“Our research shows that mothers and fathers diagnosed with schizophrenia were about twice as likely to have a child diagnosed with autism,” said Julie Daniels of the University of North Carolina, Chapel Hill, who worked on the study. The teams research has also been confirmed by earlier studies on the same topic.

“We also saw higher rates of depression and personality disorders among mothers, but not fathers,” she said in a statement.

The study of families in Sweden with children born between 1977 and 2003 involved 1,227 children diagnosed with autism. They were compared with families of nearly 31,000 children who did not have autism. Sweden’s detailed health registry provides a wealth of data for such studies.

The association between a child’s autism and mental illness in the parent was strongest with schizophrenia, and was less powerful when the mother suffered from depression or personality disorders. There was little association between autism and parental addiction to alcohol or drugs or certain other types of mental illness.

It is now increasingly recognized that a large microbiota of chronic intraphagocytic biofilm-like and L-form bacteria (the Th1 pathogens) cause mental disorders such as schizophrenia and depression. There are a great number of patients on the Marshall Protocol who suffer from depression and their symptoms, as would be expected if the disease has a bacterial cause, fluctuate in response to antibiotic type and dosage. Many patients are reporting recovery from depression after several years of using the MP to kill the pathogens at the heart of their disease. Patients with OCD, bipolar disorder, and other mental afflictions are also reporting similar patterns.

The Chapel Hill team’s research makes it quite clear that the pathogens that cause mental illness can easily be passed down the maternal line. For one thing, the chronic bacterial forms that cause these diseases can easily survive in the egg that eventually becomes a new child. The child may also inherit bacterial-induced genetic mutations from the mother that create an environment inside the infant’s cells that is more hospitable to the Th1 pathogens. Furthermore, mothers generally pass a great deal of the bacteria they harbor to their infants during the first weeks of life – weeks when the infants’ adaptive immune systems are not yet up and running, but cuddling and close contact are common.

The fact that mothers with mental diseases known to be caused by the Th1 pathogens are in some cases twice as likely to have an autistic child confirms the fact that autism is almost surely a Th1 disease as well.

Unfortunately mainstream medicine remains largely oblivious to this reality. Daniels and team, as well as most other autism researchers, are unfortunately trying to find a connection between various genes they believe might cause mental diseases in order to come up with a hypothesis to explain the above research. Not surprisingly, no genetic connections have turned up.

The fact that the mothers of autistic children tend to suffer from a high degree of mental illness unfortunately poses a problem for many autistic children who can potentially reverse their disease by doing the Marshall Protocol – a treatment that kills the Th1 pathogens over the course of several years. Children on the MP need a strong support network and constant guidance. If the mother of an autistic child is sick with a Th1 condition herself, she will be less able to create the stable environment that an autistic child needs in order to succeed on the MP. Consequently, mothers of autistic children are prime candidates for the MP. Their circumstances enforce the reality that often, an entire family must make the effort to rid themselves of Th1 disease and successfully conquer their illnesses together.

In a study published this month in the Journal of Clinical Psychiatry, researchers at the University of Salt Lake City in Utah, reported that although boys with attention-deficit hyperactivity disorder (ADHD) appear to be more impulsive and troubled than their female counterparts, in adulthood the condition seems to have more impact in women than in men.

“We found that adult women with ADHD frequently have high levels of emotional symptoms as well as the cognitive problems found in ADHD,” Dr. Frederick W. Reimherr, head of the study, told Reuters Health.

Reimherr and colleagues analyzed data collected from two clinical trials of the medication Strattera, known generically as atomoxetine, in adults with ADHD. In all, the researchers collected information on ADHD symptoms and treatment response in 515 individuals, about a third of whom were women.

More women (75 percent) had combined-type ADHD than did men (62 percent). Women also had higher scores on measures of anxiety and depression and had more sleep problems. Poor temper control, mood volatility, and emotional over-reactivity were more common in women (37 percent) than in men (29 percent). In contrast to results of studies involving children, “women were more impaired than men on ADHD scales in our study,” the investigators conclude.

The study supports my hypothesis, namely because the researchers found that in childhood – a time before puberty and hormonal development – boys actually appeared to be more troubled by the symptoms of ADHD then their female counterparts.

But after puberty, as both women and men reached adulthood, this situation completely reversed. Later in life it was women, rather than men, who started to suffer from more severe symptoms of ADHD. This strongly suggests that differences in hormonal expression between the sexes could explain why adult women tend become more susceptible to the Th1 pathogens that cause numerous forms of cognitive dysfunction. As described in my presentation, the nuclear receptors – such as the androgen, progesterone, and estrogen receptors – fluctuate during the female menstrual cycle and during pregnancy. This is in contrast to males, in which the activity of the receptors remains fairly constant.

Since the nuclear receptors transcribe antimicrobial peptides (AMPs) that are able to kill the Th1 pathogens, the fact that their expression fluctuates in women may allow for periods when the Th1 pathogens can more easily infect a variety of tissues including those of the brain. Furthermore, since the Vitamin D Receptor is expressed in the cycling endometrium, women have more VDRs then men. Thus, they are disproportionately affected by the negative effects of VDR blockage, blockage that again leads to a decrease in AMP production and a more hospitable environment for pathogens.

I would love to see a research team (or many research teams!) track rates of Th1 disease in childhood, middle age, and then during the years after women go through menopause. My guess is that the rate of certain Th1 diseases that affect more women then men during early adulthood might even out after women become postmenopausal – a time when menstruation and pregnancy no longer cause fluctuations in nuclear receptor expression.