People will forgive you for being wrong, but they will never forgive you for being right – especially if events prove you right while proving them wrong. Thomas Sowell
“Scientists publish only positive findings and not negative ones, and I cannot think of a single study in the vast human oxytocin literature that was replicated by an independent research group.”
This 2015 German paper with 342 references described:
“Increasing evidence that milk is not “just food” but represents a sophisticated signaling system of mammals.
This paper highlights the potential role of milk as an epigenetic modifier of the human genome paying special attention to cow milk-mediated overactivation of FTO [a gene associated with fat mass and obesity] and its impact on the transcriptome of the human milk consumer.”
The author declared “no competing interests” and “There are no sources of funding.” He presumably wasn’t pressured into writing this paper.
The paper wasn’t agenda-free, however. The main thesis was:
“Persistent milk-mediated epigenetic FTO signaling may explain the epidemic of age-related diseases of civilization.”
There were separate sections on how milk may promote:
Breast cancer
Prostate cancer
Obesity
Metabolic syndrome
Coronary heart disease
Early menarche
Type 2 diabetes
Neurodegenerative diseases
I don’t eat or drink dairy products because I’m lactose-intolerant. I coincidentally don’t have any of the diseases mentioned in the paper.
My life experiences haven’t led me to share the author’s sense of alarm, or to attribute other people’s problems to their consumption of milk products. However, more than a few problems I’ve had are things I’ve done to myself through actions or inaction that may have turned out differently if I had better information.
So I curated this article in case we’re insufficiently informed about the harmful epigenetic effects of milk. What do you think?
“The progress that has been made by studies that have investigated the relationship between depression, early trauma, the HPA axis and the NR3C1 [glucocorticoid receptor] (GR) gene.
Gene linkage studies for depression, as well as for other common complex disorders, have been perceived by some to be of only limited success; hence the focus on GWAS[genome-wide association studies]. However, even for simple traits, genetic variants identified by GWAS are rarely shown to account for more than 20% of the heritability.
Epigenetic changes are potentially reversible and therefore amenable to intervention, as has been seen in cancer, cardiovascular disease and neurological disorders.”
“Adverse maternal environments can lead to increased fetal exposure to maternal cortisol, which can cause infant neurobehavioral deficits. The placenta regulates fetal cortisol exposure and response, and placental DNA methylation can influence this function.
Placental FKBP5 methylation reduces expression in a genotype specific fashion, and genetic variation supersedes this effect. These genetic and epigenetic differences in expression may alter the placenta’s ability to modulate cortisol response and exposure, leading to altered neurobehavioral outcomes.”
The authors listed seven human studies conducted 2008-2015 “investigating interactions between methylation of NR3C1, depression and early adversity”:
“Newborn offspring exposed to maternal depression in utero had increased methylation at [a GR CpG site] as well as adverse neurobehavioural outcomes.
Unlike the majority of animal studies examining NR3C1 methylation, many types of potential stressors, sometimes at different developmental stages, have been used to represent early human adversity.
Substantial differences can be expected in the nature of stresses prenatally compared with postnatally, as well as their developmental consequences.”
Seven human studies over the past eight years was a very small number considering both the topic’s importance and the number of relevant animal studies during the period.
Is the topic too offensive for human studies? What makes people pretend that adverse prenatal and perinatal environments have no lasting consequences to the child?
“Many more studies will be needed before effects directly attributable to early life trauma can be separated from those relating to tissue type.
Although investigators have amassed a considerable amount of evidence for an association between differential methylation and HPA axis function in humans, a causal relationship still needs to be fully established.”
Factors that disrupt neurodevelopment may be the largest originators of epigenetic changes that are sustained throughout an individual’s entire lifespan.
Are the multitude of agendas that have resources thrown at them more important than ensuring the well-being of a human before and after they are born?
“Dopamine fluctuations encode an integration of RPEs [reward prediction errors, the difference between actual and expected outcomes] with counterfactual prediction errors, the latter defined by how much better or worse the experienced outcome could have been.
How dopamine fluctuations combine the actual and counterfactual is unknown.”
“The idea that “what could have been” is part of how people evaluate actual outcomes is not new. But no one expected that dopamine would be doing the job of combining this information in the human brain.”
Some caveats applied:
Measurements of dopamine were taken only from basal ganglia areas. These may not act the same as dopamine processes in other brain and nervous system areas.
The number of subjects was small (17), they all had Parkinson’s disease, and the experiment’s electrodes accompanied deep brain stimulation implantations.
Because there was no control group, findings of a study performed on a sample of people who all had dysfunctional brains and who were all being treated for neurodegenerative disease may not apply to a population of people who weren’t similarly afflicted.
The researchers didn’t provide evidence for the Significance section statement:
“The observed compositional encoding of “actual” and “possible” is consistent with how one should “feel” and may be one example of how the human brain translates computations over experience to embodied states of subjective feeling.”
The subjects weren’t asked for corroborating evidence about their feelings. Evidence for “embodied states of subjective feeling” wasn’t otherwise measured in studied brain areas. The primary argument for “embodied states of subjective feeling” was the second paragraph of the Discussion section where the researchers talked about their model and how they thought it incorporated what people should feel.
The study’s experimental evidence didn’t support the researchers’ assertion – allowed by the reviewer – that the study demonstrated something about “states of subjective feeling.” That the model inferred such “findings” along with the researchers’ statement that it “is consistent with how one should “feel” reminded me of a warning in The function of the dorsal ACC is to monitor pain in survival contexts:
“The more general message you should take away from this is that it’s probably a bad idea to infer any particular process on the basis of observed activity.”
“These precise, real-time measurements of dopamine-encoded events in the living human brain will help us understand the mechanisms of decision-making in health and disease.”
It’s likely that repeated hubris is one way researchers respond to their own history and feelings, such as their need to feel important as mentioned on my Welcome page.
The Parkinson’s patients were willing to become lab rats with extra electrodes that accompanied brain implantations to relieve their symptoms. Findings based on their playing a stock market game didn’t inform us about “mechanisms of decision-making in health and disease” in unafflicted humans. As one counter example, what evidence did the study provide that’s relevant to healthy humans’ decisions to remain healthy by taking actions to prevent disease?
The unwarranted extrapolations revealed a belief that the goal of research should be to explain human actions by explaining the actions of molecules. One problem caused by the preconceptions of this widespread belief is that it leads to study designs and models that omit relevant etiologic evidence embedded in each of the subjects’ historical experiences.
This belief may have factored into why the subjects weren’t asked about their feelings. Why didn’t the study’s design consider as relevant subject-provided evidence for feelings? Because the model already contrived explanations for feelings underlying the subjects’ actions.
“Early stage [diet-induced] obesity, before the onset of diabetes or metabolic syndrome, produced deficits on cognitive tasks that require the prefrontal cortex.
These results strongly suggest that obesity must be considered as a contributing factor to brain dysfunction.”
The difference in the diets of the adult male subjects was that the control group ate 10% fat (20% protein, 70% carbohydrates) whereas the obese group ate 45% fat (20% protein, 35% carbohydrates). Significant changes in body weight were present after the first two weeks on the diets, but testing didn’t begin until after eight weeks.
I thought the study design prematurely terminated the experiments. The study didn’t justify the ultimate purpose of conducting rodent experiments, which is to find possible human applicability.
One study design possibility would have been to continue through old age to find how the conditions progressed. Another possibility would have been to reverse the high-fat diet to find whether the conditions reversed.
“Placebo effects can be translated to a real-life setting in the short-term reduction of stress, anxiety and symptoms of depression in a non-patient population.
In treating psychological distress, placebos may be useful addition to the treatment repertoire.“
The researchers provided a self-administered 3-day course of fake “anti-stress treatment spray” and told the participants the spray was either “oxytocin” or “serotonin” with these results:
“Both the ‘serotonin’ and ‘oxytocin’ treatment sprays were effective in reducing symptoms of depression; however, only those in the ‘oxytocin’ group reported less stress and anxiety as compared with controls. Overall, the ‘oxytocin’ was perceived as more effective.”
Will this study of non-patients be used to try to justify manipulating patients’ perceptions of their stress, anxiety, and depression?
“It is known that increased circulating glucocorticoids in the wake of excessive, chronic, repetitive stress increases anxiety and impairs Brain-Derived Neurotrophic Factor (BDNF) signaling.”
The study had several statements that were unconvincingly supported by the study’s findings. One such statement in the Conclusions section was:
“This study supports the view that early-life adversity may induce long-lasting epigenetic changes in stress-related genes, thus offering clues as to how intergenerational transmission of anxiety and trauma could occur.”
However, the study’s evidence for “intergenerational transmission of anxiety and trauma” as summarized in the Limitations section was:
“This study did not directly associate child behavior or biology to maternal behavior and biology.”
In another example, the Discussion section began with:
“The severity of maternal anxiety was significantly correlated with mean overall methylation of 4 CpG sites located in exon IV of the BDNF promoter region as measured from DNA extracted from mothers’ saliva.
In addition, methylation at CpG3 was also significantly associated with maternal exposure to domestic violence during childhood, suggesting that BDNF gene methylation levels are modulated by early adverse experiences.”
The researchers assessed five DNA methylation values (four individual sites and the overall average). The CpG3 site was “significantly associated with maternal exposure to domestic violence during childhood” and the three other CpG sites’ methylation values were not.
IAW, the researchers found only one of four sites’ methylation values significantly associated to only one of many studied early adverse experiences. This finding didn’t provide sufficient evidence to support the overarching statement:
“BDNF gene methylation levels are modulated by early adverse experiences.”
To make such a generally applicable statement – more than one BDNF gene’s methylation levels could be directly altered by more than one early adverse experience – the researchers would, AT A MINIMUM, need to provide evidence that:
The one category of significantly associated early adverse experience directly altered the one significantly associated CpG site’s DNA methylation level
Other categories of early adverse experiences were fairly represented by the one significantly associated experience category
Other categories of early adverse experiences could directly alter other BDNF genes’ DNA methylation levels
The significantly associated DNA methylation level of only one out of four CpG sites was fairly represented by the overall average of the four sites
Other BDNF gene’s methylation levels were fairly represented by the overall average of the four sites
If researchers and sponsors must have agendas, a worthwhile, evidence-supported one would be to investigate prenatal and perinatal epigenetic causes for later-life adverse effects.
As Grokking an Adverse Childhood Experiences (ACE) score pointed out, environmental factors that disrupt neurodevelopment may be the largest originators of epigenetic changes that are sustained throughout an individual’s entire lifespan.
What’s the downside of conducting studies that may “directly associate child behavior or biology to maternal behavior and biology” during time periods when a child’s environment has the greatest impact on their development?
When prenatal and perinatal periods aren’t addressed, researchers and sponsors neglect the times during which many harmful epigenetic consequences may be prevented. It is known.
“Mitochondrial function in the nucleus accumbens, a brain region relevant for motivation and depression, is a critical mediating factor in the subordinate status displayed by high-anxious rats.
Treatment with nicotinamide, an amide form of vitamin B3 that boosts mitochondrial respiration, into the NAc [nucleus accumbens] of high-anxious rats at a time point before the social encounter and at a dose that increased accumbal mitochondrial respiration, abolished the disadvantage of high-anxious animals to become dominant against low-anxious animals.
Our findings highlight a key role for brain energy metabolism in social behavior and point to mitochondrial function in the nucleus accumbens as a potential marker and avenue of treatment for anxiety-related social disorders.”
The researchers handled individual differences of the outbred subjects by separating them into high-, intermediate-, and low-anxiety categories according to their responses on two tests. The high- and low-anxiety subjects were matched by weight, age, and social experience.
Here are a few examples of the researchers thoroughly ruling out confounding factors:
“Differences in social competitiveness are not related to overall differences in social motivation or sociability.
Although social competition did significantly increase corticosterone compared with baseline levels, there were no significant differences between anxiety groups at either time point.
Microinfusion of either ROT, MA, or 3NP [mitochondrial respiration inhibitors] reduced the success of treated animals to win the social contest.
Importantly, these treatments did not induce side effects on social investigation or auto-grooming during social competition, or alter locomotor activity, anxiety, or sociability in additional experiments.
Furthermore, these inhibitor treatments did not produce neurotoxic effects, as the drugs were infused at low doses and we confirmed the absence of lesion and neuronal death.
The effects of complex I or complex II inhibition on social competition were specific for the NAc, as infusions of the same inhibitors into the BLA [basolateral amygdala] had no effect on social dominance and did not affect general locomotor activity.
We further showed that, unlike infusion of muscimol [a GABA receptor agonist] in the BLA that interferes with BLA-dependent auditory fear conditioning, 3NP did not affect conditioning in this task, discarding that neuronal inactivation could be a general mechanism whereby impairing mitochondrial function would affect putative functions from the affected brain region.
The impact of mitochondrial function in social competition described here is not mediated by oxidative stress.”
“The coordinated actions of BDNF and glucocorticoids promote neuronal plasticity and that disruption in either pathway could set the stage for the development of stress-induced psychiatric diseases.
Genetic strategies that disrupted GR [glucocorticoid receptor] phosphorylation or TrkB [the BDNF receptor] signaling in vivo impaired the neuroplasticity to chronic stress and the effects of the antidepressant fluoxetine.
We demonstrate that fluoxetine prevented the neuroplasticity of chronic stress by priming GR phosphorylation at BDNF-sensitive sites.”
It wasn’t too difficult to see how many of the stressors had human equivalents during infancy/early childhood:
“To determine the plasticity of GR phosphorylation upon changes in the endogenous levels of BDNF and glucocorticoids, mice were exposed to a chronic unpredictable stress that included one daily random stressor for 10 consecutive days from P21 [immediately after weaning] to 1 mo of age.
Chronic unpredictable stress includes one of the following daily random stressors (wet bedding, no bedding, food deprivation, crowded cage, 2 h or 6 h restraining, forced swim, tail suspension).”
But who would give fluoxetine – Prozac – to a human infant or young child to prevent “the neuroplasticity of chronic stress” from having adverse effects?
http://www.pnas.org/content/112/51/15737.full “Neurotrophic-priming of glucocorticoid receptor signaling is essential for neuronal plasticity to stress and antidepressant treatment”
“The two major populations of human prefrontal cortex neurons..the excitatory glutamatergic projection neurons and the inhibitory GABAergic interneurons which constitute about 80% and 20% of all cortical neurons, respectively.
Major differences between the neuronal subtypes were revealed in CpG, non-CpG and hydroxymethylation (hCpG).
A dramatically greater number of undermethylated CpG sites in GLU versus GABA neurons were identified. These differences did not directly translate into differences in gene expression and did not stem from the differences in hCpG methylation, as more hCpG methylation was detected in GLU versus GABA neurons.
Notably, a comparable number of undermethylated non-CpG sites were identified in GLU and GABA neurons, and non-CpG methylation was a better predictor of subtype-specific gene expression compared to CpG methylation.”
The researchers performed numerous cross checks to test the results of their methodologies. This was necessary because, for example, studies such as A human study of changes in gene expression point out that current technologies such as the 450K array:
“Queries only 1.6% of all CpGs in the genome and the CpG selection is biased towards CpG islands.”
From the Discussion section:
“The higher abundance of hmCpG sites in GLU versus GABA neurons appears indicative of a difference in transcriptional potential between the neuronal subtypes. The increased hydroxymethylation could enable certain genes (e.g. activity-dependent genes) to be more readily induced in GLU versus GABA neurons.
These findings emphasize the importance of even subtle differences in the promoter CpG methylation for neuron subtype-specific gene expression. They also suggest that differences in CpG methylation within gene bodies and distal regulatory elements are not always directly reflected in differences in gene expression between neuronal subtypes.
The functional relevance of the association between gene expression and distal non-CpG methylation remains to be characterized.
Our data suggest that, compared to GABA interneurons, GLU projection neurons are characterized by more permissive chromatin state that is less constrained by repressive DNA methylation marks and is instead controlled by more dynamic means of transcription inhibition, such as non-coding RNAs and/or histone modifications.”
“If common risk variants determined by the recent genome wide associated studies (GWAS) for several neuropsychiatric diseases including schizophrenia (SCZ), autism spectrum disorder (ASD), major depressive disorder (MDD), and Alzheimer’s disease (AD) significantly overlap.
These findings strongly suggest an association between the epigenetic specification of both GABA and GLU neurons and SCZ. Risk variants associates with ASD, MD, or AD were not enriched.
An alternative explanation of our negative results could be the involvement of different developmental stages and/or brain regions in different diseases.”
The current study performed more detailed analyses, but on fewer subjects. The emphasis was on demonstrating an improved methodology.
Both studies’ findings regarding disease were of effects, not causes. That both study designs were limited to the postmortem prefrontal cortex reminded me of the old joke about looking for lost keys under the street light because the light was better there. At least the current study acknowledged the existence of other areas to search.
“Although only a small minority of patients withautismhave a mitochondrial disease, many patients with mitochondrial myopathies have autism spectrum disorder symptoms.
These symptoms may be the presenting symptoms, which presents a diagnostic challenge for clinicians.
The case of a 15-year-old boy with a history of autism spectrum disorder and neurocardiogenic syncope, admitted to the inpatient unit for self-injury, whose young mother, age 35, was discovered to suffer from mitochondrial myopathy, dysautonomia, neurocardiogenic syncope, Ehler-Danlos syndrome, and other uncommon multisystem pathologies likely related to mitochondrial dysfunction.”
I was somewhat taken aback by the Abstract and Introduction statements:
“All autism spectrum disorders are known to be heritable, via genetic and/or epigenetic mechanisms, but specific modes of inheritance are not well characterized.
This form of ASD is known to be heritable, as are all forms of ASD, despite the previous belief to the contrary, though the mechanisms of inheritance, both genetic and epigenetic, are not well characterized.”
I didn’t see the “known to be heritable” phrase mentioned in the referenced review. However, I also didn’t see anything stated in the review or cited from its 217 references that disproved this phrase.
I shouldn’t have been surprised by “despite the previous belief to the contrary” in the above quotation. I’d guess that the physicians frequently encountered parents who needed such beliefs when faced with their child’s condition.
A relevant hypothesis of Dr. Arthur Janov’s Primal Therapy is: a major function that our cerebrums have evolutionarily adapted is to use ideas and beliefs to repress pain and make us more comfortable.
I value this inference as an empathetic method of interpreting people’s behaviors and expressions of thoughts and feelings.
When a “known to be heritable” phrase can unleash pain, it likely won’t be understood in its appropriate context. Among the physicians’ challenges was a barrier that kept the parent’s pain from being felt – the belief.
2023 update – After all the medical gaslighting on display this decade, I don’t what it would take for me to trust a medical professional anymore. These doctors ‘knew’ somehow that autism was heritable, yet couldn’t describe mechanisms of inheritance? Please. Why were medical professionals trusted in the first place?
From one of the articles in a freely-available Genome editing publication:
“Genomic studies frequently point to the important role that the full collection of epigenetic patterns in a cell nucleus has in complex diseases such as diabetes or schizophrenia, notes Tim Reddy, a genomics researcher also at Duke University. “In a lot of these cases, it really seems to be not a DNA mutation that impacts the protein sequence, but a change in how genes are regulated.”
Reddy says that he was surprised at the extent to which the expression of a target gene increased when a histone in an enhancer region was acetylated. “That result started to convince me that the acetylation of histones may be a direct cause of gene activation.”
Because of its simplicity and versatility, CRISPR–Cas9 opens up an opportunity. “If we want to target a region in the genome, we can have that targeting molecule here tomorrow for five dollars,” says Reddy.”
Reading this article and several of the publication’s other articles revealed the widespread belief that the goal of research should be to explain human conditions by explaining the actions of molecules.
One problem caused by this preconception is that it leads to study designs and models that omit relevant etiologic evidence embedded in each of the subjects’ historical experiences.
This 2015 George Washington study compared human and chimpanzee brain attributes to find:
“The morphology of the human cerebral cortex is substantially less genetically heritable than in chimpanzees and therefore is more responsive to molding by environmental influences.”
“We found that the anatomy of the chimpanzee brain is more strongly controlled by genes than that of human brains, suggesting that the human brain is extensively shaped by its environment no matter its genetics.
Though our findings suggest that the increased plasticity found in human brains has many benefits for adaptation, it is also possible that it makes our brain more vulnerable to many human-specific neurodegenerative and neurodevelopment disorders.”
The study demonstrated an aspect of how natural selection of species leading to Homo sapiens – after humans and chimpanzees shared a common ancestor – favored our increased capacity to adapt to our environments.
“CpGs that differ between schizophrenia patients and controls that were enriched for genes related to development and neurodifferentiation.
The schizophrenia-associated CpGs strongly correlate with changes related to the prenatal-postnatal transition and show slight enrichment for GWAS[genome-wide association study] risk loci while not corresponding to CpGs differentiating adolescence from later adult life.
Only a fraction of the illness-associated CpGs, 4.6%, showed association to nearby genetic variants in the meQTL [methylation quantitative trait loci] analysis, further suggesting that these findings may be more related to the epiphenomena of the illness state than to the genetic causes of the disorder.
These data implicate an epigenetic component to the developmental origins of this disorder.”
It wasn’t surprising in 2015 to find “an epigenetic component to the developmental origins of this disorder.” From the supplementary material:
“Diverse chromatin states suggest vastly different epigenetic landscapes of the prenatal versus postnatal human brain.
Approximately half of the CpGs had DNAm [DNA methylation] levels positively correlated with expression across the lifespan, and half had DNAm levels negatively correlated.
These results suggest that many of the epigenetic changes occurring between prenatal and postnatal life in prefrontal cortex manifest in the transcriptome, and that the directionality of association is not strictly linked to the location of the CpG or DMR [differentially methylated region] with respect to an annotated gene.
Diagnosis-associated CpGs were relatively small compared with those differentially methylated between fetal and postnatal samples.”
The studied brain area was limited to the dorsolateral portion of the prefrontal cortex, which isn’t mature in humans until we’re in our late teens/early twenties.
The researchers ignored brain areas that were fully developed or further along in development – such as the limbic system – during “the prenatal-postnatal transition.”
The researchers intentionally blinded themselves from discovering “many of the epigenetic changes occurring between prenatal and postnatal life” possibly associated with schizophrenia and these more-developed brain areas.
Where’s the evidence that the developmental origins of schizophrenia have no associations with brain structures whose development closely approximates their lifelong functionalities at birth?
The study’s limitations didn’t hamper researcher hubris in a press release for a site that touts business news, such as:
“This conclusion, while perhaps not the final verdict on the subject, is hard to resist given this remarkable evidence”
Did the spokesperson really understand GWAS? Or was he trying to exploit public ignorance of GWAS?
“Recent developments in the research of ASD [autistic spectrum disorder] with a focus on epigenetic pathways as a complement to current genetic screening.
Not all children with a predisposing genotype develop ASD. This suggests that additional environmental factors likely interact with the genome in producing ASD.
Increased risk of ASD is associated with mutations in genes that overlap with chromatin remodeling proteins, transcriptional regulators and synapse-associated proteins. Interestingly, these genes are also targets of environmentally induced changes in gene expression.”
Evidence was discussed for both broad and specific epigenetic ASD causes originating in the prenatal environment:
Maternal stress:
“Prenatal stress exerts a profound epigenetic influence on GABAergic interneurons by altering the levels of proteins such as DNMT1 and Tet1 and decreasing the expression of various targets such as BDNF.
Ultimately, this results in reducing the numbers of fully functional GABAergic neurons postnatally and a concomitant increased susceptibility toward hyperexcitability. The delayed migration of GABAergic interneuron progenitors results in reduced gene expression postnatally which is likely the consequence of increased amounts of DNA methylation.
The net effect of stress during early development is to disrupt the balance of excitatory/inhibitory neuronal firing due to the loss of function associated with disrupted neuronal migration and maturation.”
Prenatal nutrition:
“Exposure to a wide range of environmental toxins that impact neurodevelopment also result in global DNA hypomethylation. This model was extended to connect pathways between dietary nutrition and environmental exposures in the context of DNA hypomethylation. More recently, this hypothesis was expanded to show how dietary nutrients, environmental toxins, genome instability and neuroinflammation interact to produce changes to the DNA methylome.”
Maternal infections:
“Inflammation, autoimmunity and maternal immune activation have long been suspected in the context of aberrant neurodevelopment and ASD risk.”
Exposure to pollutants, medications, alcohol
This was a current review with many 2015 and 2014 references. However, one word in the reviewers’ vernacular that’s leftover from previous centuries was “idiopathic,” as in:
“Idiopathic (nonsyndromic) ASD, for which an underlying cause has not been identified, represent the majority of cases.”
It wasn’t sufficiently explanatory to use categorization terminology from thousands of years ago.
Science has progressed enough with measured evidence from the referenced studies that the reviewers could have discarded the “idiopathic” category and expressed probabilistic understanding of causes. They could have generalized conditional origins of a disease, and not reverted to “an underlying cause has not been identified.”
Another word the reviewers used was “pharmacotherapeutic,” as in:
“The goal for the foreseeable future is to provide a better understanding of how specific genes function to disrupt specific biological pathways and whether these pathways are amenable to pharmacotherapeutic interventions.”
Taking “idiopathic” and “pharmacotherapeutic” together – causes for the disease weren’t specifically identified, but the goal of research should be to find specific drug treatments?
Of course reviewers from the Department of Psychiatry, The Psychiatric Institute, University of Illinois at Chicago are biased to believe that “the design of better pharmacotherapeutic treatments” will fulfill peoples’ needs.
Are their beliefs supported by evidence? Without using drugs, are humans largely incapable of therapeutic actions such as:
Preventing epigenetic diseases from beginning in the prenatal environment?
Treating epigenetic causes for and alleviating symptoms of their own disease?
Surface Your Real Self 