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Psychosocial vulnerability and early life adversity as risk factors for central sensitivity syndromes

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Abstract

The aim of this narrative review of the epidemiology of central sensitivity syndromes is to provide a summary of the role of early life adversity and psychosocial / psychological factors, in the epidemiology of six main syndromes: (i) fibromyalgia / chronic widespread pain; (ii) headache / migraine; (iii) irritable bowel syndrome; (iv) temporomandibular joint disorder; (v) interstitial cystitis; and (vi) endometriosis / vulvodynia / chronic pelvic pain.

The occurrence of each of the above syndromes varies between each other and between studies. Prevalence ranges from interstitial cystitis, with a prevalence of approximately 14.5 per 100,000, to headache, with some estimates of lifetime prevalence to be around 66%. Precise risk estimates vary between studies, conditions, and exposures, although there is consistent evidence to suggest an association between early life adversity and central sensitivity syndromes (based on the six syndromes under investigation). In further support of this, a number of studies have also demonstrated dose-risk associations.

There is also considerable consistency in the literature to suggest a strong association between negative psychological and psychosocial factors, and the occurrence of central sensitivity syndromes and, again, there is some evidence of a dose-risk relationship. The majority of studies in this field are cross-sectional or retrospective in design, and caution is advised when interpreting results. It is possible – indeed there is some evidence – that some findings may be subject to recall bias, and reverse causation is also a potential concern. However, there are also a number of prospective studies which provide more robust evidence.

Source:  Jones GT. Psychosocial vulnerability and early life adversity as risk factors for central sensitivity syndromes. Curr Rheumatol Rev. 2015 Dec 30. [Epub ahead of print]


Editor's Note:  The nature/nurture debate continues in the world of chronic diseases such as fibromyalgia, ME/CFS, etc.  Hopefully, studies such as this one will provide much needed evidence about the role of each and help put to rest the idea that "it's all in our head".

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One thought on “Psychosocial vulnerability and early life adversity as risk factors for central sensitivity syndromes”

  1. IanH says:

    This statement is nonesense: “

    “There is also considerable consistency in the literature to suggest a strong association between negative psychological and psychosocial factors, and the occurrence of central sensitivity syndromes and, again, there is some evidence of a dose-risk relationship. . . . . .However, there are also a number of prospective studies which provide more robust evidence.

    There is NO robust evidence for early life psychosocial adversity and central sensitivity and certainly none for FM. Many studies, even if they are 100% biophysical often say in their conclusions that psychological factors should be explored. God knows why, lets uncover the physiology first.

    To say that FM or ME/CFS are central sensitivity disorders is to state half the picture. Central sensitivity is a feature but it is NOT the illness. Its like saying a brain tumor is headaches.

    There is more evidence that FM is caused by a set of overlapping genes mainly causing stiff tissue induced TLR4 mediated hyperimmunity. The evidence for stiff tissue induced macrophage hyperfunction in the presence of LPS is becoming clearer.

    In fact I would now go so far as to say that many cases, if not all are in some way caused by a genetic predisposition to form stiff tissue with aging combined with a genetic tendency for macrophages TLR4 attack on strained neuromuscular tissue. The underlying requirements are excess LPS, often due to a leaky gut

    Start with a common premise which has been shown to be true:

    macrophages on stiff tissue will have an increased output of TLR4 in the presence of LPS. So if a person has the following risk factors they will have elevated pro-inflammatory leukocyte output towards pro inflammatory cytokine signalling and consequent oxidative stress in the nervous system:

    1. genes promoting early stiff neuro-muscular tissue formation with aging
    2. poor gut function and heightened LPS transfer (this also has its own risk factors)
    3. physical trauma which also increases stiff tissue formation, sometimes via persistent musculo-skeletal pain especially spinal.
    4. systemic stresses which are related to increased neuromuscular stiffening. these can also alter blood flow.

    Following on:
    persistently raised TLR4 output will establish a pro-inflammatory effect of TLR4 on the nervous system and consequent neural damage or irritation. (Bearing in mind that TLR4 has positive effects under normal conditions and will be “anti-inflammatory and neuroprotective). For many with a condition like FM find that the symptoms wax and wain ie a remission state can be experienced – TLR4 acting as an anti-inflammatory and neuroprotective agent might explain this.

    We know that some things exacerbate the condition:
    poor diet and gut disorder
    soft tissue strain injury or overdoing it
    poor sleep
    low physical fitness (cardiopulmonary)

    Now, while all the evidence is not there, doesn’t this make more sense to explain FM. It certainly does to many who suffer from FM. Most of the people with FM who I have spoken with FM find this idea that FM (central sensitivity) is related to psychological history bizarre. The neuro-inflammatory model makes MUCH MUCH more sense to us all.

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