anna

Thanks for the post

Kitt it does get worse!!! With studies like this one: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3365276/ "Moreover, in postural tachycardia syndrome, which commonly occurs with hypermobility (and may have a common basis in collagen variants), heart rate acceleration compensates for dysfunctional vasoconstriction giving rise to physiological symptoms (e.g. palpitations and light-headedness) that are shared with panic and anxiety states.3 Such deregulated responses are likely to affect neural processes supporting emotional feelings.4,5 Differences in the structural integrity of temporal and parietal cortices may underlie wider behavioural phenotypical expression of hypermobility: abnormalities in superior temporal cortex are also seen in autism.11 Inferior parietal cortex can affect proprioceptive awareness and hypermobility is itself linked to dyspraxia.1 Our findings suggest that processes compromising function in neuro-developmental conditions may occur in individuals with hypermobility, putatively enhancing vulnerability to stress and anxiety."

So so sorry this has happened, it is sad that your hubby has put himself first and not thought of the consequences of his actions. Hugs

Dani you may find the following article of interest http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821781/ Prevalence of Joint Hypermobility and Patterns of Articular Manifestations in Patients with Inflammatory Bowel Disease

Thank you Kitt I will have a good listen to this and report back lol

Sadly sometimes people can find it difficult to start to understand what some folk go through and it looks like you have a case of that with your situation, well let me say you are not mad for being ill and worn out with all that you have going on. Your poor friend may be a tad too needy at the moment and it might be time to let this butterfly go on her way, do not feel too bad about this you need all your strength to look after you and your children. You have tried explaining not much else you can do maybe write again telling her that you do really care about this relationship but no longer have the energy to keep it going your end but it would be wonderful if she could keep in touch to see how you and your daughter are doing. Gentle hugs to you and your poor poorly daughter, Take care Anna

Would the net deficiency theory, link into what is coming out of the sports medicine at the moment I read an article by a Professor Tim Noakes which got me thinking about the whole deconditioning thing again! http://www.pponline.co.uk/encyc/how-physiological-biochemical-and-neural-systems-influence-your-training-and-competition-performance-152 The muscle recruitment: (central fatigue) model The argument This model proposes that it is not the rate at which either oxygen or fuel are supplied to muscle that limits its performance but rather the processes involved in skeletal muscle recruitment (activation), excitation and contraction. It suggests that the brain concentration of the neurotransmitter serotonin, and possibly others including dopamine and acetylcholine, alters the neural impulses from the brain to the exercising muscles to reduce skeletal muscle activation - the actual mass of muscle that is active during any exercise. Alternatively, fatigue may be induced by inhibitory reflexes arising from the exercising muscles and feeding back to the spinal chord. The evidence A number of studies have shown that manipulating central nervous system neurotransmitter concen-trations, particularly by increasing dopamine and reducing serotonin, can enhance exercise performance, and vice versa. There is also direct evidence for reduced central nervous system drive to muscle after fatiguing muscle contractions. I have already described the clear evidence that fatigue at high altitude is caused by reduced activation of exercising muscles by the central nervous system and that a central 'governor' must be involved in causing fatigue when liver glycogen stores are depleted. It is also likely that heat-induced fatigue is controlled by the central nervous system, as it cannot be explained by any other model. In all these cases, reduced central activation of muscle would function as a protective mechanism to prevent organ damage. A contrasting finding that electrical activity within the skeletal muscles actually rises during exercise at a constant workload is usually inter-preted as evidence for increased activation by the central nervous system to compensate for a prog-ressive failure of muscle fibre contractile function. But competitive athletes do not work at a constant rate. And our own studies of prolonged exercise, including bouts of self-chosen high-intensity work, show a progressive reduction in power output during successive bouts of high intensity exercise. This response is very strongly suggestive of central rather than peripheral fatigue. The fact that a relatively small percentage of the available muscle mass (perhaps as little as a maximum of 40%) is ever recruited, even during maximal exercise, remains a perplexing enigma. And proponents of any model of peripheral limitations for exercise performance need to explain why the body does not recruit all its available muscle mass to produce the necessary force under varying exercise conditions as so-called 'peripheral fatigue' develops. An alternative view I have argued that a reduced central activation of the exercising muscles may be necessary to protect humans under specific conditions. I believe these control mechanisms are necessary to prevent the following potentially dangerous developments: * myocardial ischaemia during high-intensity exercise; * muscle ATP depletion and rigor during high intensity exercise; * myocardial ischaemia or cerebral hypoxia during exercise at altitude; * falling blood pressure during exercise in patients with chronic heart failure; * heatstroke during prolonged exercise in the heat; * brain damage from hypoglycaemia during prolonged exercise, when liver glycogen stores are depleted.

I still find the article lacks something, now I am reading the article from the angle of an EDSer, with symptoms of ANS dysfunction, that has 3 children with the EDS and very odd ANS stuff going on. I found that the article is a tad unhelpful: "Ehlers-Danlos Syndrome Ehlers-Danlos syndrome (EDS) is a heterogeneous dis- order that includes several forms, all linked to se- quence variations in genes encoding for fibrillar pro- teins and/or collagen processing enzymes leading to reduced structural integrity of connective tissue. Joint hypermobility, which is characteristic of EDS type III associated with sequence variations in tenas- cin X, has been frequently associated with POTS.47-49 However, the mechanistic relationship between these 2 entities is incompletely defined. Whereas tenascin X sequence variations affect car- diovascular tissue leading to valvular disease,50 the hypothesis that impaired integrity of vascular con- nective tissue leads to impaired venous return and secondary orthostatic tachycardia has not yet been convincingly tested. EDS III is also characterized by early onset of chronic pain, particularly in the shoul- ders, hands, and knees,51 which may be disabling due to associated anxiety, depression, and a somato- sensory amplification state52; this may lead to sec- ondary hypersympathetic responses triggered by fear of pain on standing." the hypothesis that impaired integrity of vascular con- nective tissue leads to impaired venous return and secondary orthostatic tachycardia has not yet been convincingly tested. It is true it has not yet been convincingly tested but does not mean it will not show up when tests are done just that they have not found the tests to give light to this theory. From what I have read such testing would be possibly proved post-mortem but I can not find any research on EDS done on tensile integrity of non vascular EDSers vasculature. this may lead to sec- ondary hypersympathetic responses triggered by fear of pain on standing. Why not include the research coming out of Europe: Mild to moderate neuromuscular involvement is commonly present in various types of EDS, with a remarkable relation between residual TNX level and degree of neuromuscular involvement, compatible with a dose-effect relationship. The findings of this study should increase awareness of neuromuscular symptoms and signs in EDS patients and improve clinical care. It also points to a possible role of the extracellular matrix in muscle and peripheral nerve function. Neuromuscular involvement in various types of Ehlers-Danlos syndrome Adapted from: Voermans NC, van Alfen N, Pillen S, Lammens M, Schalkwijk J, Zwarts MJ, van Rooij IA, Hamel BC, van Engelen BG. Ann Neurol. 2009;65:687-97. Surly having inherently poorer functioning musculature than a 'normal' person, backs up the theory of poor muscle pump in EDSers with POTs symptoms.

Two out of 3 of my children get like this, well the feeling of doom and gloom more that dread, they have found herbal remedies for anxiety and stress have helped a great deal. The ones they use contain Passion flower, valerian and hops, it does seem to calm down their adrenaline rushes.

The following link is to do with neck instability in paediatric medicine but you may find some of the article of interest as this is all well established medical information: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2656787/

Well I found this article about fitness may get some of you thinking! http://www.pponline.co.uk/encyc/how-physiological-biochemical-and-neural-systems-influence-your-training-and-competition-performance-152

Do you have any Autism in your family?

the issue is not the increase, but the sustained increase abbyw from what I have read you are definitely right it is the sustained increase one of 30 beats or more from supine to standing. Many Dr.'s are still fixed on the HR must be over 120 bpm which is why the many get that look when you say you feel bad but you HR is under that magic 120bpm rate. Katybug I could not help but post that chart because I am sure many of us here have been told you are fine your HR is very good nothing to worry about lol.

Normal Results For resting heart rate: Newborns (0 - 3 months old): 100 - 150 beats per minute Infants (3 - 6 months old): 90 - 120 beats per minute Infants (6 - 12 months old): 80 - 120 beats per minute Children 1 - 10 years: 70 - 130 beats per minute Children over 10 and adults (including seniors): 60 - 100 beats per minute Well-trained athletes: 40 - 60 beats per minute The more I read the more I think that the whole heart rate issue needs to be clearly understood by Dr's which I feel at the moment many Dr's do not think further that the numbers. According to this chart I am athletic that is a laugh lol

It is quite easy these days to find the right research articles to fit ones theory if you have the mind to blatantly exclude proven research that states a different outcome. This sort of approach does not help anyone with our symptoms get to the bottom of what is really going on.

You may all find this article of interest: http://www.practicalpainmanagement.com/pain/neuropathic/clinical-recognition-central-abnormal-neuroplasticity "The two hallmarks of a patient with CAN are one whose pain is constant and whose peripheral, originating pain site is either absent or healed and doesn’t respond to local and peripheral treatments such as injections, topical medications, prolotherapy, physical or electromagnetic measures, or anti-inflammatory agents. These patients characteristically exhibit sympathetic outflow signs with symptoms of tachycardia, hypertension, vasoconstriction, diaphoreses, piloerection, nausea, anxiety, and insomnia. Hormonal disturbances are extremely common as indicated by elevated serum cortisol and pregnenolone until such time as pituitary and adrenal exhaustion occurs and serum levels of some pituitary and adrenal hormones drop below normal. Pain control and treatment in these patients is difficult as tissue loss and cell rearrangement may render some medications rather ineffective. Practitioners may have to be creative and experiment to find a good pain control regimen. At this time, there is only symptomatic but no curative treatment. Understanding that some chronic pain patients have CAN rather than a peripheral pain problem should lead investigators to look for, and find, some curative approaches. For now, clinical identification and profiling of suspected CAN is the first step."

I understand where prof. Aziz is coming from lots of Dr.'s seem to be going down the route that EDS is just Joint hypermobility and it is very very common in the general poulation. I think much of this comes from the fact that they can not find the genetic faults that cause EDS3 and half of EDS1 until they do we are stuck I think!!

It is either one because they are really fed up at not being able to find a real answer or two they are being somehow guided by the insurance giants, who much prefer the it's all in your head theory as the treatments are much cheaper in the long run and if they do not work they can always turn around and say it is your own fault for net getting better, you are not trying hard enough to overcome your problem, we can no longer support you! I am in the UK by the way so our medical system is quite different to yours in in the USA but we still have a big nasty insurance company advising our government and health service,they love the biopsychosocial model of health care!!! The biopsychosocial model claims that a disease or disorder is explained through biological, psychological, and social factors. Interestingly, it is a model which has been adopted by this company, who the government consulted on regarding Welfare Reform. They provide insurance and rehabilitation services. OPPs sorry rant over I promise.

The thing that confuses me a tad is that migraine's are noted as common in EDS patients more so that non EDS folk, so is their more of a link to EDS than we think?!

I am going to post this on private UK EDS group and see what they think Issie I will post back an response to this article later. This has got me quite fed up really but I know it was going this way for some time as my children's old cardiologist kept pointing out that he could not find any evidence of arterial resistance or something like that thus could not see how my children's EDS could be related unless it was not due to the theory that blood vessels are too elastic! So I am guessing as these top research places can not find out what is going on they are going to say it is all in your head because you are worried about the pain you are in because you are over sensitive!!

Ehlers-Danlos Syndrome Ehlers-Danlos syndrome (EDS) is a heterogeneous disorder that includes several forms, all linked to sequence variations in genes encoding for fibrillar proteins and/or collagen processing enzymes leading to reduced structural integrity of connective tissue. Joint hypermobility, which is characteristic of EDS type III associated with sequence variations in tenascin X, has been frequently associated with POTS.47, 48, 49 However, the mechanistic relationship between these 2 entities is incompletely defined. Whereas tenascin X sequence variations affect cardiovascular tissue leading to valvular disease,50 the hypothesis that impaired integrity of vascular connective tissue leads to impaired venous return and secondary orthostatic tachycardia has not yet been convincingly tested. EDS III is also characterized by early onset of chronic pain, particularly in the shoulders, hands, and knees,51 which may be disabling due to associated anxiety, depression, and a somatosensory amplification state52; this may lead to secondary hypersympathetic responses triggered by fear of pain on standing. This bit EDS III is also characterized by early onset of chronic pain, particularly in the shoulders, hands, and knees,51 which may be disabling due to associated anxiety, depression, and a somatosensory amplification state52; this may lead to secondary hypersympathetic responses triggered by fear of pain on standing. in my opinion is a load of rubbish. It is basically saying that folk with EDS are worried about pain all the time so they get POTs symptoms what a load of rubbish Grrrr

It is really good that it is helping, will have to look into this.

Just found a more detailed version: Proof That Irritable Bowel Syndrome Is not really In your Head Irritable bowel syndrome may make life miserable for those afflicted -- an believed ten percent or more from the populace. And what irritates lots of of them even more is that they typically are labeled as hypochondriacs, considering the fact that bodily results in for irritable bowel syndrome have never been discovered. Now, biologists in the Technische Universitaet Muenchen (TUM) have drop new mild about the make a difference: They have identified mini-inflammations in the mucosa in the gut, which upset the sensitive stability with the bowel and they are accompanied by sensitization from the enteric nervous method. Flatulence, constipation and diarrhea, nausea and abdomen cramps: Irritable bowel syndrome (IBS) can transform digestion into a nightmare. Regular visits towards the bathroom are often accompanied by rest disturbances, head aches, and backaches. In Germany on your own, some 7 million individuals are affected from the dysfunction -- and through the indisputable fact that their irritable bowel syndrome can often be deemed psychosomatic. It is because the organic cause in the disease hasn't been uncovered, and for that reason the varied therapeutic interventions are disappointing for both of those the clients and their medical practitioners. That may shortly change, nonetheless, due to the fact now, for the initially time, biologists in Munich have nailed down hidden physical triggers of this bowel condition. Professor Michael Schemann's investigate crew for the TUM Section for Human Biology has managed to display that micro-inflammations of your mucosa trigger sensitization on the enteric nervous system, therefore producing irritable bowel syndrome. Making use of ultrafast optical measuring solutions, the scientists were equipped to demonstrate that mediators from mast cells and enterochromaffin cells specifically activate the nerve cells while in the bowel. This hypersensitivity of the enteric anxious program upsets communication in between the gut's mucosa and its anxious process, as venture leader Prof. Schemann clarifies: "The irritated mucosa releases improved amounts of neuroactive substances like as serotonin, histamine and protease. This cocktail created by the body could be the actual induce of the unpleasant IBS issues." The TUM scientists in human biology are blazing a path as they follow this lead. Their present concentrate is usually to what extent nerve sensitization correlates with all the severity of indications. Operating with colleagues from Amsterdam, they have got by now substantiated the medical relevance of their outcomes: Irritable bowel signs improved after remedy with the antihistamine recognised for its immune-stabilizing influence within the treatment solution of allergic reactions these kinds of as hay fever. Thanks to funding within the German Investigate Foundation (DFG), the researchers are actually investigating whether the improved signs or symptoms are accompanied by a normalization of nerve activity. Thriving identification of your active factors could allow the event of helpful medication to deal with irritable bowel syndrome. Even now, nevertheless, the TUM workforce have designed life much easier for most IBS patients, in they have revealed that the chronic ailment does have physical causes and isn't just "in their heads." Qualifications: As direct creator on the article in "Gastroenterology", exploration assistant Dr. Sabine Buehner obtained the five,000-euro Norgine Gastro Award for outstanding study and discovery within the area of gastroenterology. The task "The pathophysiology of irritable bowel syndrome: Effect of mucosal biopsy supernatants from people with irritable bowel syndrome to the enteric anxious system" is funded through the German Investigation Foundation (DFG

http://news.bio-medicine.org/?q=biology-news-1/proof-that-a-gut-wrenching-complaint----irritable-bowel-syndrome----is-not-in-your-head-14976

This is all very interesting I think I will have to bring the B12 issue up with my children's EDS/POTS next week.