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Fibromyalgia and Chronic Fatigue Syndrome

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Slide set to accompany the public lecture on Fibromyalgia and Chronic Fatigue Syndrome.

Publicada em: Saúde e medicina
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Fibromyalgia and Chronic Fatigue Syndrome

  1. 1. Fibromyalgia Part 1 Marcus Webb The NutriCentre, Park Crescent February 1st 2012 (Fibromyalgia Part 2 scheduled for 6th June 2012)
  2. 2. Where do you start? What is it?Why does it occur? Can it be treated? Is it curable?
  3. 3. 11 out of the 18 needed • Occiput • C5-C7 region • Mid-trapezius • Supraspinatus • 2nd rib, costochondral area • Lateral epicondyle • Gluteal upper quadrant • Greater trochanter • Knees, medial fat padWolfe F, Smythe HA, Yunus MB, et al. The American College of Rheumatology 1990 Criteria for the Classification ofFibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33(2):160-72.
  4. 4. Some history & background • UK prevalence: 2.0 – 4.7 % • Second only to OA as a cause of chronic pain • Diagnosed 7 x more frequently in women • Typical age range 45-60 • No diagnostic tests (X-rays, scans, blood tests) • Diagnosis of exclusion to be on the safe side • Confirmed by clinical & physical examination • Regular review needed to check for symptom changes White KP, Harth M. Classification, epidemiology, and natural history of fibromyalgia. Curr Pain Headache Rep. 2001;5(4):320-9. Gran JT. The epidemiology of chronic generalized musculoskeletal pain. Best Pract Res Clin Rheumatol. 2003;17(4):547-61. Expert Panel And Consensus Panel Myopain 1992. Consensus Document On Fibromyalgia: The Copenhagen Declaration. Fibromyalgia Association UK. Guidance on management of Fibromyalgia for the multidisciplinary team.
  5. 5. Thoughts & observations There is no real agreement on what actually causes FM There are some very strong associations between FM and another rather mysterious chronic condition; CFS – (NB. ME is not CFS) However, there appears to be some common themes in both; • Sleep disturbance • Anxiety syndromes / depression • Subtle changes in metabolic hormones such as thyroid & cortisol • Low blood pressure • Exposure to a traumatic event or illness – physical or emotional • Irritable bowel and/or irritable bladder (interstitial cystitis) • Subtle changes in carbohydrate metabolism / glucose regulation
  6. 6. Fibromyalgia part 1 (Today) will focus on; • A review of possible causal factors • A review of 2 key symptoms; 1. Pain 2. Sleep disturbance •Practical management tips
  7. 7. Fibromyalgia part 2 (6th June 2012) will focus on; • A review of any advances since part 1’s talk • A review of; 1. Mood disorder, anxiety & depression 2. Low blood pressure 3. Irritable bowel & interstitial cystitis •Practical management tips
  8. 8. Causes
  9. 9. Causes 1.Genetic There is evidence that genes involved in the serotonin and dopamine systems can exist in many forms play a role in the development of FMS. These ‘polymorphisms’ are not specific for FMS and are also associated with other functional disorders and depression.
  10. 10. The genetic - neuroendocrine cascade
  11. 11. Causes 3.Stress triggers Home / work / kids / relationships… life! Change of life / work / domestic circumstance Loss of ‘control’ over life events / work events Illness – chronic or acute Trauma – RTA, trivial falls, surgery… Any combination of the above to the threshold of ‘tipping point’ Stress reaction: Alarm phase, fatigue phase, exhaustion phase
  12. 12. Stress Normal Hypothalamic Hypothalamus Pituitary Axis response to stress CRH Anterior pituitary ACTH Adrenal gland Cortisol Kidney Metabolic effects
  13. 13. Stress “Blunted” Hypothalamic Pituitary Hypothalamus Axis response to chronic / unresolved stress CRH Anterior pituitary  ACTH Adrenal gland Cortisol Kidney Metabolic effects
  14. 14. NB: Pregnenolone is derived from cholesterol and is the precursor of DHEA… the building block for all other steroid hormones; eg.sex hormones, gluco and mineralocorticoids
  15. 15. The Cortisol Spectrum Pathologic Pathologic Natural Adaptive state of high state of low physiology cortisol cortisol Normal physiology progressing to Cushing’s Addison’s Stage 1 – Stage 2 – Stage 3 disease disease adrenal functional adoptions• ‘Lemon on match • Fatigue & weaknesssticks’ appearance • Low BP / heart rate• Puffy face & hirsuit • Dark skin patches• Thin easily bruised • Chronic diarrhoeaskin • Loss of appetite• Heavy sweating • Salt craving• Slow healing • Sluggish movements• Infertility, low libido • Weight loss• High blood sugars • Low Na & high K• Osteoporosis • Normal sex steroids• Weight gain • Painful muscles• Depression / mood • Irritable / depressedswings • Sweating• High thirst / DM • Headaches• High BP • 90% of cortex to be• Low K & high Na damaged in Addison’s
  16. 16. Normal adrenal stress profile
  17. 17. Stage 1. The acute ‘Alarm-Phase’
  18. 18. Stage 1. The acute ‘Alarm-Phase’ profile
  19. 19. Stage 1. Alarm (acute) phase - Super HeroPhase Achiever, super efficient Perfectionist / type-A personality Multitasking Thriving on challenges / deadlines Exercises regularly
  20. 20. Stage 2. Adrenal ‘fatigue’
  21. 21. Stage 2. Adrenal ‘fatigue’ profile
  22. 22. Stage 2. Adrenal Fatigue – Cracks starting to show phase Getting cranky Loosing focus Memory suffering / ‘brain fog’ Sleep disturbance starting… fatigued but can’t sleep Eating pattern / food choices changing Starting to notice fatigue setting in Notices unfamiliar aches and pains
  23. 23. Stage 3. Adrenal ‘exhaustion’
  24. 24. Stage 3. Adrenal ‘exhaustion’ profile
  25. 25. Stage 3. Adrenal Exhaustion – Crash & burn phase Sleep deregulation Medically unexplained fatigue Medically unexplained digestive upsets Medically unexplained pain syndromes Medically unexplained Immune dysfunction Medically unexplained infection prone system Mood disorder CFS / FM
  26. 26. A novel model No effects Normalindividuals taking Brief phase of exercise regular exercise deprivation (7 days) Fatigue Mood disturbance Prior to exercise deprivation Muscular pains this group also had asymptomatic; Hypo-functioning HPA ANS disturbance Low NK cell responsiveness Pre-existing hypo-active stress regulating system J. Psychosom Res 2004;57:391-8 Trends Endocrinol Metab 2004;15:55-9 J Psychosom Res 2001;51:571-6
  27. 27. A dysfunction in the stress-regulating systems may antedate the onset of FM/CFS Concept supported by the characteristic history of a pre-morbid lifestyle characteristics “Never could sit still…” “I always kept very busy…” “I needed the gym even after a busy day…” “I thrived on challenges and problem solving…”Sufferers appear to have a need to hyper-stimulate theirhypo-responsive systems to obtain a feeling of well-being Burn Out CFS/FM
  28. 28. Sleep
  29. 29. Stage-1 (slow theta waves) Phase between awake & 5-15 minsStage-5 sleep Stage-2 (bursts of spindle waves)(REM sleep) Increase BP, temp & Heart & breathing The Sleep Cycle brain slows relaxed muscles 4-6 cycles per night 90-110 mins per cycle 20 mins into delta sleep Lower Stage-3 (slow delta Repair body temp waves, transitionStage-4 (deep phasedelta sleep) & BP drops phase before deep 30 mins into deep sleep sleep)
  30. 30. Sleep disturbance Over three quarters of FM patients suffer from non-restorative sleep Interestingly, sleep deprivation in normal subjects induces myalgic symptoms that resemble FM In normal folk sleep induces; 1. A reduced SNS activity 3. Promotion of PNS activity 5. Transient reduction in circulating cortisol Moldofsky H. Management of sleep disorders in fibromyalgia. Rheum Dis Clin North Am. 2002;28(2):353-65. Moldofsky H, Scarisbrick P, England R, Smythe H. Musculosketal symptoms and non-REM sleep disturbance in patients with “fibrositis syndrome” and healthy subjects. Psychosom Med. 1975;37(4):341-51. Meerlo P, Koehl M. Sleep restriction alters the HPA response to stress. J Neuroendrcrinology. 14 (2002):397-402
  31. 31. Normal Sleep Profile A good sleep Hypothalamus _ + Inhibits release Inhibits release CIF CRH of cortisol of cortisol release release Pituitary _ ATC H Adrenal CortexCIF – corticotropin inhibiting factor ReducedCRH – corticotropin releasing hormone CortisolACTH – adrenocorticotrophic hormone
  32. 32. Sleep disturbance / poor sleep Poor or disturbed sleep is associated with; 1. SNS activation 3. Changes the ways the neuroendocrine system reacts to stress 5. In acute states: Increase in circulating cortisol 7. In acute states: High cortisol levels are associated with ‘brain fog’ in which the normal functioning of the frontal lobes are influenced by the uncoordinated activity of other cortical regions 9. In chronic states: Reduction in number of brain system serotonin receptors and dysfunctional cortisol awakening response (CAR). 11. A shift in brain system function towards that of a true mood disorder Meerloa P, Sgoifob A, Sucheckic D. Restricted and disrupted sleep: Effects on autonomic function, neuroendocrine stress systems and stress responsivity. Sleep Medicine Reviews (2008) 12, 197–210 Drummond S, Brown G. Altered brain response to verbal learning following sleep deprivation. Nautre. 403 (2000):655
  33. 33. Acute phase Sleep Disturbance Stress / SNS _ Hypothalamus + Stimulates Inhibits release CIF CRH of CIF and release of facilitates CRH & cortisol release enhances Pituitary cortisol release ATC H + Adrenal CortexCIF – corticotropin inhibiting factor IncreasedCRH – corticotropin releasing hormone CortisolACTH – adrenocorticotrophic hormone
  34. 34. In chronic or unresolved stress situationsLoss of the predictable peak level (50-75% increase onawakening level) normally seen 30 mins after awakening.Tests for morning cortisol levels best taken on a typical day, notover a holiday or atypical day so it accurately reflects a ‘real-life’cortisol awakening response (CAR).
  35. 35. Cortisol Awakening Response Normal range Flattened CAROn awakening 10 mins later 20 mins later 30 mins later 60 mins later (normally peek level)
  36. 36. Practical tips for sleep management – the basicsDo not consume alcohol near bedtime or caffeine after 4:00 pm.Avoid ‘stimulus’ in the late evenings – TV, radio, music, computer…Don’t go to bed too early!Understand that with increasing age the need for sleep can reduce.Do not use your bed for problem solving or doing work.Care with fluids to avoid nocturnal bladder activity!Turn the bedside clock round to avoid ‘clock-watching’Turkey roll and glass of milk… the tryptophan trickTake a hot bath before bed.Keep your bedroom cool.
  37. 37. Practical tips for sleep management – useful natural remedies500mg Calcium & 200mg Magnesium taken at bedtime.200 – 300mg Elthea-100 containing L-theanine (Enzymatic Therapy, USA)taken half an hour before bed.500mg Phosphatidylserine (Nature’s Way, USA) taken 4 hours before bed.50 – 200mg enteric coated 5-HTP (Webber, Canada) 1 hr before sleep –give it 4-6 weeks to work, don’t use if on antidepressants.1-3 x capsules Dr T’s sleep formula (Enzymatic Therapy, USA) – wildlettuce, hops, Jamacian dog wood, valerian taken 30 – 90 mins before bed.Delta wave sleep CD…
  38. 38. Phosphatidylserine (PS) & acute stress/cortisolmanagement Placebo given with exercise (cycling) to simulate biological stress, known to increase ACTH & Cortisol levels as seen in this response curve 50 and 75mg PS given with exercise (cycling) to simulate biological stress but the ACTH/Cortisol response is significantly ‘blunted’. Neuroendocrinology.1990; 52:243-248
  39. 39. L-Theanine – a great ‘leveler’ Significant increase in Alpha-wave propagation following 30-40 mins ingestion of between 50-200mg L-theanine Trends Food Sci Tech 1999; 10:199-204. Alternative & Complementary Therapies 2001,April; 7:91-95
  40. 40. Pain
  41. 41. Basic Pain Pathway; basic scheme PainAscending Descendingpathway (modulating) pathway Dorsal horn Peripheral nerve Injury
  42. 42. Mayo Clin Proc. 2011;86(9):907-911
  43. 43. Basic Pain Pathway; Pain the pain gate Higher centers regulate the amount of descending control on the pain gate; complex personal and experiential influences. Peripheral nerveAscending Descendingpathway (modulating) pathway Pain gate in Injury dorsal horn Pain gate neurons contains complex mixture of; 3.Opioid receptors Interneuron 4.GABA receptors 5.Glutamate receptors 6.5-HT receptors
  44. 44. The effects of weather (changes in atmosphericpressure) on FM and rheumatic pain Weather conditions significantly influence day-to-day symptoms in FM patients Annals of Rheumatic Diseases 1990; 49: 158-159
  45. 45. Practical tips for pain management – Anti-inflammatory diet
  46. 46. Practical tips for pain management – useful natural remedies1000 – 4000mg Fish oils (Nature’s Way Mega-EFA) : DHA & EPA, good evidence.200-600mg Magnesium (citrate, chelate or glycinate) : Mixed evidences, may alsohelp with migraines, care with high dose… lose bowels!1000-2000iu Vitamin D3 : low levels associated with chronic pain syndromes.1000 – 2000mg methylsufonylmethane (Opti-MSM, Hadley Wood Healthcare) :long history of use in pain and allergy management, mixed reviews but safe.500 – 1000mg Acetyl-L-carnitine (Nature’s Way, USA) : especially useful in nervepain & diabetic neuropathy as well as cellular (mitochondrial) ATP synthesis fromdietary fats.50 – 300mg Alpha-lipoic acid (Nature’s Way, USA) : especially useful in nerve pain& diabetic neuropathy, may even slow the progression of nerve damage.500 – 1500mg Celadrin (Hadley Wood Healthcare): especially good for joint pain &‘stiffness’
  47. 47. Jacob Teitelbaum MD Books & special formulas
  48. 48. Energy Revitalization formula
  49. 49. Energy Revitalization formula
  50. 50. Ongoing research – Jacob Teitelbaum MD Journal of Chronic Fatigue Syndrome One published approach, known as SHINE, shown to be of help; Sleep Hormones Infections Nutrition Exercise Teitelbaum J. Bird B. Greenfield RM. Weiss A. Muenz L. Gould L. Effective Treatment of Chronic Fatigue Syndrome and Fibromyalgia—A Randomized, Double-Blind, Placebo-Controlled, Intent to Treat Study. Journal of Chronic Fatigue Syndrome Vol. 8, No. 2, 2001. PP3-28.
  51. 51. The SHINE protocol Methods: 72 FMS patients (38 active & 34 placebo) received all active or all placebo therapies. Patients were treated for:1. Adrenal insufficiency subclinical thyroid 2. Disordered sleep 3. Suspected neural hypotension 4. Opportunistic infections 5. Suspected nutritional deficiencies.
  52. 52. The SHINE protocol Results: Long-term follow-up (mean 1.9 years) of the active group showed continuing and increasing improvement over time, despite patients being able to wean off most treatments.
  53. 53. The SHINE protocol Conclusions: Significantly greater benefits were seen in the active group than in the placebo group for all primary outcomes
  54. 54. Patient often ask “is FM is curable?”I tend to reply “well…yes and no…”In my view… • FM is not “curable” in the way most people view the term “cure” • FM is not simply “caught” it is “developed ” as part of a complex syndrome • Primary FM may represent a “slow burn” condition • Secondary FM may represent the “tipping point” in a persons life • The pain & disability are real despite a normal investigative work up
  55. 55. Contact details:Marcus Webbmarcus.webb@btinternet.comHadley Wood Healthcare0208 441 8352www.hadleywoodhealthcare.co.uk

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