Schizophrenia Gene: Is This the Answer We’ve All Been Waiting For?





Susanne.Posel-Headline.News.Official- schizophrenia.gene.chromosome4.cannabis.antidepressantsSusanne Posel ,Chief Editor Occupy Corporatism | Co-Founder, Legacy Bio-Naturals

 

Beth Stevens, an assistant professor of neurobiology from Boston Children’s Hospital (BCH), co-authored a study showing the correlation between specific genes and schizophrenia.

It has been long established that chromosome 6 (C6), a region within DNA, is “the strongest genetic predictor” of a person’s risk toward developing schizophrenia; however, this new research points to other genes within this region – specifically complement component 4 (C4).

C4 is involved in immune system function.

Interestingly, after deciphering data from C4 in 28,800 post mortem brain samples from cadavers who were diagnosed with schizophrenia, and 36,000 more samples from persons that were not suffering from the disease, the researchers’ uncovered higher levels of C4 activity present in those with the disease.

Other theories as to how schizophrenia develops have to do with outside stimuli, such as exposure to death at an early age.

In 2014, researchers from the University of Manchester (UM) released a study stating that children who are exposed to death during childhood are at risk for developing psychotic disorders such as schizophrenia and bipolar.

According to the findings, only .4% of those children participating in the study developed schizophrenia and .17% developed other psychotic disorders, psychosis or bipolar states.

The researchers wrote “that the risks are highest for children who have experienced a suicide in the ‘nuclear family’ (brothers, sisters, parents).”

The conclusion of the study stated that there was “an increased risk of ‘all psychosis’ was associated with deaths in the nuclear family and risk increased the earlier in childhood the death occurred. Risks associated with exposure to suicide were higher compared with exposure to deaths from accidents which in turn were higher than risks associated with other deaths from natural causes. The largest risk was seen in children exposed ages 0-3 years and risks reduced as age of exposure increased.”

Another suspected culprit of this mental disorder is allegedly cannabis.

According to psychiatrists at the Institute of Psychiatry at King’s College London (IPKCL) there is an increased risk of developing schizophrenia with the use of cannabis.

This study claims that of the 2,082 participants, 1,011 were cannabis users and of those it was shown through genetic testing certain “people [are] genetically predisposed to schizophrenia [and] more likely to use cannabis, and to use it in greater amounts than those who had no schizophrenia risk genes.”

Organizations such as the National Alliance on Mental Illness (NAMI) helped create the perception that there is an “overwhelming consensus from mental health professionals is that marijuana is not helpful—and potentially dangerous—for people with mental illness.”

Despite recent findings, cannabis has been used to successfully treat “mental disease” and conditions such as:

• Insomnia
• Migraines
• Anxiety
• Depression
• Bipolar disorder

Cannabis has been shown to “slow down the rate of neurotransmitters in the brain” which assists in the relief of overloaded neural stimulation that leads to chronic headaches and migraines; as well as diminishes pain, nausea and ocular sensitivities.

But the most damning evidence that schizophrenia is caused by outside stimuli was produced by a Harvard School of Public Health (HSPH) and Gillings School of Global Health (GSGH) study that found “children and young adults initiating therapy with antidepressants at high-therapeutic (rather than modal-therapeutic) doses seem to be at heightened risk of deliberate self-harm.”

These antidepressants highlighted in the research included Celexa, Zoloft and Prozac.

This study showed that high doses of psychostimulants, psychotropic and mood stabilizers are regularly prescribed by psychiatrists which causes homicidal and suicidal behaviors in as little as the initial 3 months of treatment.

In their conclusion, the researchers warned that their “findings offer clinicians an additional incentive to avoid initiating pharmacotherapy at high-therapeutic doses and to closely monitor patients starting antidepressants, especially youth, for several months.”


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