This document provides an overview of fibromyalgia including what it is, possible causes, symptoms, and treatment approaches. It discusses fibromyalgia as a condition with widespread pain and tender points, and notes that the cause is unknown but may involve genetic and environmental factors like physical or emotional trauma. Common symptoms are described as pain, sleep disturbances, fatigue, and mood issues. The document outlines a framework for understanding fibromyalgia as a dysregulation of the stress response and hypothalamic-pituitary-adrenal axis. Practical management tips focus on diet, natural remedies, pain management, and improving sleep. A follow up session is scheduled to provide more detail on topics like mood issues, gastrointestinal problems, and advances in understanding fibromyalgia.

1. Fibromyalgia
Part 1
Marcus Webb
The NutriCentre, Park Crescent
February 1st 2012
(Fibromyalgia Part 2 scheduled for 6th June 2012)

3. Where do you start?
What is it?
Why does it occur?
Can it be treated?
Is it curable?

7. 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 pad
Wolfe F, Smythe HA, Yunus MB, et al. The American College of Rheumatology 1990 Criteria for the Classification of
Fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33(2):160-72.

9. 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.

10. 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

11. 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

12. 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

13. Causes

14. 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.

15. The genetic - neuroendocrine cascade

17. 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

18. Stress Normal
Hypothalamic
Hypothalamus Pituitary Axis
response to
stress
CRH
Anterior pituitary
ACTH
Adrenal gland
Cortisol
Kidney
Metabolic
effects

19. Stress “Blunted”
Hypothalamic Pituitary
Hypothalamus Axis response to
chronic / unresolved
stress
CRH
Anterior pituitary
 ACTH
Adrenal gland
Cortisol
Kidney
Metabolic
effects

20. 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

21. 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 & weakness
sticks’ appearance • Low BP / heart rate
• Puffy face & hirsuit • Dark skin patches
• Thin easily bruised • Chronic diarrhoea
skin • 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 / depressed
swings • Sweating
• High thirst / DM • Headaches
• High BP • 90% of cortex to be
• Low K & high Na damaged in Addison’s

22. Normal adrenal stress profile

23. Stage 1. The acute ‘Alarm-Phase’

24. Stage 1. The acute ‘Alarm-Phase’ profile

25. Stage 1. Alarm (acute) phase - Super Hero
Phase
Achiever, super efficient
Perfectionist / type-A personality
Multitasking
Thriving on challenges / deadlines
Exercises regularly

26. Stage 2. Adrenal ‘fatigue’

27. Stage 2. Adrenal ‘fatigue’ profile

28. 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

29. Stage 3. Adrenal ‘exhaustion’

30. Stage 3. Adrenal ‘exhaustion’ profile

31. 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

32. A novel model
No
effects
Normal
individuals 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

33. 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 their
hypo-responsive systems to obtain a feeling of well-being
Burn Out
CFS/FM

34. Sleep

36. Stage-1 (slow theta waves)
Phase
between
awake & 5-15 mins
Stage-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, transition
Stage-4 (deep phase
delta sleep)
& BP drops phase before deep
30 mins into deep sleep sleep)

37. 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

38. Normal Sleep
Profile
A good sleep
Hypothalamus _
+
Inhibits release
Inhibits release CIF CRH
of cortisol of cortisol
release release
Pituitary
_ ATC
H
Adrenal
Cortex
CIF – corticotropin inhibiting factor Reduced
CRH – corticotropin releasing hormone Cortisol
ACTH – adrenocorticotrophic hormone

39. 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

40. 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
Cortex
CIF – corticotropin inhibiting factor Increased
CRH – corticotropin releasing hormone Cortisol
ACTH – adrenocorticotrophic hormone

41. In chronic or unresolved stress situations
Loss of the predictable peak level (50-75% increase on
awakening level) normally seen 30 mins after awakening.
Tests for morning cortisol levels best taken on a typical day, not
over a holiday or atypical day so it accurately reflects a ‘real-life’
cortisol awakening response (CAR).

42. Cortisol Awakening Response
Normal range
Flattened CAR
On awakening 10 mins later 20 mins later 30 mins later 60 mins later
(normally peek level)

43. Practical tips for sleep management – the basics
Do 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 trick
Take a hot bath before bed.
Keep your bedroom cool.

44. Practical tips for sleep management – useful natural remedies
500mg 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) – wild
lettuce, hops, Jamacian dog wood, valerian taken 30 – 90 mins before bed.
Delta wave sleep CD…

45. Phosphatidylserine (PS) & acute stress/cortisol
management
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

46. 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

47. Pain

48. Basic Pain Pathway;
basic scheme
Pain
Ascending Descending
pathway (modulating)
pathway
Dorsal horn
Peripheral nerve
Injury

49. Mayo Clin Proc. 2011;86(9):907-911

50. 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 nerve
Ascending Descending
pathway (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

51. The effects of weather (changes in atmospheric
pressure) on FM and rheumatic pain
Weather conditions significantly influence day-to-day
symptoms in FM patients
Annals of Rheumatic Diseases 1990; 49: 158-159

52. Practical tips for pain management – Anti-inflammatory diet

53. Practical tips for pain management – useful natural remedies
1000 – 4000mg Fish oils (Nature’s Way Mega-EFA) : DHA & EPA, good evidence.
200-600mg Magnesium (citrate, chelate or glycinate) : Mixed evidences, may also
help 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 nerve
pain & diabetic neuropathy as well as cellular (mitochondrial) ATP synthesis from
dietary 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’

54. Jacob Teitelbaum MD
Books & special formulas

55. Energy Revitalization formula

56. Energy Revitalization formula

57. 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.

58. 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.

59. 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.

60. The SHINE protocol
Conclusions: Significantly greater benefits were seen in the active group than in
the placebo group for all primary outcomes

61. 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

62. Contact details:
Marcus Webb
marcus.webb@btinternet.com
Hadley Wood Healthcare
0208 441 8352
www.hadleywoodhealthcare.co.uk