metals in the pathogenesis of Alzheimer’s disease (AD) has grown considerably. In particular, aluminum (Al) neurotoxicity was suggested after its discovery in the senile plaques and neurofibrillary tangles that represent the principal neuropathological hallmarks of AD.

“Al is omnipresent in everyday life and can enter the human body from several sources, most notably from drinking water and food consumption… [O]ther elements present in drinking water, such as fluoride, copper, zinc, or iron could also have an effect on cognitive impairment or modify any Al neurotoxicity.”

Indeed, dozens of studies have shown that fluoride causes brain damage and lowers IQ. Fluoride emitted by aluminum plants has also been implicated in animal disease. Farmers in Iceland, for example, claim their animals are being sickened by environmental fluoride contamination — some to the point of having to be euthanized. Others report higher rates of tooth damage and infertility among their livestock. (You can learn more about the damaging effects of fluoride exposure here.)

Another related study linked occupational exposure to aluminum to the development of pulmonary fibrosis, a condition in which scarring on your lungs make it difficult to breathe. In this case, the exposure occurred during sanding of Corian material.

All in all, it seems reasonable to conclude that the combination of aluminum, fluoride, and/or a number of other toxins, can promote Alzheimer’s disease in addition to a number of other health problems. (You can learn more here.)

Pesticides Can Also Wreak Havoc with Brain Function

Pesticides, for example, have also been shown to have an adverse effect on neurological function and brain health In one study, farmers exposed to organochlorine insecticides had a 90 percent increased risk of depression compared to those who didn’t use them. Exposure to fumigants increased the risk of depression by 80 percent. People exposed to pesticides are also more likely to have Parkinson’s disease.

Glyphosate is also known to damage the liver and kidneys, significantly increase the risk of cancer, and enhance the damaging effects of other chemical residues and toxins.

Of course, when it comes to toxins in general, unless the chemical is acutely toxic, the real harm occurs when your body becomes chronically overloaded with them, and most people today are exposed to thousands and perhaps tens of thousands of different chemicals on a regular basis. And farmers are not the only ones at risk for adverse effects from pesticide exposure: Glyphosate can be found in most processed foods in the Western diet courtesy of GE sugar beets, corn, and soy — and is even found in tampons, vaccines, it is literally everywhere.

While nearly one billion pounds of glyphosate is doused on both conventional and genetically engineered (GE) crops worldwide each year, GE crops receive the heaviest amounts. Meats from animals raised in confined animal feeding operations (CAFOs) may also contain higher amounts of glyphosate residues, as GE soy is a staple of conventional livestock feed.

Unfortunately, glyphosate doesn’t just stay within the boundary of conventional and GMO crops; it spreads — as documented in this report — contaminating everything, including organics, completely disrupting the natural balance of soil biology.

It’s also crucial to understand that glyphosate contamination is systemic, meaning it is integrated into every cell of the plant, from root to tip. Normally, you need to thoroughly wash your produce to remove topical pesticide residues, but you simply cannot remove glyphosate from your produce. This is part and parcel of what makes GE foods so harmful to your health — it’s not just an issue of topical contamination, as with many other agricultural chemicals sprayed on crops.

Synergistic Poisoning from Aluminum and Glyphosate Implicated in Autism Research

Dr. Stephanie Seneff, a senior research scientist at Massachusetts Institute of Technology (MIT), has been instrumental in educating people about the hazards of glyphosate. In the video below, she explains how aluminum and glyphosate act together as synergistic poisons that promote autism. Based on the current trend, Dr. Seneff predicts that by 2025, half of all children born will be diagnosed with autism. Clearly, we must identify leading environmental factors contributing to this frightening trend. Lack of vitamin D caused by inadequate sun exposure is one factor. Nutritional deficiencies caused by poor diet are another.

Environmental toxins must not be overlooked however, and some toxins—glyphosate and aluminum included—are far more hazardous and ubiquitous than others, and are therefore likely to contribute to a greater degree. As Dr. Seneff explains, glyphosate’s mechanism of harm renders it particularly problematic. Indeed, according to Dr. Seneff, glyphosate is possibly “the most important factor in the development of multiple chronic diseases and conditions that have become prevalent in Westernized societies”, including but not limited to:

Autism Gastrointestinal diseases such as inflammatory bowel disease, chronic diarrhea, colitis, and Crohn’s disease Obesity
Allergies Cardiovascular disease Depression
Cancer Infertility Alzheimer’s disease
Parkinson’s disease Multiple sclerosis ALS and more

Tips for Avoiding These Pernicious Toxins

It seems quite clear that aluminum exposure plays a role in neurodegenerative diseases like Alzheimer’s. Other neurotoxins such as fluoride and glyphosate add to the toxic burden. The best way to protect yourself is to be careful about your choices in food and personal products, and minimize your use of vaccines and other drugs that are often contaminated with aluminum. Optimizing your dietary sulfur is also essential, as your body needs sulfur to manufacture its number one weapon against aluminum overload: glutathione.

By taking a few steps to protect yourself, you’ll minimize your exposure while maximizing your body’s ability to rid itself of this toxic metal, which will move you toward a long and healthy life well into your senior years. For additional tips and strategies that can help prevent and/or treat Alzheimer’s, please see my previous article “Two Exciting Alzheimer’s Advances: A Novel Early Detection Test Using Peanut Butter, and a Study Evaluating Coconut Oil.

The following list offers a number of suggestions for items to avoid, to reduce your exposure to aluminum, fluoride, glyphosate, and other brain-harming components:

Processed foods and sodas. This will help you avoid both GE ingredients (which tend to be contaminated with glyphosate) and aluminum. In addition, replacing processed foods with whole organic foods will drastically reduce your sugar/fructose intake, which will help normalize your insulin and leptin sensitivity. This is in fact one of the best strategies for protecting and preserving your brain function and overall health. Fructose and gluten are other dietary factors that promote Alzheimer’s, and are best avoided as much as possible.
Mechanically de-boned chicken, which tends to be high in fluoride as a result of the processing.
Dental amalgams. Dental amalgam fillings, which are 50 percent mercury by weight, are one of the major sources of heavy metal toxicity. However, you should be healthy prior to having them removed. Once you have adjusted to following the diet described in my optimized nutrition plan, you can follow the mercury detox protocol and then find a biological dentist to have your amalgams removed.
Cosmetics and personal care products containing aluminum, such as antiperspirants (including salt crystals, made of alum), lotions, sunscreens, and shampoos.
Vaccines containing either mercury (thimerosal) and/or aluminum.
Aluminum-containing drugs, such as antacids, analgesics, anti-diarrheals, and others
Anticholinergics and statin drugs. Drugs that block acetylcholine, a nervous system neurotransmitter, have been shown to increase your risk of dementia. These drugs include certain nighttime pain relievers, antihistamines, sleep aids, certain antidepressants, medications to control incontinence, and certain narcotic pain relievers.Statin drugs are particularly problematic because they suppress the synthesis of cholesterol, deplete your brain of coenzyme Q10 and neurotransmitter precursors, and prevent adequate delivery of essential fatty acids and fat-soluble antioxidants to your brain by inhibiting the production of the indispensable carrier biomolecule known as low-density lipoprotein.
Fluorinated medications, including Cipro.
Fluoridated water
Fluoridated toothpaste and fluoride gel treatments.
Non-stick cookware will outgas fluoride, but also avoid other aluminum-containing products, such as cans, foil, juice pouches, tins, and water bottles.

Is Ultrasound During Pregnancy Linked to Autism?

Study actually reveals ultrasound to be safe, says F. Perry Wilson, MD

A study appearing in JAMA Pediatrics is being reported as showing a link between ultrasound during pregnancy and autism spectrum disorder. But in this Deep Dive analysis, F. Perry Wilson, MD, suggests that the study actually reveals ultrasound to be a safe procedure in this regard. What’s more, the senior author agrees.

The rate of autism spectrum disorder has risen dramatically over the past several decades.

Now, much of that rise has been attributed to an increased recognition and diagnosis of the syndrome, but most experts believe some environmental factor is contributing. While we don’t have a great idea of what that factor is, we’re getting more confident in what it isn’t. First, it isn’t vaccines, either the content or the schedule. I eagerly await your angry emails.

Second, after reading this article in JAMA Pediatrics, I’m fairly certain it’s not prenatal ultrasound.

But I very much doubt that’s the story you’re going to hear with regards to this study. On the contrary, I think you’re going to hear a lot of outlets saying something like “New study links ultrasound during pregnancy with autism”.

First things first – why was this question even studied? Aren’t we always telling our patients that ultrasounds are super safe? Well, ultrasonic energy is energy, and while it may not do much damage as it passes into say, your gallbladder, it may do quite a bit more harm to a developing fetal brain. Some animal studies, in fact, have demonstrated that ultrasonic energy can alter neuronal migration, and at least one study showed that mice exposed to ultrasound in utero had poorer socialization than mice not so exposed.

In other words, there is biological plausibility here. But prior studies looking at ultrasound exposure in pregnancy, including one randomized trial, showed no link with autism.

But these studies were blunt tools – looking at ultrasound as a binary, yes/no type of exposure. Did you get one or not?

The study in JAMA Pediatrics, in contrast, is much more precise. The researchers took 107 kids with autism spectrum disorder and matched them to 104 kids with other developmental anomalies and 209 kids with typical development. They then went back and tallied up all their ultrasounds in utero, but not just the number. They looked at the duration of ultrasound, the frame rate, whether Doppler was used, and also the thermal and mechanical indices – metrics that quantify exactly how much energy is delivered to the imaged tissues.

In total, 9 different ultrasound metrics were assessed. The effect was assessed over the entire pregnancy and in trimester 1, 2, and 3.

Now assessing this much detail is a double-edged sword. If you count it up, we have more than 30 statistical tests here. Some of these were bound to turn up as statistically significant by chance alone as there was no correction done for multiple comparisons.

And that’s just what happened.

Depth of ultrasound was found to be associated with ASD, but none of the other metrics were. Well, duration of ultrasound was associated with ASD in the first two trimesters, but in the opposite direction of what would be hypothesized, with longer duration of ultrasound being protective.

Should we conclude, then, that we should be careful how deep we set our ultrasound scanners? Almost certainly not. There is a very good chance this is a false positive. Even if it’s not, depth of ultrasound is largely determined by anatomy, and maternal body habitus. The observed link may be explained by maternal adiposity.

But more impressive than this is the lack of association with thermal or mechanical index – the biological factors previously hypothesized to mediate any adverse ultrasound effects. If ultrasound is causative in ASD, you would really think that more ultrasonic energy delivered would be worse. This study essentially rules out that possibility, and to me, rules out the possibility that increased ultrasonography in pregnancy is driving the autism epidemic.

But if you don’t take my word for it, ask senior author Dr. Jodi Abbott, whom I spoke with last week about the study results:

“Given the information investigated very very thoroughly, none of the parameters previously associated with harm were found to be different in these populations.”

In other words – the search goes on. But if excellent researchers like Dr. Abbott and her colleague Dr. Paul Rosman continue their in-depth analyses, the search will lead to answers.

Why 80% of Us Are Deficient In Magnesium

We thirst for magnesium rich water.

Magnesium deficiency is often misdiagnosed because it does not show up in blood tests – only 1% of the body’s magnesium is stored in the blood.

Most doctors and laboratories don’t even include magnesium status in routine blood tests. Thus, most doctors don’t know when their patients are deficient in magnesium, even though studies show that the majority of Americans are deficient in magnesium.

Consider Dr. Norman Shealy’s statements, “Every known illness is associated with a magnesium deficiency” and that, “magnesium is the most critical mineral required for electrical stability of every cell in the body. A magnesium deficiency may be responsible for more diseases than any other nutrient.” The truth he states exposes a gapping hole in modern medicine that explains a good deal about iatrogenic death and disease. Because magnesium deficiency is largely overlooked, millions of Americans suffer needlessly or are having their symptoms treated with expensive drugs when they could be cured with magnesium supplementation.

One has to recognize the signs of magnesium thirst or hunger on their own since allopathic medicine is lost in this regard. It is really something much more subtle then hunger or thirst but it is comparable. In a world though where doctors and patients alike do not even pay attention to thirst and important issues of hydration, it is not hopeful that we will find many recognizing and paying attention to magnesium thirst and hunger, which is a dramatic way of expressing the concept of magnesium deficiency.

Few people are aware of the enormous role magnesium plays in our bodies. Magnesium is by far the most important mineral in the body. After oxygen, water, and basic food, magnesium may be the most important element needed by our bodies; vitally important, yet hardly known. It is more important than calcium, potassium or sodium and regulates all three of them. Millions suffer daily from magnesium deficiency without even knowing it

In fact, there happens to be a relationship between what we perceive as thirst and deficiencies in electrolytes. I remember a person asking, “Why am I dehydrated and thirsty when I drink so much water?” Thirst can mean not only lack of water but it can also mean that one is not getting enough nutrients and electrolytes. Magnesium, Potassium, Bicarbonate, Chloride and Sodium are some principle examples and that is one of the reasons magnesium chloride is so useful.

A man with magnesium deficiency

You know all those years, when doctors used to tell their patients ‘its all in your heads,’ were years the medical profession was showing its ignorance. It is a torment to be magnesium deficient on one level or another. Even if it’s for the enthusiastic sport person whose athletic performance is down, magnesium deficiency will disturb sleep and background stress levels and a host of other things that reflect on the quality of life. Doctors have not been using the appropriate test for magnesium – their serum blood tests just distort their perceptions. Magnesium has been off their radar screens through the decades that magnesium deficiencies have snowballed.

Symptoms of Magnesium Deficiency

The first symptoms of deficiency can be subtle – as most magnesium is stored in the tissues, leg cramps, foot pain, or muscle ‘twitches’ can be the first sign. Other early signs of deficiency include loss of appetite, nausea, vomiting, fatigue, and weakness. As magnesium deficiency worsens, numbness, tingling, seizures, personality changes, abnormal heart rhythms, and coronary spasms can occur.

A full outline of magnesium deficiency was beautifully presented in a recent article by Dr. Sidney Baker. “Magnesium deficiency can affect virtually every organ system of the body. With regard to skeletal muscle, one may experience twitches, cramps, muscle tension, muscle soreness, including back aches, neck pain, tension headaches and jaw joint (or TMJ) dysfunction. Also, one may experience chest tightness or a peculiar sensation that he can’t take a deep breath. Sometimes a person may sigh a lot.”

“Symptoms involving impaired contraction of smooth muscles include constipation; urinary spasms; menstrual cramps; difficulty swallowing or a lump in the throat-especially provoked by eating sugar; photophobia, especially difficulty adjusting to oncoming bright headlights in the absence of eye disease; and loud noise sensitivity from stapedius muscle tension in the ear.”

“Other symptoms and signs of magnesium deficiency and discuss laboratory testing for this common condition. Continuing with the symptoms of magnesium deficiency, the central nervous system is markedly affected. Symptoms include insomnia, anxiety, hyperactivity and restlessness with constant movement, panic attacks, agoraphobia, and premenstrual irritability. Magnesium deficiency symptoms involving the peripheral nervous system include numbness, tingling, and other abnormal sensations, such as zips, zaps and vibratory sensations.”

“Symptoms or signs of the cardiovascular system include palpitations, heart arrhythmias, and angina due to spasms of the coronary arteries, high blood pressure and mitral valve prolapse. Be aware that not all of the symptoms need to be present to presume magnesium deficiency; but, many of them often occur together. For example, people with mitral valve prolapse frequently have palpitations, anxiety, panic attacks and premenstrual symptoms. People with magnesium deficiency often seem to be “uptight.” Other general symptoms include a salt craving, both carbohydrate craving and carbohydrate intolerance, especially of chocolate, and breast tenderness.”

Magnesium is needed by every cell in the body including those of the brain. It is one of the most important minerals when considering supplementation because of its vital role in hundreds of enzyme systems and functions related to reactions in cell metabolism, as well as being essential for the synthesis of proteins, for the utilization of fats and carbohydrates. Magnesium is needed not only for the production of specific detoxification enzymes but is also important for energy production related to cell detoxification. A magnesium deficiency can affect virtually every system of the body.

Water rich in magnesium can prevent magnesium deficiency
Like water we need magnesium everyday. There is an
eternal need for magnesium as well as water and when
magnesium is present in water life and health are enhanced.

One of the principle reason doctors write millions of prescriptions for tranquilizers each year is the nervousness, irritability, and jitters largely brought on by inadequate diets lacking magnesium. Persons only slightly deficient in magnesium become irritable, highly-strung, and sensitive to noise, hyper-excitable, apprehensive and belligerent. If the deficiency is more severe or prolonged, they may develop twitching, tremors, irregular pulse, insomnia, muscle weakness, jerkiness and leg and foot cramps.

If magnesium is severely deficient, the brain is particularly affected. Clouded thinking, confusion, disorientation, marked depression and even the terrifying hallucinations of delirium tremens are largely brought on by a lack of this nutrient and remedied when magnesium is given. Because large amounts of calcium are lost in the urine when magnesium is under supplied, the lack of this nutrient indirectly becomes responsible for much rampant tooth decay, poor bone development, osteoporosis and slow healing of broken bones and fractures. With vitamin B6 (pyridoxine), magnesium helps to reduce and dissolve calcium phosphate kidney stones.

Magnesium deficiency may be a common factor associated with insulin resistance. Symptoms of MS that are also symptoms of magnesium deficiency include muscle spasms, weakness, twitching, muscle atrophy,  an inability to control the bladder, nystagmus (rapid eye movements), hearing loss, and osteoporosis.  People with MS have higher rates of epilepsy than controls.  Epilepsy has also been linked to magnesium deficiencies.[1]

Another good list of early warning symptoms suggestive of magnesium insufficiency:

  • Physical and mental fatigue
  • Persistent under-eye twitch
  • Tension in the upper back, shoulders and neck
  • Headaches
  • Pre-menstrual fluid retention and/or breast tenderness

Possible manifestations of magnesium deficiency include:

  • Low energy
  • Fatigue
  • Weakness
  • Confusion
  • Nervousness
  • Anxiousness
  • Irritability
  • Seizures (and tantrums)
  • Poor digestion
  • PMS and hormonal imbalances
  • Inability to sleep
  • Muscle tension, spasm and cramps
  • Calcification of organs
  • Weakening of the bones
  • Abnormal heart rhythm

Severe magnesium deficiency can result in low levels of calcium in the blood (hypocalcemia). Magnesium deficiency is also associated with low levels of potassium in the blood (hypokalemia). Magnesium levels drop at night, leading to poor REM (Rapid Eye Movement) sleep cycles and unrefreshed sleep. Headaches, blurred vision, mouth ulcers, fatigue and anxiety are also early signs of depletion.


We hear all the time about how heart disease is the number one health crisis in the country, about how high blood pressure is the “silent killer”, and about how ever increasing numbers of our citizens are having their lives and the lives of their families destroyed by diabetes, Alzheimer’s disease, and a host of other chronic diseases.

Signs of severe magnesium deficiency include:

  • Extreme thirst
  • Extreme hunger
  • Frequent urination
  • Sores or bruises that heal slowly
  • Dry, itchy skin
  • Unexplained weight loss
  • Blurry vision that changes from day to day
  • Unusual tiredness or drowsiness
  • Tingling or numbness in the hands or feet
  • Frequent or recurring skin, gum, bladder or vaginal yeast infections

But wait a minute, aren’t those the same symptoms for diabetes? Many people have diabetes for about 5 years before they show strong symptoms. By that time, some people already have eye, kidney, gum or nerve damage caused by the deteriorating condition of their cells due to insulin resistance and magnesium deficiency. Dump some mercury and arsenic on the mixture of etiologies and pronto we have the disease condition we call diabetes.

Magnesium deficiency is synonymous with diabetes and is at the root of many if not all cardiovascular problems.

Magnesium deficiency is a predictor of diabetes and heart disease both; diabetics both need more magnesium and lose more magnesium than most people. In two new studies, in both men and women, those who consumed the most magnesium in their diet were least likely to develop type 2 diabetes, according to a report in the January 2006 issue of the journal Diabetes Care. Until now, very few large studies have directly examined the long-term effects of dietary magnesium on diabetes. Dr. Simin Liu of the Harvard Medical School and School of Public Health in Boston says, “Our studies provided some direct evidence that greater intake of dietary magnesium may have a long-term protective effect on lowering risk,” said Liu, who was involved in both studies.

The thirst of diabetes is part of the body’s response to excessive urination. The excessive urination is the body’s attempt to get rid of the extra glucose in the blood. This excessive urination causes the increased thirst. But we have to look at what is causing this level of disharmony. We have to probe deeper into layers of cause. The body needs to dump glucose because of increasing insulin resistance and that resistance is being fueled directly by magnesium deficiency, which makes toxic insults more damaging to the tissues at the same time.

When diabetics get too high blood sugars, the body creates “ketones” as a by-product of breaking down fats. These ketones cause blood acidity which causes “acidosis” of the blood, leading to Diabetic Ketoacidosis (DKA), This is a very dangerous condition that can lead to coma and death. It is also called “diabetic acidosis”, “ketosis”, “ketoacidosis” or “diabetic coma”. DKA is a common way for new Type 1 diabetics to be diagnosed. If they fail to seek medical advice on symptoms like urination, which is driving thirst they can die of DKA.

Oral magnesium supplements reduce erythrocyte[2] dehydration.[3] In general, optimal balances of electrolytes are necessary to maintain the best possible hydration. Diabetic thirst is initiated specifically by magnesium deficiency with relative calcium excess in the cells. Even water, our most basic nutrient starts having a hard time getting into the cells with more going out through the kidneys.

Autism and Magnesium Deficiency

When dealing with autism spectrum and other neurological disorders in children it is important to know the signs of low magnesium: restless, can’t keep still, body rocking, grinding teeth, hiccups, noise sensitive, poor attention span, poor concentration, irritable, aggressive, ready to explode, easily stressed. When it comes to children today we need to assume a large magnesium deficiency for several reasons.

1) The foods they are eating are stripped of magnesium because foods in general, as we shall see below are declining in mineral content in an alarming way.

2) The foods many children eat are highly processed junk foods that do not provide real nutrition to the body.

3) Because most children on the spectrum are not absorbing the minerals they need even when present in the gut. Magnesium absorption is dependent on intestinal health, which is compromised totally in leaky gut syndromes and other intestinal problems that the majority of autism syndrome disorders.

4) Because the oral supplements doctors rely on are not easily absorbed, because they are not in the right form and because magnesium in general is not administered easily orally.

Modern medicine is supposed to help people not hurt them, but with their almost total ignorance of magnesium doctors end up hurting more than they help for many of the medical interventions drive down magnesium levels when they should be driving them up. Many if not most pharmaceutical drugs drive magnesium levels into very dangerous zones and surgery done without increasing magnesium levels is much more dangerous then surgery done with.

The foundation of medical arrogance is actually medical ignorance and the only reason ignorance and arrogance rule the playing field of medicine is a greed lust for power and money. Human nature seems to be at its worst in modern medicine when it should be at its best. It is sad that people have to suffer needlessly and extraordinarily tragic that allopathic medicine has turned its back on the Hippocratic Oath and all that it means.

For additional research on Magnesiun Deficiency, read the following articles:

Consult our Magnesium research database on the therapeutic role of magnesium in over 190 conditions:

Additional Resources

  • [2] Red blood cells are also known as RBCs, red blood corpuscles (an archaic term), haematids or erythrocytes (from Greek erythros for “red” and kytos for “hollow”, with cyte translated as “cell” in modern usage). The capitalized term Red Blood Cells is the proper name in the US for erythrocytes in storage solution used in transfusion medicine.
  • [3] J. Clin. Invest. 100(7): 1847-1852 (1997). doi:10.1172/JCI119713. The American Society for Clinical Investigation

These Major Mental Illnesses Share Unexpected Levels of Gene Activity

How is autism linked to schizophrenia?


On the surface, diverse mental health conditions like autism, alcoholism, and schizophrenia seem to have few things in common with one another.

A fresh look at the genes being expressed in the brains of individuals diagnosed with one of five mental illnesses reveals an unexpected degree of overlap, suggesting many psychiatric disorders are more similar than their symptoms would suggest.

Five years ago, a team of researchers used data supplied by the Psychiatric Genomics Consortium experiment to show people with autism spectrum disorder (ASD), attention deficit-hyperactivity disorder, bipolar disorder, major depressive disorder, and schizophrenia often share a handful of genetic variations.

While somewhat unexpected, it also didn’t say much about how those genes might relate to any of those conditions.

A follow-up study has added new details to the discovery, revealing levels of similarity between diverse disorders that aren’t just surprising, but downright counterintuitive.

The international team of scientists produced what’s known as a transcriptomic profile on 700 brain samples taken from deceased patients who had been diagnosed with either ASD, schizophrenia, bipolar disorder, depression, or alcoholism.

This gave them a library of not just the genes present in these specimens, but of their relative activity in the brain’s outer layer, the cortex.

These libraries were then compared with samples taken from just under 300 patients who had no diagnoses, as well as close to 200 individuals who had inflammatory bowel disease.

While we might expect conditions with related symptoms to share similar gene expressions, these results were a lot harder to explain.

Bipolar and depression are both classified as mood disorders, for instance, so there’d be no surprise if they shared fundamental biochemistry.

The fact the transcriptome for bipolar had more in common with schizophrenia came as quite a shock.

“This is not what clinicians would’ve expected,” says psychiatric geneticist Kenneth Kendler from Virginia Commonwealth University.

“It certainly suggests the idea that these are sharply different kinds of disorders is not valid.”

Links were also found between schizophrenia and autism. This isn’t exactly a revelation, but the research did show that many of the genes in both conditions are more active in those with ASD.

Genes known to be related to the rate at which neurons fire in the brain were found to be quieter in samples taken from people with ASD, schizophrenia, and bipolar disorder.

Besides a bunch of interesting correlations, the team failed to find any similarity between alcoholism and the other four illnesses.

Previous research on twins had suggested individuals with alcohol dependence and depression are more likely to share certain genes, hinting at an overlap in neurology.

If there is, this research suggests those shared genes aren’t expressing themselves. The team found no similarity in transcriptome between samples from people diagnosed with alcoholism and those with depression.

Studies such as these show just how fuzzy the concept of disease is, especially when it comes to mental health.

Far from having distinct boundaries, genetic research is revealing how tangled the roots of seemingly diverse mental illnesses really are.

“We’re beginning to see the bits of the puzzle starting to slowly get clearer,” says Kendler.

Which is a great thing for improving how we diagnose and treat suffering in people who experience mental illness.

Over 2,000 Newly Discovered Biological Markers Could Help Explain How Autism Develops

Scientists have discovered a swathe of biochemical regions that look to be deeply involved with the risk factors behind autism spectrum disorder (ASD).

Researchers have identified more than 2,000 of these regulatory regions – markers on top of our DNA that affect how our genetic machinery operates on a functional level – which are involved in learning and strongly associated with ASD.


While we know many cases of ASD are tied to differences in our genetic coding, the findings suggest epigenetic factors affecting non-genetic sequences of DNA could account for the development of the condition in many individuals.

“Our proof-of-concept study demonstrates the feasibility of going after genetic components of autism that are outside of genes and may eventually lead to improvements in the diagnosis and treatment of autism,” says neuroscientist Lucia Peixoto from Washington State University.

Epigenetics is a burgeoning field of science looking at how we inherit traits and changes from environmental or external sources, not just the DNA code that otherwise instructs how our bodies should grow and function.

These kinds of epigenetic mechanisms – which modify how our DNA is expressed at a molecular level – mean experiences in childhood can change our genetic code ever after, with things like babies being biochemically transformed by the amount of cuddles they receive.

Even more amazingly, these changes can persist beyond one lifespan –meaning things your parents did before you were born could have an impact on your own health.

In some cases, epigenetic ‘memories’ can be passed down as far along as 14 generations, so there’s clearly a lot more than just DNA affecting our biological destiny.

In their own study, Peixoto and her team experimented with mice that were placed in a box and given a small shock, which conditioned them to associate the box with an unpleasant experience.

When DNA from the animals’ hippocampus (which processes memory) was later analysed, the researchers found that chromatin – macromolecules that help ‘package’ DNA inside cells – had become more accessible.

With a new bioinformatics tool they developed called DEScan (Differential Enrichment Scan), the team identified 2,365 regions which were epigenetically regulated following the mouse’s conditioning. Interestingly, genes near many of these regions are known risk genes for ASD.

One of the more well-known autism risk genes is called Shank3, which is missing in a small percentage of autism patients. In a previous study, researchers found that by switching this gene on in mice that were engineered without the active Shank3 gene, autism symptoms could be reversed.

In the present research, the team analysed a clinical study involving more than 700 children (some 550 of which had autism), and found that one of the regulatory regions they identified in mice – called rs6010065 – is indeed associated with ASD in humans.

There’s obviously still a huge amount of research to be done here before we know more about how these epigenetic controls might be impacting the development of autism in children, but the researchers are convinced we could have a bright new lead to follow up on.

“One of the major challenges in the genetics of disease is understanding the role of the vast portions of the genome that regulate gene expression,” says one of the researchers, neuroscientist Ted Abel from the University of Iowa.

“[A]ctivity-dependent changes in chromatin accessibility may hold the key to understanding the function of this ‘dark matter’ of the genome and may provide novel insights into the nature of autism and other neurodevelopmental disorders.”

The autism paradox

How an autism diagnosis became both a clinical label and an identity; a stigma to be challenged and a status to be embraced

In 1991, Donna Williams, a little-known Australian writer, released her memoir Nobody Nowhere: The Remarkable Autobiography of an Autistic Girl. The book sold astonishingly well and became an international hit, spending 15 weeks on The New York Times bestseller list. Williams recalled her frustration that ‘people were forever saying that I had no friends’, when this didn’t bother her at all. When she retreated from the outside world, she said, it was not because she didn’t understand words (a common misconception), but because she simply couldn’t relate to them, which forced her to ‘shut down’ her senses and ‘meaning systems’. High-pitched sounds, touch and light became simply ‘intolerable’, she explained.

In the early 1990s, narratives told from the perspective of autistic people were virtually unheard of. At the time, most scientists depicted autism as an illness or ‘mental disorder’, and the focus was on identifying and ultimately eradicating it. Lorna Wing, a British psychiatrist, had developed the clinical classification back in the 1960s that stuck. She claimed that autistic people were ‘impaired’ in three areas: in social interaction, communication and imagination. Various methods were used to identify these ‘impairments’, from puzzles and games to family testimony. Psychologists and neuroscientists went on to try to develop quick-fix behavioural interventions, as well as to search for ‘autistic genes’. However, after much hype, the idea that the autism diagnosis resided in a unique genetic code quickly faded from view.

Meanwhile, increasing numbers of children around the world were found to fit the prototype, and diagnosed accordingly. Yet Wing’s ‘impairment’ model of autism carved up human psychology in a way that was oddly definitive and unambiguous. It captured and contained an important aspect of human identity, but in a very artificial fashion. In retrospect, perhaps the definition was always just too perfect to go without dissent?

While adults such as Williams began to challenge the false clarity of the scientific account, the global ‘neurodiversity’ movement took shape online, where internet activists on new forums attacked the notion that autism was an ‘illness’ or ‘impairment’. Jim Sinclair, the American co-founder of the advocacy group Autism Network International, argued that most of the population were just ‘neurotypical’, and that wider society should not ‘treat’ autistic people as sick or abnormal. Judy Singer, an Australian sociologist and autism advocate, said that those with neurological difference should claim the label ‘neurodiverse’, and form a new political group equivalent to those aligned by class, race or gender. These activists said that there were positive aspects to the identity, and that having autistic members was good for wider society. Approaches to autism, they argued, should not be about ‘eliminating’ it, but rather about making society as a whole more inclusive.

These debates point to an apparent paradox in our understanding of autism: is it a disorder to be diagnosed, or an experience to be celebrated? How can autism be something that must be ‘treated’ at one level, but also praised and socially accommodated at another? Many people in the neurodiversity community say that autism is just a natural variant in the human condition. But should autistic individuals have the same legal rights as everyone else? Or are their needs different, and if so, how? If we are invited to be skeptical of clinical approaches, how can we decide who qualifies for additional support? The fundamental conundrum is that, over its troubled history, views have shifted about whether autism is part of a narrative description of an individual’s developing life, or whether it’s a measurable category that others have the right to count, demarcate and define.

It is tempting to see human psychology as simply a feature of existence, but in fact it has both a history and a politics. Historians have long argued that diagnostic categories are imbricated in their specific social and political settings. For example, the diagnosis of ‘hysteria’ was produced in the context of 19th-century misogynistic investigation. The idea of ‘intelligence’ was crystallised only as part of a sustained political project to revolutionise the education system at the start of the 20th century. The concept of ‘mental deficiency’ was formulated in the context of mid-20th-century eugenic institutions and concerns. This is not to claim that there are no biochemical correlates to any condition. However, the historian’s interest is not in either invalidating or proving the existence of any category; it is more about understanding how diagnostic tools get employed to direct resources and attention to certain areas at certain times.

The truth is that it is incredibly difficult to pin down the definition of ‘autism’. Ever since the early 20th century, the theory of autism has been a device for thinking through the early stages of psychological development, and it has been plagued with controversy about its status for just as long. It is no coincidence that the very idea of neurodiversity arose from specific, targeted criticisms of the autism diagnosis, a category that served its own role in the social and political structures of the past. Neurodiversity advocates are now legitimately reclaiming the autism label and making it their own, taking power away from psychologists and psychiatrists. Before we address contemporary concerns, it is worth reflecting on how we arrived at this juncture.

In the mid-20th century, a major fault-line appeared between psychoanalytic approaches to autism, and the strategies of statistical psychologists. Between 1910 and 1950, the most significant attempts to categorise, carve up and understand child development came in two distinct forms: psychoanalysis and intelligence-testing.

Child psychoanalysis built on Sigmund Freud’s idea that the trajectory of a person’s life was driven by instincts and desires that took root in childhood, and could be analysed via individual testimony and case histories. Intelligence-testing built on the French psychologist Alfred Binet’s attempt to quantify and order human capacities and capabilities. These influential human sciences had very different goals. Psychoanalysis gave voice to the unique and idiosyncratic experiences of ‘the individual’, at the same time that capitalism was thriving, and family ties were losing power and influence. Intelligence-testing, meanwhile, served the bureaucratic objective of categorising and sorting out child types for an ever-expanding education and institutional-care system.

The attempt to quantify autism radically transformed the meaning of the term

Against this backdrop, the Austrian-American psychiatrist Leo Kanner is commonly credited with coining the term ‘autism’ in 1943. However, autism was, in fact, described in young children long before this. The Swiss developmental psychologist Jean Piaget described many instances of ‘autism’ in his work in the 1920s, and went into great detail to define it as the first form of ‘thought’ in early infancy. Piaget and his contemporaries considered autism a kind of ‘symbolic’ thinking, in which visual imagery and hallucinations dominated an individual’s thoughts, and affected the ability to think logically and relate socially. Kanner’s understanding was similar; he drew from psychoanalysis to argue that autistic children thought in a bizarre, fantastical way that made it difficult to relate to others. Kanner did try to claim autism as a specific ‘syndrome’ – but his efforts were frequently challenged by other specialists, who thought he was describing a kind of ‘amentia’, ‘mental deficiency’, or low intellectual capacity. In the 1940s and ’50s, the definition of autism was hotly contested, and the only thing that psychological specialists had to support their position were case descriptions of individuals.

After the Second World War, both Freudian psychoanalysis and Binet’s intelligence classifications began to look increasingly shaky. Pre-war narratives of ‘progress’ had been shattered, and Nazism made social divisions based on human ‘types’ politically noxious. Autism research of the 1960s responded by creating a whole new paradigm of human development, one that was more suitable to the demands of the post-war social climate and a radical reorganisation of state services. Alongside the creation of the welfare state, psychological specialists made the first attempts to classify autism as a universal diagnostic category that could be recognised around the world. But in order to enable this universal definition, they stopped using case descriptions, and instead started counting – using the techniques of intelligence-testing and quantification to capture the complexity of ego-development and social interaction.

In the mid-1960s, the British psychiatrist John Wing, husband of Lorna Wing, supervised a South African colleague, Victor Lotter, to create the first epidemiological study of autism anywhere in the world. Lotter made his way to the unimpeachably ‘normal’ county of Middlesex in the United Kingdom, and began to count all the children with autism who lived there. He included children based on a list of behaviours such as ‘jumping’, ‘flapping’, ‘toe walking’, ‘solitary’, and ‘behaves as if deaf’. One of the leading child psychiatrists in the UK at the time, Mildred Creak, had said that it was impossible to create a definitive list of behaviours for the purposes of diagnosis; an inability to form relationships stood at the heart of the condition, and this was not measurable. However, Wing and Lotter insisted that it was possible to standardise autism in this way and, moreover, the fact that they could count the children whom it affected would prove them right.

Wing and Lotter’s project to measure autism was part of a larger push to quantify children’s mental states. It was also a criticism of reasoning that relied on psychoanalytic case descriptions and narratives to make claims about psychological truth. Most importantly, the attempt to quantify autism radically transformed the meaning of the term. Whereas in the early 20th century ‘autism’ referred to states of excessive fantasy, hallucinations and vivid dreams, the quantifiable ‘autism’ of the 1960s came to mean the exact opposite of what it had meant previously. It was only after 1960 that autism, as a diagnosis, came to be seen as an impairment, lack or absence, of thought. This is the model of autism that is coming under fire from neurodiversity advocates today; yet it had its own important social and political work to do in the past.

What many people don’t know is that the rise of the autism diagnosis went hand in hand with a certain reforming zeal for social-scientific measurement and progressive change. The critique of the psychoanalytic method got caught up in this push. Before the growth of the autism diagnosis, it largely fell to psychoanalysts to monitor children’s psychological growth. These practitioners were trained to see development as a fluid and variable process, and they thought in terms of individual desires and needs, not clear-cut categories of difference. However, psychoanalysts were not trained to deal with large groups of children who had been crudely classed as ‘mentally deficient’ or ‘ineducable’, and who had primarily been treated within long-stay institutions or ‘subnormality hospitals’ in the early part of the 20th century.

In the early 1970s, the UK, the United States, and many other Westernised countries went through a process of closing down these large, state-run institutions. Therefore, when all children entered the education system, there was a distinct lack of expertise in understanding their individual developmental needs. In the UK, world-renowned psychoanalysts such as John Bowlby and Donald Winnicott had focused on the role of the mother, examining the separations that had occurred during the Second World War. But the new generation of 1960s autism psychologists were concerned to see psychoanalysts apparently blaming women for the problems of their children; perhaps, they thought, the issues were constitutional.

Of course, many psychoanalysts were able to grasp the complex interplay between genetic and environmental factors, as were those advocating for the autism diagnosis. However, by the 1970s, it was clear that giving a child an autism diagnosis was a surefire way to ensure that this child received special educational services and support. The voices of those who had resisted the category on the grounds that it was clumsy and crass were silenced, and accused of propagating myths of mother-blame. Couldn’t they see that the label was vital to social progress for people who had been marginalised?

In this way, the autism diagnosis became the beacon of a new kind of inclusion, and a gesture of generosity towards psychological difference. Its impact was remarkable. In the UK, which set the global standard of autism, Lorna Wing and the National Autistic Society used it to repeatedly campaign to the UK government for specific services for those diagnosed. From the early 1960s, they argued that the standard education system did not cater to autistic children, and that new schools and special services needed to be established.

Of course, this was a political argument, driven by political need – yet, like all good social scientists of the time, they wanted scientific proof that such political moves were necessary. In an attempt to fully measure the needs of this newly definable population, Wing and her collaborator, the clinical psychologist Judith Gould, conducted a statistical study of the number of children in a population sample who had ‘impairments in social interaction’. This study, published in 1979, has been used as the benchmark for almost every epidemiological study of autism worldwide since. Wing and Gould argued that one could measure social ‘capacity’ in children, in a similar way that one would measure intellectual capacity, and use this as a convenient measure for the categorisation of all children. Autism was then defined as part of a wider ‘continuum’ or ‘spectrum’, into which social ‘impairments’ could be grouped. This was the birth of the ‘autism spectrum’.

Autism grew up as resistance to a neoliberal agenda, a tool for sheltering people from global capitalism

It’s ironic that the expansion of autism as a medical diagnosis was powered via the growth of studies that weren’t particularly interested in refining it as a medical category; rather, they viewed it as a tool by which the state could reliably measure social ‘impairment’. Yet both medical researchers and government advisors took autism very seriously, and the diagnosis was used increasingly in education and healthcare settings around the world. The 1987 edition of the Diagnostic and Statistical Manual – often referred to as the psychiatric bible – drew from Wing and Gould’s definition of autism almost word-for-word.

As the diagnosis became established, the label became a marker of biological difference associated with ideas of ‘handicap’, ‘disability’ and ‘disorder’. It was frequently described as an impenetrable puzzle. In fact, the National Autistic Society featured a person trapped in a puzzle piece as its logo for many years, and numerous campaigns depicted autistic children as being locked away or trapped in some way. The ‘impairment’ model was always presented as specific and measurable, but there was often an underlying sense that it must be more complicated than it seemed.

Yet autism, as both a medical condition and a political catalyst, was ultimately a phenomenal ‘success’. The diagnosis was by no means flawless, but it served a vital role in reorganising social services, and advancing the rights of individuals who needed specialised social care. By the 1990s, unique educational and social services had been established around the world, and new approaches to integrating children within mainstream education had taken hold. By the 2000s, diagnoses of autism began to skyrocket in the UK and elsewhere. A growing awareness of autism, and the establishment of the ‘spectrum’, were among the biggest factors in this ascendancy.

The diagnosis gained a foothold at the end of the 20th century not only because it ensured special educational services. It also slotted neatly into new models of social and economic liberalism in the 1980s and ’90s that aspired to dismantle systems of social welfare. Neoliberalism has arguably led to the ‘death of the social’, as the British sociologist Nikolas Rose notedin 1996, because it encouraged individuals to engage in a market for welfare products in order to boost their own advantage. In the case of autism, the diagnosis protected certain people from the mass demolition of social welfare systems in the 1980s.

It should be no surprise, then, that the most unwavering support for the autism diagnosis occurred under the UK prime minister Margaret Thatcher and the US president Ronald Reagan. It provided a kind of protection for citizens who were considered ‘impaired’ in their social function, and thus entitled to support in a way that others were not. In other words, autism as we know it today grew up as a kind of resistance to a neoliberal agenda, a tool for sheltering certain people from the growing challenges of global capitalism. And in the years since, it has become an important means of affirming identity.

Autism has a history. So just how far have we come in our understanding of it? In many ways, the modern neurodiversity movement is revolutionary. The fact that it is formed primarily of people who have either received a diagnosis, or who self-identify with autism, is an important and persuasive validation of its aims. When Sinclair proudly told the parents of autistic children in 1993: ‘Don’t mourn for us,’ it galvanised many who were fed up with being seen as pitiable and ‘impaired’. Since then, the movement has grown exponentially. The principle of neurodiversity is widely recognised as a legitimate model for thinking about human difference, even as researchers continue to search for ‘cures’ and treatments.

Intriguingly, in some ways the idea of ‘neurodiversity’ represents an extraordinary revival of psychoanalytic approaches to individual development. These methods elevated personal narratives as the only means to access human truth, and preceded psychiatric attempts to contain autism as an ‘impairment’ or ‘disorder’. Interestingly, the discussions in online forums today don’t look too different from all-out celebrations of psychoanalytic reasoning. Online dialogues about autism and gender contain echoes of psychoanalysts’ interests in the relation between sexuality and development, albeit in new and innovative forms. What we’re witnessing, it seems, is a shift away from standardising and statistical models to a more expansive appreciation of human difference. This is a fantastic idea, as long as our political and social structures can adapt to support it.

As we saw, the idea of ‘neurodiversity’ came about as a critique of the definition of autism that arose in the 1960s and solidified in the 1980s. However, for all its flaws, the ‘impairment’ approach was also an engine of social inclusion and a buffer against neoliberal cuts to state spending. Dismantling the impairment framework has the potential to create new problems.

Whether autism is seen as a ‘disorder’ or a source of value is hugely consequential in economic terms

The difficult political question is this: if governments don’t use scientific criteria and diagnoses to identify people with autism, how can they judge eligibility for representation or access to special services? Autism advocates have frequently clashed with parental groups and charities that persist, they say, in presenting autistic children as ‘sick’, ‘trapped’ and ‘impaired’. Meanwhile, the neurodiversity movement offers alternatives and new models of inclusion, but also pushes for political representation for a group that’s increasingly difficult to define. And in any case, no one thrives under political agendas that don’t support universal public services or a model of ‘the social’ at all. The transformation we’re witnessing now has the potential to revolutionise public perceptions, but it also risks reducing social support if the political shift isn’t carefully handled.

Perhaps we need to think about what it would it mean to turn away from a model of social support that relied on clinical diagnoses to function? It’s here that the autism paradox could really bite. In May 2017, a news story broke that a group of National Health Service commissioners in south-west London were planning to cut diagnoses of autism in an attempt to modernise and streamline existing services. Many saw this as a euphemism for massive public-service cuts, and some observers unfairly attacked the neurodiversity movement for romanticising autism and criticising the legitimacy of the science. It is clear that we are walking a thin line in the fight for resources, and whether autism is seen as an ‘impairment’ or a source of value is hugely consequential in economic terms. In fact, the neurodiverse, scientific and parental communities are increasingly overcoming these problems in creative and productive ways, but they are not always so easy to conquer at the level of health and social care administration.

To date, most attempts to categorise human development reach a peak at which they generate more problems than they can explain. Psychoanalytic theories of ‘maternal deprivation’ reached their zenith when the political model they supported was no longer viable. The same thing happened with post-war intelligence-testing, so the idea of ‘intelligence’ had to be recast. Autism research in the 1960s ‘solved’ many problems of the previous generations, by finding ways to support individuals who had previously been excluded – but it also began to fail those individuals as soon as it started making population-wide claims about how autistic people were ‘impaired’. Autism diagnoses were the foundation of social support, but individual dignity and identity were lost in the process. Many neurodiversity advocates are now clawing back these rights to tell individual stories. Yet this activism takes place against an unfortunate backdrop of grave threats to the public services that support autistic individuals.

Is there really an autism paradox? Or is this actually a paradox of human difference, and of what it means to delineate human types while also offering people the best opportunity to thrive. If we are to think creatively about how to identify difference without stigmatising it, it pays to think historically about how autism research got us to this point. Such history offers a rather humbling lesson: that it might very well be impossible to measure, classify and quantify an aspect of human psychology, without also muting attempts to tell the story differently.

Exposure to Ozone Kicks Up Chances of Autism 10-Fold in at-Risk Kids

“The increase in risk is striking.”

Having a higher number of copies of genes has been shown to raise the risk of a child developing autism, as has early exposure to various pollutants in the mother’s environment.

Researchers have now shown that when these two factors are combined, an individual has 10 times the chance of developing the condition, demonstrating the importance of stepping beyond the question of nature versus nurture and looking at the bigger picture.

The analysis by a team led by scientists from Pennsylvania State University is one of the first to examine genetic differences across the whole genome in conjunction with environmental factors surrounding an individual as it develops.

Autism Spectrum Disorder (ASD) covers a variety of behaviours involving social interactions and communications, presenting with degrees of severity.

“There are probably hundreds, if not thousands, of genes involved and up until now – with very few exceptions – these have been studied independently of the environmental contributors to autism, which are real,” says Penn State researcher Scott B. Selleck.

Those genes can affect numerous functions in the brain, potentially affecting a bunch of different neurological circuits that influence anything from social interactions to eye contact.

The question on just how heritable autism is has long been debated, with some early twin studies estimating as much as 90 percent of the condition is the result of genes passed down from parents.

Other researchers suggest the environment shares more of the blame, with the consensus now hovering around 50 percent genetics, 50 percent environment.

This new study shows how complicated the story just might be when it comes to such complex neurological conditions.

“Our team of researchers represents a merger of people with genetic expertise and environmental epidemiologists, allowing us for the first time to answer questions about how genetic and environmental risk factors for autism interact,” says Selleck.

Research involved 158 children with autism who were selected through a previous study, and 147 controls who were closely matched in age and demographic.

The team examined a feature called copy-number variations (CNVs); sequences that have been duplicated at least once to form repeats through the genome.

Previous research on individuals with ASD has already shown a higher tendency for their genomes to contain more CNVs than the rest of the population, and that the more of these repeats an individual has, the lower their measures of social and communication skills.

In addition to the subjects’ genetic variations, the team analysed their family’s residential history, comparing the addresses with data on air quality from the US Environmental Protection Agency (EPA) Air Quality System.

“This allowed us to examine differences between cases of autism and typically developing controls in both their prenatal pollutant exposure and their total load of extra or deleted genetic material,” says researcher Irva Hertz-Picciotto from University of California Davis.

Each risk factor on its own – larger numbers of CNV and high amounts of particulate in the air – was found to elevate the risk of autism, in line with previous research.

Once they started to combine the figures, one result in particular stood out.

Ozone, as one of the pollutants examined, hasn’t previously been considered a hugely significant risk factor for ASD.

The gas, consisting of three oxygen atoms, is formed from other pollutants such as nitrogen oxides and volatile organic compounds, which react in the presence of sunlight. Those molecules are generally released in vehicle exhaust, industrial processes, and electrical utilities.

The effect of ozone on those with high CVN numbers ramps up the chances of developing the condition, more than either would account for on their own.

Compared with those the bottom quarter of CNV numbers, and the bottom quarter of ozone exposure, there is a ten-fold risk of developing autism for those in the top quarter for both measures.

“This increase in risk is striking, but given what we know about the complexity of diseases like autism, perhaps not surprising,” says Selleck.

While the study didn’t analyse the cause, the researchers did speculate that ozone could increase the number of reactive oxygen species, such as peroxides, that are known to cause stress to cells and damage DNA.

It’s possible that having more variations of genes responsible for certain autism-related functions could open individuals to more oxidation damage.

The researchers acknowledge their sample size was relatively small, and since ozone occurs in conjunction with numerous other pollutants, there could be confounding factors that need to be pulled apart. It also doesn’t point at a single cause, instead hinting at one way a number of key genes could be affected by the environment.

Still, given the complexities of the condition, the study does show how variables we’ve previously dismissed might be working in combination.

“It demonstrates how important it is to consider different types of risk factors for disease together, even those with small individual effects,” says Selleck.

Egyptian study confirms autism is caused by mercury in vaccines

Ever heard of metabolic brain disease? A team of nine scientists from top Egyptian medical schools and universities may have just confirmed that one in every 50 American children has it, and its primary cause could be mercury in vaccines.

How was this determined? Exposure to mercury can be measured by analyzing children’s urinary porphyrins – excreted organic compounds that act as biomarkers for mercury toxicity. Not only does the presence of mercury in urine and blood expose the long-known link between metabolic brain disease (autism) and vaccines, but the severity of autism (and its broad array of symptoms) is directly correlated with the levels of exposure to this known neurotoxin. Yes, you read that correctly.

Image: Egyptian study confirms autism is caused by mercury in vaccines

To put the nails in the coffin for any doubters or skeptics, of the 100 children studied, the 40 with autism spectrum disorder (ASD) had significantly higher mercury levels than their non-autistic siblings and the other healthy children in the study. In addition, the children with the most severe versions of metabolic brain disease revealed the highest levels of mercury exposure. For years and years, natural health enthusiasts have been screaming about the dangers of vaccines and mercury-loaded dental fillings, and now the truth comes out – and scientifically proven at that.

Disordered urinary porphyrin metabolism – the smoking gun of the autism–mercury connection

Six American studies have linked autism to mercury exposure by analyzing disordered porphyrin metabolism in autistic kids, but the mass media has been prohibited from publishing them or even discussing them at all because their sponsors are Big Pharma conglomerates. That is why you never hear anything about them on television, in newspapers or on mainstream media websites.

Another study published this past June was carried out by an international team of scientists who measured pro-inflammatory neuro peptides that indicate the presence of mercury in blood. The results showed a “positive linear relationship between mercury levels and the severity of autism symptoms.”

The previously mentioned study done by the scientists from Egyptian medical schools included analyzing the mothers of autistic children who had multiple dental “silver” amalgams (mercury-loaded fillings), which the scientists said most likely contributed to the children’s body levels of mercury. You could call these the “silver bullets” from the “smoking gun.”

Special note: Ethyl mercury in thimerosal (used for vaccines, especially flu shots) is at least 50 times as toxic to human tissue as the methylmercury in amalgams and fish, and can prove to be twice as persistent in the brain. When mercury is injected into the blood and muscle tissue, it bypasses normal protective human filters, such as the lungs, digestive organs and the skin. This is also how mercury can cross the blood/brain barrier.

It’s not just mercury causing metabolic brain disease, but also lead and aluminum

In 2015, a paper published in Behavioral Neurology by a group of researchers from the National Institute of Standards revealed results of a study of 100 autistic children with significantly high levels of mercury, lead and aluminum that may have resulted from environmental exposure. Aluminum is often also found in vaccines, and lead has been revealed to be in most U.S. tap water, sometimes at alarming levels (think of Flint, Michigan, here).

Detoxification by chelating agents could play a major role in improving the lives and mental and social capacities of children afflicted with metabolic brain disease. Remember, autism is a neurodevelopmental disorder that appears during infancy or childhood (not at birth), with a broad array of communication and learning impairments, from mild to moderate to severe. It is rarely, if ever, inherited, but rather brought on by an overload of neurotoxins either consumed, injected or ingested from environmental factors, or all of the above.

Realize the CDC has formally admitted to covering up the autism-mercury-vaccine link

Mercury is the most toxic non-radioactive element on earth and the second most poisonous element known to mankind, second only to uranium, yet, for some reason, it’s still used in vaccines as a preservative, even when there are several other options that are not toxic that would do the same job. It is scientific fact that human brain neurons permanently disintegrate in the presence of mercury within one hour of exposure. Thimerosal is a mercury containing preservative (about 50 percent mercury), and the World Health Organization warned about its use in vaccines way back in 1990.

Plus, mercury is a cumulative poison, meaning the body has difficulty removing it and it accumulates significantly over time. Some infants receive more mercury in one day than the WHO recommends as a maximum for adults for three months worth of exposure. One scientific fact most Americans do not know is that aluminum (listed as aluminum phosphate) in vaccines greatly increases the toxicity of mercury (listed as thimerosal), therefore caution about minimum mercury tolerance is severely underestimated.

Does the CDC mix vaccines with aluminum and mercury in combination? Absolutely. The Diptheria and Tetanus “toxoid” inoculations have “trace” amounts of mercury combined in the same vaccine with aluminum. What’s in the whooping cough vaccine? Aluminum phosphate and formaldehyde. Mix that aluminum phosphate with a flu shot laced with mercury and measure the level (potency) of mercury and see what that does to the central nervous system and the brain. Remember, aluminum makes the vaccine more “powerful.”

Since 2002, the CDC has been covering up the link between autism and the MMR vaccine. Dr. William W. Thompson, a senior scientist and epidemiologist at the US Centers for Disease Control and Prevention (Immunization Safety Branch) confessed to the vaccine-autism connection in a confession letter (an email Dr. Thompson wrote to officials at CDC via his attorneys). After being silent about the cover-up for over a decade, Dr. Thompson said he could no longer stand to look at parents whose children were suffering from autism and keep silent about the whole conspiracy, so he blew the whistle.

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For Those With Autism, Eye Contact Isn’t Just Weird, It’s Distressing

For many people with autism, avoiding eye contact isn’t a sign that they don’t care – instead, it’s a response to a deeply uncomfortable sensation.

Researchers have discovered a part of the brain responsible for helping newborns turn towards familiar faces is abnormally activated among those on the autism spectrum, suggesting therapies that force eye contact could inadvertently be inducing anxiety.


Autism spectrum disorder is a term used to describe a variety of conditions that make communicating and socialising a challenge, and is often accompanied by restricted and repetitive behaviours.

A defining characteristic of autism spectrum disorder is a difficulty in making or maintaining eye contact, a behaviour that not only makes social interactions harder, but can lead to miscommunication among cultures where eye contact is taken as a sign of trust and respect.

Those with the condition typically claim it feels “unnatural” or express anxiety over making eye contact, but psychologists have been uncertain if the discomfort is sensory or stems from conflict over the social importance of looking a person in the eye when you communicate.

Previous research suggested the latter, but a team of neurologists from the Massachusetts General Hospital in the US suspected the problem might be over-sensitivity of the parts of the brain responsible for emotional perception.

In part, they were persuaded to search for a neurological cause by reports from those diagnosed with the condition, who claimed looking into the eyes of others was stressful, that it “feels yucky“, or even that “it can actually make my eyes burn or water while doing it.”

Specifically, the researchers looked to a part of the brain called the subcortical system, a variety of structures that integrates information from the outer cortex with the peripheral senses to give rise to movements and other behaviours.

Within this system are pathways that carry visual information from the eyes to parts of the brain that stimulate emotions, and helps newborn babies recognise and turn to familiar faces and influence a range of other social actions.

Previous research on whether this part of the brain was overactive in people with ASD produced mixed results, possibly over confusion whether subjects actually looked at the eyes in the faces used in the studies.

To address this conflict, the researchers used functional magnetic resonance imaging (fMRI) to measure differences in the activation of the parts of the subcortical system responsible for processing faces in 23 adult and child volunteers with ASD and 20 controls.

The participants all received scans as they watched two versions of clips of faces displaying emotions such as fear, anger, or happiness; one normal, and another with a red cross between the eyes to attract attention.

While the face-recognition subcortical region was active in both groups, the areas were highly active in those with ASD when they were forced to focus around the eye region, especially when the faces expressed fear.

“The findings demonstrate that, contrary to what has been thought, the apparent lack of interpersonal interest among people with autism is not due to a lack of concern,”says lead researcher Nouchine Hadjikhani.

“Rather, our results show that this behaviour is a way to decrease an unpleasant excessive arousal stemming from overactivation in a particular part of the brain.”

The results are interesting, however shouldn’t be overstated. For one thing, the researchers admit that without using eye-tracking technology they couldn’t match the time spent looking at the eyes with the duration of overactivation in the subcortical system.

They also hadn’t matched the subjective claims of uncomfortable sensations made by individuals with their particular brain activity, leaving room for doubt.

But the research is enough to force a rethink on the consequences of coercing children with autism to practice making eye contact.

“The findings indicate that forcing children with autism to look into someone’s eyes in behavioural therapy may create a lot of anxiety for them,” says Hadjikhani.

Instead, she suggests slow habituation towards eye contact could be a more appropriate way to handle eye contact in the long run without causing stress.

Understanding that eye contact can induce a physical discomfort and isn’t simply a case of learning to fake it could also help others in society understand the cultural complexities of facial expressions, and accept not everybody is being shifty as they avoid meeting your gaze.

Source:Nature Scientific Reports.