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Autism and the SSRI connection

Reading time: 6 minutes

SSRI antidepressants taken during pregnancy are amplifying the effects of inflammation in the depressed mother-to-be to increase the risk of autism in the child, major new research has discovered

It was only 10 years ago that biologists were describing the fetus as a fortress, immune to anything the mother might eat, drink or inhale. Today, we know different. A mother who smokes or drinks alcohol can affect her baby, and the unborn child’s healthy development can also be impaired by malnutrition, obesity, infection and autoimmune conditions.

These recent discoveries have unlocked billions of dollars of research funding as scientists have scrambled to understand the inexorable rise of autism in children and its possible link to toxins crossing the placenta. In the US, the incidence of autism is increasing by around 24 percent every two years, and America’s Centers for Disease Control and Prevention (CDC) has estimated that one in 44 eight-year-old boys has the condition, which represents 2.3 percent of the boys of that age.

Although it’s now known that toxins can breach the placenta, most scientists still hold to the theory that genetics is usually responsible for autism. Studies of twins have discovered that 70 percent are likely to be autistic, which does support the genetics theory, and other studies have identified genetics as a major factor in 30 to 80 percent of autistic children.

But the genetics theory can’t explain the explosion in autism in recent years, a phenomenon that seemed to start around 30 years ago, although the rise can, in part, be explained by a greater understanding of the condition and its complexity of symptoms, along with better screening programs.

It’s the drugs

Ever since it was recognized that the fetus can be affected by toxins, prescription drugs have been in the frame as a likely suspect. Although the theory that the MMR vaccine might be responsible has been roundly discredited by scientists, the suspicion about a link to pharmaceutical drugs—and antidepressant SSRIs (selective serotonin reuptake inhibitors) in particular—hasn’t gone away. It’s been fueled by the tantalizing observation that the rise in autism coincided with the introduction of SSRIs in 1990.

Up to 20 percent of pregnant women have depression, and 80 percent of these are given an SSRI, considered the safer option among antidepressants. In the US, around 3.6 million children are born every year, suggesting that around 570,000 of them are exposed to SSRI toxicity while in the womb—although we still don’t know how many of them go on to develop autism. Once the mother starts taking an SSRI, the maternal serum starts to change until eventually 80 percent of it contains the drug.

Most researchers accept that SSRIs are a factor in autism’s development, but the results have always been diluted by the possibility that the depression’s inflammation, rather than the antidepressant, is the major cause, or, as researchers put it, there are “confounding factors” that muddy the waters.

The whammy doubles

But it’s not that either the drug or the depression raises the risk of autism, but that both work synergistically, as major new research has discovered. The study is the first to track the biological course of the SSRI as it reaches the placenta, and the researchers have found that inflammation, a common feature of depression—as well as viral and bacterial infections—is amplified by the SSRIs. This toxic mix is affecting the neurodevelopment of the fetus.1

Researchers at the University of Virginia carried out a series of experiments on laboratory mice, who were given water with Prozac (fluoxetine), one of the most celebrated SSRIs. The pregnant mice were given a viral infection to create an inflammatory response, and some were also given the SSRI.

What happened next was extraordinary. The maternal fetal interface (MFI), which communicates with the biological processes outside the womb, started to respond to both the inflammation and the drug—at the expense of the fetus’s healthy neurodevelopment.

“Even brief disruption of the delicate maternal fetal interface milieu has the potential to alter nutrient, waste and gas exchange with the developing embryo which may have severe consequences,” the researchers say.

Serotonin (5-HT) isn’t only the feel-good chemical in the adult brain; it also plays a key role in the fetus’s neurodevelopment, “critically influencing the brain structure and function of the developing fetus,” say researchers from the School of Public Health in Tel Aviv, and so the drugs, which target the chemical, could be interfering with this vital process.2

The Virginia researchers agree. Inflammation on its own alters serotonin levels, and so too do the SSRIs, and the combination of the two creates a different response again. “We found that mothers who encountered an immune challenge during pregnancy showed a totally different signature in the placenta when they were on SSRIs compared to mothers who weren’t,” said Kristine Zengeler, one of the researchers.

Not so bad

Before the study was published, researchers had reckoned that SSRIs represent only a small risk.  One study estimated that the drugs were responsible for just 1 percent of autistic babies. A research team from the University of Bristol in the UK compared 4,429 autistic children to a group of 43,277 non-autistic children of a similar age; a history of maternal depression increased the risk by 50 percent, and some of those women were also taking an SSRI. But correlation doesn’t establish cause, the researchers say, and depression itself could be more of a factor than the drugs.3

Others didn’t see any association at all. Researchers at the Women’s College Hospital in Toronto analyzed 35,000 births in which 2,837 mothers took antidepressants, and 2 percent of their children developed autism. The rate of autism among children exposed to SSRIs was 4.51 per 1,000 person-years, and 2.03 in those who were not exposed to the drugs. Although the drugs doubled the risk of autism, the researchers said it didn’t prove that SSRIs were responsible, as other factors could be at play.4

All of this leaves the doctor between a rock and a hard place. Faced with a pregnant woman with depression, what does a doctor do? If they don’t treat the depression, inflammation can affect the fetus’s growth and cause low birth weight, and it could also disturb the mother-baby bond. But prescribing SSRIs means toxins cross the placenta and even afterward enter maternal milk, and so a breastfed baby is still being fed SSRIs after birth.

But reaching for the prescription pad—or not—may be a simplistic response to a deeper problem.  Understanding the underlying cause of depression is vital, and there are scientifically proven alternative remedies that don’t affect the fetus.

We still can’t put a number on children who are autistic due to SSRIs, but it is more significant than earlier research had suggested. We also understand the mechanism and the amplifying effect of SSRIs on inflammation, and this means doctors can no longer proffer the drugs as a safe option for depressed mothers-to-be.

The mold connection

Depression may have many causes, but one that is usually overlooked is mold.

Karen Thomas (NaturallyRecoveringAutism.com), one of the world’s leading experts on autism, whose Naturally Recovering Autism program has helped thousands of parents with autistic children, says depression can be a symptom of mold biotoxin illness, sometimes known as chronic inflammatory response syndrome, a genetic defect that affects up to 29 percent of the world’s population.

“People with this genetic defect do not have the ability to dispel toxins when exposed to mold they absorb from water damaged buildings,” she explained.

Other factors she’s witnessed include Candida infection, heavy metals, Lyme disease and parasites, and she recommends a detox program as the first step to recovery.

Treating depression naturally

Instead of prescribing an SSRI, doctors could be recommending healthier diets and alternative remedies that have been scientifically proven to ease depression.

Adding resveratrol-rich foods—such as grapes and raspberries—to the diet can alleviate symptoms, and there’s a double-whammy effect with raspberries and other berries as they also contain anthocyanins, chemicals that inhibit monoamine oxidase enzymes linked to depression. Drinking green tea can also help.1

Raw herbs and parts of plants—such as the leaves, roots, flowers and seeds—can help ease depression. Plants such as Hypericum perforatum, Crocus sativus, Camellia sinensis and Panax ginseng contain properties that help with depression.

Supplements such as omega-3 fatty acids, anthranilic acid (vitamin L1), L-tryptophan and 5-hydroxy-L-tryptophan can improve mood. Aside from supplements, mushrooms are rich in L-tryptophan, while fish, walnuts, beans and eggs contain omega-3s.2

Herbs that have antidepressant qualities include St John’s wort, as do the sedative-hypnotics valerian and melatonin, and the nootropic “smart drug” ginkgo biloba, while there’s plenty of evidence to support the use of the supplement SAMe (S-adenosyl methionine).3

Autism has become an epidemic, affecting around one in 10 children.  It also happened to Karen Thomas’s son, who was diagnosed when he was five.  She was offered an array of drugs to suppress the symptoms and to help him cope with life—but Karen wanted to find a non-drug alternative approach.

She spent years researching autism and the many therapies available—and came to understand that autism isn’t a ‘mental’ problem, it’s biological.  And, as with most problems, it all starts in the gut.

Today, Karen’s son has no signs of autism and lives a full life.

On this webinar Karen will outline what we can do if we have a child—or grandchild—who’s been diagnosed with autism.

CLICK HERE TO READ MORE, PURCHASE, OR FOR SUBSCRIBERS, DOWNLOAD FOR FREE!

References
Main Article
  1. Brain Behavior and Immunity, 2023; 108: 80–97
  2. Frontiers in Psychiatry, 2020; 11: 555740
  3. BMJ, 2013; 346: f2059
  4. JAMA, 2017; 317(15): 1544–52
  Treating depression naturally
  1. Nutr Neurosci, 2017; doi: 10.1080/1028415X.2015.1103461
  2. Psychiatr Pol 2015; 49(3): 435–53
  3. Focus, 2018; 16(1): 2–11
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