Psychologists argue mental illness is less about genetics and more about life experiences


Image: Psychologists argue mental illness is less about genetics and more about life experiences

It wasn’t long ago scientists believed that most mental illnesses, including autism, major depression, bipolar disorder, schizophrenia and attention deficit hyperactivity disorder (ADHD), were a result of genetics, but that is beginning to change.

Psychologists are now warning that too much money is being spent on researching the genetic and biological factors of mental illness, instead of understanding what they say is the real cause: “social crises such as unemployment or childhood abuse,” according to the Telegraph.

If this theory is in fact true, that would mean the medical establishment (Big Pharma, hospitals, and doctors) is drugging people with harmful psychotropics simply because they’re going through a tough time – a situation or condition that could probably be resolved through safer and more effective treatments, like meditation, exercise, a strong support network, and talk therapy.

Examining the triggers of mental illness

The Telegraph writes that “while there has been some success in uncovering genes which make people more susceptible to various disorders, specialists say that the true causes of depression and anxiety are from life events and environment, and research should be directed towards understanding the everyday triggers.”

Yet, the Medical Research Council (MRC), a governmental agency that coordinates and funds medical research in the UK, has blown hundreds of millions of dollars investigating the biological causes of mental illness. The same is true for research done in the U.S..

A few years ago, the National Institute of Health funded a study that sifted through thousands of genetic markers searching for genetic commonalities among patients with the most common mental illnesses: autism, major depression, bipolar disorder, schizophrenia and ADHD.

Researchers said they found genetic variations associated with the five most common disorders. But Peter Kinderman, Professor of Clinical Psychology at the University of Liverpool, says “genes are involved, but not very much.”

Kinderman told BBC Radio 4’s Today program:

“Of course every single action, every emotion I’ve ever had involves the brain, so to have a piece of scientific research telling us that the brain is involved in responding emotionally to events doesn’t really advance our understanding very much.

“And yet it detracts from the fact that when unemployment rates go up in a particular locality you get a measurable number of suicides.

“It detracts from the idea that trauma in childhood is a very very powerful predictor of serious problems like experiencing psychotic events in adult life, so of course the brain is involved and of course genes are involved, but not very much, and an excessive focus on those issues takes us away from these very important social factors.”

Why won’t the medical establishment fund mental illness studies outside of genetic factors?

Though this opinion is becoming increasingly more accepted, the medical establishment appears reluctant to divert funding away from studies on genetics and towards learning to understand the triggers of mental illness.

“It’s a tragedy actually. The UK Medical Research Council is one of the biggest funders of medical research in the UK but if you look at the things that they fund, by far the majority are things like brain scanners or gene sequencing machines, almost none of it is going towards understanding psychological mechanisms or social circumstances by which these problems develop,” said Professor Richard Bentall, of Liverpool University. “It is impossible to get funding to look at these kind of things.”

So why is the medical establishment dead set on only researching the genetic causes of mental illness?

Well, if it is accepted that the majority of mental illness is a result of stressful situations and events… that would imply the condition is much more recoverable as opposed to someone who is purportedly biologically wired with it.

In other words, drug companies couldn’t push pills as easily on individuals suffering temporarily, say from lost job or a divorce. But if a person is born with mental illness, that’s essentially justification for a life on psychotropic drugs.

The last line of the Telegraph’s report basically proves our theory: “So if by doing studies like this we can strongly implicate one area of biology it gives a new lead for drug companies to try to develop new therapies.”

DISEASE AND DEFECTIVE GENES.


In the mainstream media (and the popular consciousness programmed to consume it) defective genes are spoken about as if they were “disease time bombs,” fatalistically programmed to go off inside of us, thanks to flawed genetic contributions of our ancestors. And yet, despite common misconceptions, monogenic diseases, or diseases that result from errors in the nucleotide sequence of a single gene are exceedingly rare.  In fact, less than 1% of all diseases fall within this category…

Following the completion of the Human Genome Project (HGP) in 2003 it is no longer accurate to say that our genes “cause” disease, any more than it is accurate to say that DNA is sufficient to account for all the proteins in our body. Despite initial expectations, the HGP revealed that there are only 20,000-25,000 genes in human DNA (genome), rather than the 100,000 + believed necessary to encode the 100,000 + proteins found in the human body (proteome).

ADN_animationDid you follow that? There are not even enough genes in the human body to account for the existence of the basic protein building blocks that make it possible, much less explain the behavior of these proteins in health and disease states!

The “blueprint” model of genetics: one gene -> one protein -> one cellular behavior, which was once the holy grail of biology, has now been supplanted by a model of the cell where epigenetic factors (literally: “beyond the control of the gene”) are primary in determining how DNA will be interpreted, translated and expressed. A single gene can be used by the cell to express a multitude of proteins and it is not the DNA itself that determines how or what genes will be expressed.

Rather, we must look to the epigenetic factors to understand what makes a liver cell different from a skin cell or brain cell. All of these cells share the exact same 3 billion base pairs that make up our genetic code, but it is the epigenetic factors, e.g. regulatory proteins and post-translational modifications, that make the determination as to which genes to turn on and which to silence, resulting in each cell’s unique phenotype.

Moreover, epigenetic factors are directly and indirectly influenced by the presence or absence of key nutrients in the diet, as well as exposures to chemicals, pathogens and other environmental influences. Thoughts and emotions also play a role in how these epigenetic factors are articulated, indicating that the flow of genetic information, once thought to be strictly vertical (passage of genetic information from one cell or individual organism to its progeny by conventional heredity mechanisms), also flows horizontally and bi-directionally, opening the door back up for the human soul to return to biological science, having been reduced to a mere “ghost in the machine,” since René Descartes (1596-1650), the French philosopher and mathematician, split body and soul asunder, almost five centuries ago.

In a nutshell, what we eat and what we are exposed to in our environment directly affects our DNA and its expression.

Within the scope of this new perspective even classical monogenic diseases likeCystic Fibrosis (CF) can be viewed in a new, more promising light. In CF many of the adverse changes that result from the defective expression of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene may be preventable or reversible, owing to the fact that the misfolding of the CFTR gene product has been shown to undergo partial or full correction (in the rodent model) when exposed to phytochemicals found in turmeric, cayenne, and soybean.

Moreover, nutritional deficiencies of seleniun, zinc, riboflavin, vitamin e, etc. in the womb or early in life, may “trigger” the faulty expression or folding patterns of the CFTR gene in Cystic Fibrosis which might otherwise have avoided epigenetic activation. This would explain why it is possible to live into one’s late seventies with this condition, as was the case for Katherine Shores (1925-2004).

The implications of these findings are rather extraordinary: epigenetic and not genetic factors are primary in determining disease outcome. Even if we exclude the possibility of reversing certain monogenic diseases, the basic lesson from the post-Genomic era is that we can’t blame our DNA for causing disease. Rather, it may have more to do with what we choose to expose our DNA to, and even more surprisingly: how we choose to think and feel about our embodiment.