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I have yet to find a way to write about the connection I know exists between infant-child violent trauma caused within an abusive environment and the lifelong experience of living in a body that henceforth knows ONLY one thing for sure: Pain of Sadness. Nor can I find ANYONE who has clearly written about this subject before me as it involves Substance P and depression caused by infant-child abuse.
I know intuitively (and my body knows it) that Substance P (our pain neurostransmitter), chronic sadness, chronic depression, chronic anxiety ‘stress response’ (PTSD) and an extremely insecure and unsafe infant-toddler-child attachment-relationship environment are absolutely connected. I also believe that future research that focuses on these connections will show I am right. This is logical because ABUSE CAUSES PAIN and when this pain is extreme (and chronic), happens early in an infant-child’s life during its rapid growth during critical windows of development, and involves a failed-dangerous attachment relationship, there is no way that the Substance P system (along with all other developing physiology of a little one) could NOT be radically changed as a consequence.
I still believe that all Trauma Altered Development due to growth of a human infant 0-3 (and beyond) in an environment of violent trauma and malevolent deprivation is orchestrated by the immune system in a feedback-loop process that changes the body-brain we live in for the rest of our lives.
Sometimes when I turn to an online search regarding a topic that is front and center in my thinking I am astounded to immediately locate EXACTLY what I need. The excerpt from a research study specifically refers to Substance P, the neuropeptide of pain signaling, as being connected to the stress-fear response related – in my thinking – to interrupted early attachment:
“Substance P causes a “fight or flight” response, and there is evidence of substance P antagonists blocking this stress response via blockade of substance P receptors in the amygdala. There are multiple animal models providing evidence for this. Guinea pig pups that are separated from their mothers make vocalizations that seem to result from increased substance P released in their internal amygdala. [This bold type and italics is mine.] Substance P antagonists inhibit these vocalizations. More direct evidence has come from cats who manifest rage behavior when their medial hypothalamus is stimulated. The medial hypothalamus has direct projections to the medial amygdala. Substance P antagonists as well as antidepressants block this behavior. Similar effects have been noted in hamsters with forced intruders in their cages and in mice forced to swim. There appears to be no direct interaction between substance P antagonists and antidepressants; substance P antagonists seem to work at sites unrelated to monoamines.
Other areas of the brain that have been implicated in substance P activity are the dorsal raphe nucleus and an area of the thalamus called the habenula, which has the highest density of substance P receptors. The habenula inhibits firing of the dorsal raphe nucleus. The dorsal raphe consists of approximately 50% serotonin neurons and 50% substance P neurons.”
“It [Substance P] is thought to be the primary neurotransmitter for nociceptive [pain] information.”
2001 informative and fascinating article on Substance P (CLICK FOR FULL ARTICLE) by Harrison S, Geppetti P., Italy
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Article on cell communication and signaling from Germany (2008):
Impact of norepinephrine, dopamine and substance P on the activation and function of CD8 lymphocytes
“During the past 30 years in became evident that neurotransmitter are important regulators of the immune system. The presence of nerve fibers and the release of neurotransmitters within lymphoid organs represent a mechanism by which signals from the central nervous system influence the immune cell functions. Neurotransmitter per se cannot induce any new function in immune cells but they are mainly responsible for the “fine-tuning” of an immune response.”
“neurotransmitters are specific modulators of certain immune functions.” [bold type is mine]
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“Neurotransmitters are important regulators of the immune system, with very distinct and varying effects on different leukocyte subsets….. Conclusion: Neurotransmitters are specific modulators of CD8 + T lymphocytes not by inducing any new functions, but by fine-tuning their key tasks. The effect can be either stimulatory or suppressive depending on the activation status of the cells.”
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(Hypertension. 1997;29:510.)
© 1997 American Heart Association, Inc.
Hypothalamic Substance P Release
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From Harvard Medical School – Harvard Health Publications
Depression and pain
Hurting bodies and suffering minds often require the same treatment.
(This article was first printed in the September 2004 issue of the Harvard Mental Health Letter. For more information or to order, please go to http://www.health.harvard.edu/mental.)
“The convergence of depression and pain is reflected in the circuitry of the nervous system. In the experience of pain, communication between body and brain goes both ways. Normally, the brain diverts signals of physical discomfort so that we can concentrate on the external world. When this shutoff mechanism is impaired, physical sensations, including pain, are more likely to become the center of attention. Brain pathways that handle the reception of pain signals, including the seat of emotions in the limbic region, use some of the same neurotransmitters involved in the regulation of mood, especially serotonin and norepinephrine. When regulation fails, pain is intensified along with sadness, hopelessness, and anxiety. And chronic pain, like chronic depression, can alter the functioning of the nervous system and perpetuate itself.
The mysterious disorder known as fibromyalgia may illustrate these biological links between pain and depression. Its symptoms include widespread muscle pain and tenderness at certain pressure points, with no evidence of tissue damage. Brain scans of people with fibromyalgia show highly active pain centers, and the disorder is more closely associated with depression than most other medical conditions. Fibromyalgia could be caused by a brain malfunction that heightens sensitivity to both physical discomfort and mood changes.”
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An online chapter reading on Sadness and Depression – worth a read. Unfortunately (on page 7) the article does not state that failed safe and secure attachment with a primary caregiver(s) is probably the most neglected ‘cause’ of depression at the same time it influences genetic expression most powerfully.
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“Substance P (SP) is thought to have an impact in the pathophysiology of depression and the mechanism of action of antidepressant drugs.”
Substance P serum levels are increased in major depression: preliminary results
By Baghai et al., University of Munich, Germany, Biol Psychiatry 2003 Mar 15;53(6):538-42
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More United Kingdom research on Substance P and depression HERE
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I ask, “What happens to our development when contact with humans causes infants pain rather than brings them reward (Dopamine, a reward-related chemical)?”
Transitions in infant learning are modulated by dopamine in the amygdala
By Barr et al., Nature Neuroscience 12, 1367 – 1369 (2009)
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International research team on infant frontal cortex development at 9 months:
By Holmboe et al., Nature Neuroscience 12, 1367 – 1369 (2009)
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+SUBSTANCE P – IT’S OUR BODY’S BIOLOGICAL LINK TO FEELING EMOTIONAL AND PHYSICAL PAIN
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Interesting article:
Researcher “…Levenson thinks the heightened sadness response might be beneficial for maintaining and strengthening social ties. Sadness “is a very functional emotion,” Levenson says. “It’s an emotion that really brings people towards us and motivates them to help us.”
SEE ALSO:
+CLEAR ARTICLE ON LIFELONG INFANT-CHILD TRAUMA CONSEQUENCES
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Stop the Storm 
Interesting stuff. You’ll want to be careful with that Harvard article about depression & pain — Cymbalta was approved in 2004, the same year this “informative article” came out. Cymbalta’s big advertising kick is that it treats “the pain caused by depression.” I have no idea if the author(s) of the Harvard article had any research or financial interest in Cymbalta, but it’s something to keep in mind.
I like finding the international-based research for this reason.
“Cymbalta (duloxetine hydrochloride) is a [sic] oral dual reuptake inhibitor that enhances the levels of the neurotransmitters, serotonin and norepinephrine, which are involved in depression.”
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“Some of the newer drugs – Effexor (venlafaxine), Wellbutrin (buproprion), Remeron (mirtazapine), Serzone (nefazadone), and Cymbalta (duloxetine) – technically belong in unique classes of their own, but are generally mentioned in the same breath as the SSRIs. Effexor and Cymbalta both have dual reuptake action of serotonin and norepinephrine, not unlike the tricyclics, while Wellbutrin works mainly on both the neurotransmitter dopamine and norepinephrine. Remeron and Serzone both operate on the brain’s alpha-adrenergic-receptors (which affect norepinephrine and serotonin). The point to be made here is that there exists a sufficient variety of newer medications to offer hope to even the hardest cases, however unsuccessful previous attempts may have been.
In April, 2003, The FDA has approved Merck’s substance P/NK1 receptor antagonist, Emend (aprepitant), to treat chemo-induced nausea and vomiting. The drug is currently in phase III trials for treating depression. Substance P belongs to a class of neurotransmitters called neurokinins, made from peptides rather than the amino acids of the neurotransmitters we are more familiar with. When released from the neuron, substance P binds selectively with the neurokinin 1 (NK1) receptor – unless Emend is already there.”
from http://www.healingwell.com/library/depression/mcmanamy1.asp
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I am not an expert at anything other than being me – with a curious mind and a lot of questions. I take NO medications although I receive full disability for severe depression, dissociation, complex PTSD – whatever ‘they’ name it. I am a survivor of severe child abuse-trauma that began to alter my physiological development in adaptation to this extreme stress that began at my birth and lasted the 18 years of my childhood.
I make NO suggestions of any kind to my readers or to anyone else regarding therapy or medication. For myself, I simply know that until the time arrives in the FUTURE (not in my lifetime) that ‘drug therapy’ can actually match the source of someone’s physiological changes caused by severe infant-child abuse, I am not about to take anything ‘they’ have to offer. I’ve tried in the past — I know better now.
I was given Emend — I believe there were four pills that cost $3,000 — during my chemotherapy three years ago for breast cancer. It worked. I was/am grateful. What it seemed to me to be doing to my body was paralyzing any part of me that had to do with my digestive system! In the past the antidepressant action I experienced seemed to always be the same: they made me numb, dumb and stupid.