Monday, November 15, 2010

Treating and Beating Fibromyalgia

Note this is an abbreviated version of my feature article that appeared in the November issue of the medical journal "Townsend Letter for Doctors and Patients."

Fibromyalgia syndrome (FMS) is an illness characterized by diffuse muscle pain, poor sleep, and unrelenting fatigue.

Individuals with fibromyalgia may also experience headaches, anxiety, depression, poor memory, numbness and tingling in the extremities, cold hands and feet, irritable bowel syndrome, lowered immune function, and chemical sensitivities. Over 10 million Americans suffer with fibromyalgia; ninety percent of them are women between 25 and 45 years old. 1

Fibromyalgia is now thought to arise from a miscommunication between the nerve impulses of the central nervous system. The neurons, which supply the brain, become more excitable, exaggerating the pain sensation. This over-amplication of pain is referred to as "central sensitization". 19

Fibromyalgia patients have a reduction in their pain threshold (allodynia), an increased response to painful stimuli (hyperalgesia) and an increase in the duration of pain after nociceptor stimulation (persistent pain).

Individuals with fibromyalgia syndrome have low levels of serotonin, a 4-fold increase in nerve growth factor, and elevated levels of substance P.20 Nerve growth factor (NGF) is a member of a family of peptides known as the neurotrophins. The exposure of nociceptive sensory neurons to NGF leads to up-regulation of substance P in sensory neurons. 21

Substance P, the neuropeptide in spinal fluid, is a neurotransmitter that is released when axons are stimulated. Increased levels of substance P increase the sensitivity of nerves to pain or heighten awareness of pain. Although it’s not fully understood, fibromyalgia patients have an imbalance of the hypothalamus-pituitary-adrenal  (HPA) axis. This imbalance creates hormonal inconsistencies, which disrupt the body’s ability to maintain homeostasis.

Many of the most common fibromyalgia symptoms including widespread muscle pain, fatigue, poor sleep, gastrointestinal problems, and depression regularly occur in people with various neuroendocrine disorders, including those manifested by HPA dysfunction. 22
Researchers believe suppression of the HPA (quite likely from chronic stress), which results in lowering human growth hormone (HGH), dehydroepiandrosterone (DHEA), cortisol, and other hormones, is aggravated by the chronic pain and poor sleep associated with fibromyalgia. 23, 24

Hypothalamus-Pituitary-Adrenal Axis (HPA) Dysfunction 

The main function of the hypothalamus is homeostasis, or maintaining the body's status quo.
The hypothalamus receives and transmits messages from the nervous system and hormonally through the circulatory system. Because of its broad sphere of influence, the hypothalamus could be considered the body’s master computer. The hypothalamus receives continuous input about the state of the body, and must be able to initiate compensatory changes if anything drifts out of line.

The Hypothalamus regulates such bodily functions as:
1. Blood pressure- is often low in those with fibromyalgia.
2. Digestion- bloating, gas, indigestion, and reflux are common in FMS patients.
4. Circadian rhythms (sleep/wake cycle)- which is consistently disrupted in FMS.
6. Sex drive- loss of libido is a common complaint for FMS patients.
7. Body temperature-   is often low in FMS patients.
8. Balance and coordination- FMS patients have balance and coordination problems.
9. Heart rate- mitral valve prolapse (MVP) and heart arrhythmias are a common finding in FMS patients.
10. Sweating- it’s not unusual for FMS patients to experience excessive sweating.
11. Adrenal hormones- are consistently low in FMS patients.
12. Thyroid hormones and metabolism-hypothyroid is a common finding in FMS patients.
Recent studies show that over 43% of FMS patients have low thyroid function. It's estimated that those with FMS are 10 to 250,000 times more likely to suffer from thyroid dysfunction.25

Stress and Fibromyalgia

A survey by The Fibromyalgia Network reports that 62% of their respondents list physical or emotional stress as the initiating factor in their acquiring fibromyalgia. 32
I believe chronic stress is the underlying catalyst for the onset of HPA dysfunction and fibromyalgia. Several studies have demonstrated how chronic stress undermines the normal hypothalamic-pituitary-adrenal axis (HPA) function.33
When explaining the role of stress in fibromyalgia, I find the following analogy helps put stress and fibromyalgia into perspective.
“We are all born with a stress coping savings account. This account is filled with numerous chemicals we use to help us deal with daily stress-serotonin, norepinephrine, cortisol, magnesium, and other important hormones and nutrients. The more stress we encounter, the more stress coping chemicals we use. We replenish our stress coping savings account with adequate rest. Consistent deep restorative sleep ensures we are making more deposits than withdrawals from our stress coping account.
Since fibromyalgia patients struggle with getting a consistent good nights sleep they eventually bankrupt their stress coping account.

The Importance of a Good Night’s Sleep
Studies have shown that individuals who were prevented from going into deep sleep for a period of a week develop the same symptoms associated with FMS and CFS; diffuse pain, fatigue, depression, anxiety, irritability, stomach disturbances, and headaches. 34,35.
Sleep deprivation markedly increases inflammatory cytokines (pain causing chemicals)—by a whopping 40%. 36


Serotonin helps regulate sleep, digestion, pain, mood, and mental clarity.37
Serotonin helps:
1. Raise the pain threshold (have less pain), by blocking substance P.
2. You fall asleep and stay asleep through the night.
3. Regulate moods. “The happy hormone” reduces anxiety and reduces depression.
4. Reduce sugar cravings and over-eating.
5. Increase a person’s mental abilities.
6. Regulate normal gut motility (transportation of food-stuff) and reverse irritable bowel syndrome (IBS).

Surveys have shown that as many as 73% of FMS patients have irritable bowel syndrome.
You have more serotonin receptors in your intestinal tract than you do in your brain.

Emotionally stressful situations cause the body to release adrenaline, cortisol and insulin. These stress hormones stimulate the brain to secrete serotonin. Long term stress and poor dietary habits can deplete the body’s serotonin stores.38

Tryptophan, 5 Hydroxytryptophan  (5HTP) and Serotonin

Individuals with fibromyalgia have low levels of tryptophan38, serotonin39, and
5-HTP.40 Studies show that fibromyalgia patients have higher levels of metabolites in the kynurenine pathway, which diverts tryptophan away from serotonin production.41

Tryptophan is one of eight essential amino acids. Tryptophan is absorbed from the gut into the bloodstream and then dispersed throughout the body. Ninety percent of tryptophan is used for protein synthesis, one percent is converted to serotonin, and the balance is used to make niacin. In the formation of serotonin, tryptophan is hydroxylated to 5-hydroxy-tryptophan (5-HTP) by tryptophan hydroxylase.
5-HTP is converted to serotonin by the decarboxylase enzyme, which is vitamin B6 dependent.

Selective Serotonin Reuptake Inhibitor (SSRI) Medications
Prescription antidepressants can be helpful. However, antidepressant drugs have potential side effects including anxiety, depression, fatigue, decreased sex drive, and disruption of normal circadian rhythms.42

SSRI’s are supposed to help a patient hang onto and use their naturally occurring stores of the brain chemical serotonin. It’s like using a gasoline additive to help increase the efficiency of your cars fuel.

Most of the patients I see with fibromyalgia are running on fumes and a gasoline additive won’t help. 

Please keep in mind that several studies show that between 19-70% of those taking antidepressant medications do just as well by taking a placebo or sugar pill.43
I recommend my patients boost their serotonin levels by taking 5HTP.

5HTP and Depression

Studies (including double-blind) comparing SSRI and tricyclic antidepressants to 5HTP have consistently shown that 5HTP is as good if not better than prescription medications in treating mood disorders. Furthermore, 5HTP doesn’t have some of the more troubling side effects associated with prescription medications. 44, 45

5HTP and Sleep

5HTP has been shown to be beneficial in treating insomnia, especially in improving sleep quality by increasing REM sleep and increases the body’s production of melatonin by 200%. 46,47

5HTP and Fibromyalgia

Double-blind placebo-controlled trials have shown that patients with FMS were able to see the following benefits from taking 5HTP: 48.
• decreased pain.
• improved sleep.
• less tender points.
• less morning stiffness.
• less anxiety.
• improved moods in general, including in those with clinical depression. 49
• increased energy.

Irritable Bowel Syndrome, 5HTP and Serotonin
There are more serotonin receptors in the intestinal tract than there are in the brain. This is one reason people get butterflies in their stomach when they get nervous.50
Serotonin controls how fast or how slow food moves through the intestinal tract.51, 52
It’s common for the symptoms associated with IBS, diarrhea and constipation, to disappear within 1–2 weeks once serotonin levels are normalized with 5HTP replacement therapy.

My 5HTP and Sleep Restoration Protocol

I instruct my patients to take 50mg of 5HTP 30 minutes before bed on an empty stomach (90 minutes after or 30 minutes before eating), with 4 ounces of grape juice. I know 5HTP doesn’t have to compete with other amino acids to cross the blood brain barrier, but this routine seems to heighten the effect of 5HTP.
One of three things will happen when taking 5HTP.

1. The patient falls asleep within 30 minutes and sleeps through the night. If so, they stay on this dose until their next scheduled visit with me (typically 2 weeks).

2. Nothing happens. This is typical response to such a low dose. The patient should add an additional
50 mg. each night (up to a max of 300 mg.) until they fall asleep within 30 minutes and sleep through the night.

3. Instead of making the patient sleepy, the first dose makes them more alert. This occurs more often in CFS and chemical sensitivity patients who have a sluggish liver. If this happens, they’re to discontinue taking 5HTP at bedtime and instead take 50 mg. with food for 1–2 days. Taking 5HTP with food seems to help slow down it’s absorption, allowing the liver to process it more effectively. Taking 5HTP with food will not (usually) make a person sleepy. After 1-2 days on 5HTP with no further problems, they should increase to 100 mg. of 5HTP with each meal (300mg a day).

Can patients take 5HTP along with antidepressant medications?

Yes, patients can take 5HTP with antidepressant medications. I’ve treated thousands of patients with amino acid replacement therapy, 95% of which were already taking antidepressants when they come to see me. I’ve never had a patient report a problem with combing 5HTP with prescription drugs. It can happen, but I believe it to be rare.

Can patients take 5HTP with sleep medications?

Yes. I don’t recommend patients discontinue taking their sleep medications. Instead I suggest they start using 5HTP and increase the bedtime dose until they sleep through the night. At some point they should be able to work with their doctor and slowly wean off the prescription sleep medication. Remember all prescription sleep medications have side effects. No one has an Ambien deficiency, however, fibromyalgia patients certainly have 5HTP and serotonin deficiencies, which need to be corrected.

What if my patient is taking a prescription sleep medication and sleeping through the night?
Prescription drugs that promote deep restorative sleep include Ambien, Elavil, Trazadone, Flexeril, and Lunesta. These medications can be helpful. However, these medications have potential side effects that may cause the very symptoms associated with fibromyalgia. Ambien may cause short-term memory loss, fatigue, depression, and flu-like aches and pains.
Other common sleep inducing drugs, including benzodiazepines (Klonopin, Ativan, etc.), muscle relaxants (Zanaflex), Neurontin, and Lyrica don't promote deep delta wave sleep and therefore are not recommended. Remember the reason they’re taking these prescription drugs is because they have a serotonin (and perhaps a melatonin) deficiency, not a drug deficiency. You want them to build up their serotonin levels so that eventually they may not need prescription sleep medications. You should have them add 5HTP (50 mg.) three times daily with food. If no problems arise after 2–3 days, they should then increase to 100 mg. with each meal.

What if someone has a serotonin syndrome reaction?

A serotonin syndrome may occur if a person gets too much serotonin. This can cause rapid heartbeat, increased pulse rate, elevated blood pressure, agitation, and in its worst-case scenario, life threatening irregular heartbeats (arrhythmia).
I’ve recommended 5HTP to thousands of individuals over the last 7 years, rarely have I encountered a problem. I always start with a low dose (50 mg.) and warn the patient to stop taking it at bedtime if she has a funny reaction.

What are some of the other potential side effects of 5HTP?

Other than some patients becoming more alert when taking 5HTP at bedtime, I have had very few complaints from patients. The literature reports that individuals may have transient headaches and nausea from taking 5HTP. I have had less than half a dozen patients have one of these side effects. The headaches and any nausea usually go away after a couple of days.

What do you do when your patient still can’t fall asleep and sleep through the night even when taking 300mg of 5HTP?
If after two weeks, someone is not falling asleep and staying asleep through the night, I add melatonin. First, I make sure she is taking 5HTP as she should be and at the maximum dose of 300mg.

1. Nutrition reviews  52(7)p249 1994.
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3. Goldenberg D 1989 Fibromyalgia and its Relationship to CFS, Viral Illness and Immune Abnormalities. Journ of Rheum 16 (S19): 92)
4. Moldofsky H 1993 Fibromyalgia, sleep disorder and chronic fatigue syndrome. In: Bock G Whelan J (eds) CIBA Foundation Symposium 173. Wiley, Chichester, pp 262-279.
5. Russell IJ. Neurohormonal aspects of fibromyalgia syndrome. Rhum Dis Clin North Amer 1989;15:149-168.
6. Buskila D, Neumann L et al 1997 Increased rates of fibromyalgia following cervical spine injury. Arthritis and Rheumatism 40(3):446-452.
7. Moldofsky H 1993 Fibromyalgia, sleep disorder and chronic fatigue syndrome. CIBA Symposium 173, 1993, pp 262-279.
8. Anne Marit Mengshoel, Center for Rheumatic Diseases, The National Hospital, Akersbakken 27, N-0172 Oslo, Norway.
9. Fibromyalgia Network Newsletter October 1999p1-3.
10. Lowe J C, Garrison R L, Reichman A J, Yellin J, Thompson M, Kaufman D 1997a Effectiveness and Safety of T3 (triiothyroxine) therapy for euthyroid Fibromyalgia: a double-blind placebo-controlled response-driven crossover study. Clinical Bulletin of Myofascial Therapy 2(2/3):31-58.
11. Russell I, Vipraio G, Lopez Y et al 1993 Serum seorotonin in FMS and rheumatoid arthritis and healthy normal controls. Arthritis and Rheumatism 36(9):S2231
12. Jeffries W McK The present status of ACTH, cortisone, and related steroids in clinical medicine N Engl J Med 253:441-446;1955.
13.Selye H The general adaptation syndrome and diseases of adaptation J Clin Endocrinol Metab 6:117-230;1946.
14.Jeffries W McK. Safe Uses of Cortisone Charles C Thomas Publisher;1981.
15. Gerhard K. Endresen, Mycoplasma blood infection in chronic fatigue and fibromyalgia syndromes  2003. Rheumatology International 23(5):211-215.
16. Gail K. Adler, Neuroendocrine Abnormalities in†Fibromyalgia [abstract]Current Pain and Headache Reports 2002, 6:289-298
17. P.Koch-Sheras and A. Lemley, The Dream Sourcebook. Los Angeles: Loweel House.
18. Harding S. MD Sleep in Fibromyalgia Patients: Subjective and Objective Findings.
American Journal of the Medical Sciences. Fibromyalgia. 315(6):367-376, June 1998.
19. Staud R, Smitherman . 2002 Aug;6 Peripheral and central sensitization in fibromyalgia: pathogenetic role. Curr Pain Headache Rep. (4):259-66.
20. Russell IJ. Elevated cerebrospinal fluid levels of substance P in patients with the fibromyalgia syndrome. Arthritis Rheum.1994 Nov;37(11):1593-601
21. Woolf CJ. Nerve growth factor contributes to the generation of inflammatory sensory hypersensitivity. Neuroscience 1994; 62:327–331.
22. Gail K. Adler, Neuroendocrine Abnormalities in Fibromyalgia. Current Pain and Headache Reports 2002, 6:289-298
23. Calis M, Gokce C, et al. Investigation of the hypothalamo-pituitary-adrenal axis (HPA) by 1 microg ACTH test and metyrapone test in patients with primary fibromyalgia syndrome. J Endocrinol Invest. 2004 Jan;27(1)42-6.
24. Okifuji A, Turk DC. Stress and psychophysiological dysregulation in patients with fibromyalgia syndrome. Appl Psychophysiol Biofeedback. 2002 Jun;27(2):129-41.
25. Lowe J C, Garrison R L, Reichman A J, Yellin J, Thompson M, Kaufman D 1997a Effectiveness and Safety of T3 (triiothyroxine) therapy for euthyroid Fibromyalgia: a double-blind placebo-controlled response-driven crossover study. Clinical Bulletin of Myofascial Therapy 2(2/3):31-58.
26. Rudman, D. Growth hormone, body composition, and aging, Journal of the American Geriatrics Society. 1985;33:800-7.
27. Lopez, J. F., et al. Serotonin 1a receptor mRNA regulation in the hippocampus after acute stress. Biological Psychiatry 45: 943-947.
28. Chalmers, D. T. et al. Molecular Aspects of the Stress Axis and Serotonergic Function in Depression. Clinical Neuroscience 1: 122-128. 1993.
29. M. Biondi, A. Picardi . Psychological Stress and Neuroendocrine Function in Humans: The Last Two Decades of Research. Psychotherapy and Psychosomatics 1999;68:114-150.
30. Wisniewski TL, Hilton CW, Morse EV, et al. The relationship of serum DHEA-S and cortisol levels to measures of immune function in human immunodeficiency virus-related illness. Am J Med Sci. 1993 Feb; 305(2):79-83.
31. Altamus M, Dale JK, Michelson D, Demetrick MA, Gold PW, Straus SE Abnormalities in response to vasopressin infusion in chronic fatigue syndrome. Psychoneuroendocrinology.2001 Feb; 26(2):175-88
32. Fibromyalgia Network Newsletter October 1999p1-3.
33. Mengshoel, A. Center for Rheumatic Diseases, The National Hospital, Akersbakken 27, N-0172 Oslo, Norway.
34. P.Koch-Sheras and A. Lemley, The Dream Sourcebook. Los Angeles: Loweel  House.
35. Harding, S. Sleep in Fibromyalgia Patients: Subjective and Objective Findings.
American Journal of the Medical Sciences. Fibromyalgia. 315(6):367-376, June 1998.
36. Andrea Alberti1, et al. Plasma cytokine levels in patients with obstructive sleep apnea syndrome: a preliminary study Journal of Sleep ResearchVolume 12 Issue 4 Page 305  - December 2003.
37. Russell IJ, Vaeroy H, Javors M, Nyberg F. Cerebrospinal fluid biogenic amine metabolites in fibromyalgia/fibrositis syndrome and rheumatoid arthritis. Arthritis Rheum 1992;35:550-556.
38. Winberg S, Overli O, Lepage O. Suppression of aggression in rainbow trout (Oncorhynchus mykiss) by dietary L-tryptophan. J Exp Biol. 2001 Nov;204(Pt 22):3867-76.
39. Karl G. Henriksson, MD, PhD. Is Fibromyalgia a Central Pain State? Source: Journal: J of Musculoskeletal Pain, Vol. 10, No. 1/2,2002, pp. 45-57.
40. Yunus MB, Dailey JW, Aldag JC, et al. Plasma tryptophan and other amino acids in primary fibromyalgia: a controlled study. J Rheumatol 1992;19:90-94.
41. Hrycaj P, Stratz T, Muller W. Platelet 3H-imipramine uptake receptor density and serum serotonin levels in patients with fibromyalgia/fibrositis syndrome. J Rheumatol 1993;20:1986-1988. [letter].
42. Russell IJ, Vipraio GA, Acworth I. Abnormalities in the central nervous system metabolism of tryptophan to 3-hydroxy kynurenine in fibromyalgia syndrome. Arthritis Rheum 1993;36:S222.
43. Russell IJ. Neurohormonal abnormal laboratory findings related to pain and fatigue in fibromyalgia. J Musculoskeletal Pain 1995;3:59-65.
44.Monthly Prescribing Reference Publication Nov 2005, New York NY
45. Joan-Ramone Laporte and Albert Figueras, “Placebo Effects in Psychiatry,” Lancet 334 (1993):1206-8.
46. Byerley WF; Judd LL; Reimherr FW; Grosser BI. 5-Hydroxytryptophan: a review of its antidepressant efficacy and adverse effects.
J Clin Psychopharmacol (HUD), 1987 Jun; 7 (3): 127-37
47. Birdsall T., “5-Hydroxytryptophhan: A Clically Effective Serotonin Precursor”  Altern Med Rev 1998;3(4):271-280.
48. Puttini PS; Caruso I Primary fibromyalgia syndrome and 5-hydroxy-
L-tryptophan: a 90-day open study. Rheumatology Unit, L Sacco Hospital, Milan, Italy.
J Int Med Res 1992 Apr;20(2):182-9
49. J. Angst, B. Woggon, and J. Schoepf, “The treatment of depression with L-5-hydroxytrptophan versus Imipramine: Results of two open and one double blind study, Archiv fur Psychiatrie und Nervenkrankheiten 224 (1997): 175-86.
50. Delvaux MM. Gastroenterology Unit and Laboratory of Digestive Motility, CHU Rangueil, Toulouse, France. Stress and visceral perception. Can J Gastroenterol 1999 Mar;13 Suppl
51. Goldberg PA, Kamm MA, Setti-Carraro P, van der Sijp JR, Roth C. Modification of visceral sensitivity and pain in irritable bowel syndrome by 5-HT3 antagonism (ondansetron). Digestion 1996 Nov-Dec;57(6): 478–83A:32A–36A.
52. Johanson JF. Options for patients with irritable bowel syndrome: contrasting traditional and novel serotonergic therapies. Neurogastroenterol Motil 16(6):701-11, 2004
53. Wehr T, et al. (2001). A circadian signal of change of season in patients with seasonal affective disorder. Archives of General Psychiatry, 58(12): 1108–1114
54. Waldhauser F et al. Sleep laboratory investigations on hypnotic properties of melatonin. Psycho Pharm 1990. 100: 222–6.
55. Dollins AB, Zhadanova IV, Wurtman RJ, Lynch HJ, Deng MH. Effect of inducing nocturnal serum melatonin concentrations in daytime on sleep, mood, body temperature, and performance. Proc Natl Acad Sci USA 1994;91: 1824–28.
56. Functional Assessment Resource Manual from Great Smokies Laboratory, 1999.
57. ibid.
58. ibid.
59. Citera G, Arias MA, Maldonado-Cocco JA, Lazaro MA, Rosemffet MG, Brusco LI, Scheines EJ, Cardinalli DP. The effect of melatonin in patients with fibromyalgia: a pilot study. Clin Rheumatol 19(1):9-13, 2000.

Thursday, November 11, 2010

Are Fibromyalgia Patients Crazy?

Have you’ve been told you’re crazy, lazy or depressed? If so you’re not alone. Friends, family and doctors may try to make you think your illness isn’t real, “its all in your head.”

You often lose your train of thought mid-sentence, have strange reactions to medications, and suffer with an assortment of health problems; yet all your labs are normal. You’ve got numerous complaints including anxiety, depression, fatigue, chronic pain, insomnia, IBS, MVP, chronic sinusitis, tingling in their extremities, night sweats, chemical sensitivities, headaches, reflux, and other symptoms.

I’d be crazy too if I went days without sleeping, had diffuse chronic pain, no energy, no life, and no hope. You’ve been bounced from one doctor to another, had dozens of tests, taken numerous drugs which didn’t help, and continue to get worse, year after year. The traditional drugs of choice for fibromyalgia, including, NSAIDS, antidepressants, anticonvulsant medications, muscle relaxants, tranquilizers, and pain medications, may provide short-term relief, yet their results are often fleeting and their side-effects detrimental. It’s not unusual to be taking twelve or more prescription drugs, many of which contribute to their erratic behavior.

The sleep drugs Ambien and Lunesta may cause short-term memory loss, fatigue, flu-like symptoms, and depression. Tricyclic antidepressants, including Trazadone and Elavil, may cause early-morning hangover, mental confusion, and lethargy. SSRI drugs may cause anxiety, depression, mental blunting, and lethargy. Klonopin and other benzodiazepines may cause depression, fatigue, and decreased mental function. All of these drugs are known to deplete at least one or more essential mood-dependant vitamin, mineral, or nutrient (B6, B12, CoQ10, Folic acid, etc.). Individuals with fibromyalgia are also deficient in the brain chemicals, which help regulate mood and mental function.

Neurotransmitter Deficiencies

Research shows that the majority of fibromyalgia patients are deficient in serotonin, dopamine, and norepinephrine. These three neurotransmitters (brain chemicals) are essential for optimal mood and mental function. Serotonin, also known as the “happy hormone,” helps regulate mood, sleep, digestion, bowel movements, pain, and mental clarity. Individuals with fibromyalgia have low levels of the amino acid tryptophan, as well as 5HTP, which are needed for the production of serotonin.
L-phenylalanine derived norepinephrine, when released in the brain, causes feelings of arousal, energy, drive, and ambition. No wonder you suffer with “fibro fog.”


Stress Coping Savings Account
I like to use the analogy of being born with a stress-coping savings account. We have certain chemicals, vitamins, minerals, and hormones like serotonin, dopamine, norepinephrine, and cortisol that allow us to handle moment-to-moment, day-to-day, stress. The more stress we’re under, the more withdrawals we make. Individuals with fibromyalgia have made more withdrawals than deposits.

Serotonin re-uptake inhibitors, Lexapro, Paxil, Zoloft, and others, don’t make serotonin, they only help the brain hang onto and use serotonin more effectively. These drugs are like using a gasoline additive, but those with fibromyalgia don’t have any serotonin to re-uptake. They’ve bankrupted their stress coping savings account and depleted their serotonin. These drugs usually don’t provide long-term relief.
Fortunately, there are some tried-and-true nutritional protocols that can help build up the bankrupted stress-coping savings account.

5-Hydroxytryptophan 5HTP
Double-blind, placebo-controlled trials have shown that patients with FMS were able
to see the following benefits from increasing serotonin through 5HTP replacement therapy:
• Decreased pain.
• Improved sleep.
• Less tender points.
• Less morning stiffness.
• Less anxiety.
• Improved moods in general, including in those with clinical depression.
• Increased energy.

S-adenosyl- L-methionine  (SAMe)
S-adenosyl- L-methionine  (SAMe) increases the action of several neurotransmitters including serotonin, norepinephrine and dopamine, by binding these hormones to their cell receptors. However, patients with fibromyalgia have been shown to be deficient in this essential amino acid.
One study shows that patients taking SAMe for a period of six weeks had an improvement of 40 percent in pain reduction and 35 percent improvement in their depression.

Along with 5HTP and SAMe, I’ve found that a good optimal daily-allowance multivitamin with a free-form amino acid blend, fish oil, malic acid, and generous amounts of magnesium is essential for reversing the “brain fog,” poor energy, chronic pain, mood disorders, and sleep disturbances so common in fibromyalgia.

Please know that, while you might not think you’re the sharpest tool in the shed, with the right nutrients you can replenish your brain chemicals, build-up your stress coping savings account, and even remember where you put your car keys.


Tuesday, November 9, 2010

The Evolution of Mood Disorder Wonder Drugs


Prior to the 20th century mood disorders and mental illness were treated with a variety of obscure and often barbaric methods including frontal lobotomies (with no anesthesia), exorcisms, and shamanistic potions.

Dr. Benjamin Rush, the "father of American psychiatry," was the first to believe that mental illness is a disease of the mind and not a "possession of demons." His classic work, Observations and Inquiries upon the Diseases of the Mind, published in 1812 promoted the belief at the time, that "madness" was an arterial disease, an inflammation of the brain.
Dr. Rush wrote that as much as "four-fifths of the blood in the body" should be drawn away- Rush bled one patient 47 times, removing four gallons of blood over time. He confined others in his "Tranquilizer Chair' that completely immobilized every part of their body for long periods and blocked their sight with a bizarre wooden shroud, while they were doused in ice-cold water.

In the early 1900’s frontal lobotomies and electrical shock therapy were standard fair.
Insulin Coma Therapy was introduced into psychiatry in 1933. And within a few years, every psychiatric clinic in Germany was doing Insulin Coma Therapy. Along with all the praise it received, it was also associated with a very high mortality rate and eventually lost it’s appeal.

In 1954 the first “modern” sedative drug known as Thorazine, fueled by a huge promotion campaign by Smith, Klein & French, swept the nation. This new medication along with Haldol, spawned an additional class of drugs known as benzodiazepines (tranquilizers). The effect of taking these drugs was explicitly compared to having a lobotomy, and they were thought to induce "chemical lobotomies". Thorazine became the drug Du jour during the 1950’s and the number of individuals taking it went from 428 in 1952 to over 2,000,000 in 1957.

In the 1960’s Hoffman La Roche was successful in marketing the benzodiazepine (tranquilizers) Librium and Valium. Benzodiazepines became a frequent recommendation for any number of illnesses associated with mental stress. In fact these drugs became known as “mother’s little helper.”
To combat the ills of modern day stress, housewives, college students, and busy executives were encouraged to take these medications. Valium became the best-selling drug at that time. Klonopin, Ativan, and Xanax followed, all hailed as safer and more effective than the anti-anxiety drugs that preceded them.
In reality, all of these drugs work about the same and have similar side effects, including sleep disturbances (poor sleep), seizures, neuropsychiatric disturbances (mania, depression, suicide, etc.) tinnitus (ringing in the ears), transient memory loss (amnesia), dizziness, agitation (anxiety), disorientation, hypotension (low blood pressure), nausea, edema (fluid retention), ataxia (muscular in-coordination), tremors, sexual dysfunction (decreased desire and performance), asthenia (weakness), somnolence (prolonged drowsiness or a trance-like condition that may continue for a number of days), and headaches.
Forty percent of adults, 60 or older experience drug-induced tics or tardive dyskinesia (tremors or uncontrollable shakes) from taking a benzodiazepine drug.
Tragically, only 10 to 30% are able to successfully stop taking these drugs, most are addicted for life. (Please see my past article “SOS Save Our Seniors”).

Modern Era

In the 1960’s Merck introduced the tricyclic antidepressant drug, Amitriptyline (Elavil).
Tricyclic drugs were promoted as safer and more effective than benzodiazepines. Initially all the rage, these drugs became synonymous sedation, weight gain, loss of sex drive, nervousness, weakness, blurred vision, muscle spasms, or tremors, dry mouth, and convulsions. These drugs fell out of favor when the newer, supposedly safer, but largely over-hyped selective serotonin re-uptake inhibitor (SSRI’s) medications became available.

The first SSRI to hit the American market was Prozac in 1987 (please see my past articles “Warning Your Antidepressant May be Your Problem,” and The Depressing Truth About Antidepressants”) and was quickly hailed as the “wonder drug” of the 20th century. But like many of the so-called “wonder drugs” Prozac and the rest of the SSRI drugs haven’t lived up to all the hype. The popularity of these medications is largely due to the false belief that SSRI’s are safe, effective, and have relatively few risks. However, their side effects include-anxiety, depression, headache, muscle pain, chest pain, nervousness, sleeplessness, drowsiness, weakness, changes in sex drive, tremors, dry mouth, irritated stomach, loss of appetite, dizziness, nausea, rash, itching, weight gain, diarrhea, impotence, hair loss, dry skin, chest pain, bronchitis, abnormal heart beat, twitching, anemia, low blood sugar, and low thyroid.

In December of 2006, the FDA warned that SSRI drugs cause increased suicidality in young adults. Suicide occurs more than twice as much on antidepressants than on sugar pills in individuals under age 25. And to top it all off, studies show that up to 70% of those taking antidepressant medications do just as well by taking a placebo or sugar pill.

21st Century Psychotics
The new class of “wonder drugs” for the treatment of mood disorders are known as atypical antipsychotics - Zyprexa, Risperdal, Geodon, Ivega, Abilify, Clozril, and Seroquel. Originally used for schizophrenia and Bi-polar patients, atypicals have now become routine in the treatment of ADD, anxiety, depression, and Alzheimer’s disease.
They’re being marketed as safer and more effective than the older antipsychotic benzodiazepines – less shakes, better response. Of course like most wonder drugs they come with a steep cost- atypicals cost some 20 times more than the older psychotic drugs. The FDA has gone on record warning that there’s no proof that these drugs are safer or better and any advertisement that promotes this is false.

No problem. Even though they couldn’t promote their drugs, the drug companies could and did hire academics and doctors to recommend these drugs. 
In an attempt to squelch the debate, in 2005 the U.S. government funded a $60-million study called CATIE (Clinical Antipsychotic Trials of Intervention Effectiveness). The study concluded – first, atypicals were generally no more effective than the older drug, perphenazine (similar to Haldol) and secondly, slightly fewer people on atypicals dropped out of the study due to tremors, but the new drugs had their own distinct side effects- weight gain and diabetes.

According to Harvard trained psychiatrist, Dr Stefan Kruszewski, "the new generation of antipsychotics substantially increase the risk of obesity, diabetes type II, hypertension, cardiovascular complications, heart attacks and stroke." Persons on atypicals have been found to commit suicide two to five times more frequently than the schizophrenic population in general. Other potentials side effects include- tardive dyskinesia, low blood pressure, seen as dizziness, and possibly fainting; increased heart beat; seizures; liver problems, difficulty swallowing, sleepiness, dry mouth, dizziness, restlessness, constipation, upset stomach, weight gain, increased appetite, and tremor.

Stay tuned I’m sure there will be another antipsychotic “wonder drug” appearing in a media campaign soon. I can’t wait to hear how the new drug is safer and more effective than today’s atypicals.

1. R. H. Murphree, D.C. “Treating and Beating Anxiety and Depression With Orthomolecular Medicine.” Harrison and Hamptom Publishing Birmingham Alabama 2005.
2.Figures from Judith Swazey’s book "Chlorpromazine in psychiatry" published 1974.