Browsing Tag

rheumatology

Diseases and Conditions

Can small fiber neuropathy mimic fibromyalgia?

July 19, 2017
Small fiber neuropathy can feel like your legs and feet are on fire. Can small fiber neuropathy mimic fibromyalgia?

Can small fiber neuropathy (SFN) mimic fibromyalgia?  The simple answer is yes, but it’s more complicated… So why does a rheumatologist care about small fiber neuropathy?  The answer is very simple.  Many people get referred to a rheumatologist for fibromyalgia, which is a disease that causes widespread pain, brain fog, non-restorative sleep, and various other unexplained symptoms such as headaches.  While fibromyalgia IS NOT an autoimmune disease, small fiber neuropathy can present very similarly but CAN BE caused by autoimmune diseases.

There’s a lot of controversy in the medical community about fibromyalgia.  One group believes that it’s a separate entity, some do not believe in its existence, and some people are somewhere in the middle.  Personally, I believe that fibromyalgia likely represents many diseases that we haven’t identified yet.  Until we can categorize them into distinct entities, we’re going to have a hard time understanding them, let alone come up with effective treatments.

First, let’s review the clinical criteria that doctors use to make a diagnosis of fibromyalgia.

2010 ACR criteria for fibromyalgia

Criteria A patient satisfies diagnostic criteria for fibromyalgia if the following 3 conditions are met:

  1. Widespread pain index (WPI) ≥ 7 and symptom severity (SS) scale score ≥5 or WPI 3–6 and SS scale score ≥ 9.
  2. Symptoms have been present at a similar level for at least 3 months.
  3. The patient does not have a disorder that would otherwise explain the pain.

Number #1 are various validated pain scores.  These are rarely used in clinic but are often used for clinical trials.  It helps researchers objectively quantify pain levels at any given time.  As you can see, we don’t use trigger points to check for fibromyalgia anymore.

Small fiber neuropathy in people with fibromyalgia

So is small fiber neuropathy a feature of fibromyalgia, just like it is for diseases like Sjogren’s syndrome or are patient’s with small fiber neuropathy mistakenly diagnosed with fibromyalgia?

In one study, 46 patients with fibromyalgia and 34 normal controls were tested for small fiber neuropathy with a specialized skin biopsy.  I’ll talk more about this later on.  The researchers measured pain intensity with a survey called the Neuropathic Pain Symptom Inventory. They found that 32.6% of patients with fibromyalgia had reduced nerve fiber density on their biopsy, i.e, they had small fiber neuropathy.  Interestingly, they also didn’t find any correlation between pain scores and nerve density.

This implies three things.  First of all, the level of pain and symptoms experienced by people with fibromyalgia was the same as those with small fiber neuropathy.  So you can’t distinguish between fibromyalgia and small fiber neuropathy based on symptoms alone.  Second, about 1/3 of people diagnosed with fibromyalgia have small fiber neuropathy.  Finally, having worse nerve density doesn’t necessarily mean you’ll experience more pain.  Other studies have also found similar results.

Now this still doesn’t answer all our questions but I think it’s safe to say that testing for small fiber neuropathy should happen when there is a clinical diagnosis of fibromyalgia. Now let’s talk about small fiber neuropathy.

What is Small Fiber Neuropathy?

Small fiber neuropathy results from damage to the small, unmyelinated nerve fibers that send pain and temperature and control autonomic functions like sweating.  The following are some of the symptoms caused by SFN:

  • Burning pain
  • Numbness and tingling
  • Pain that is out of proportion
  • Cramping
  • Unexplained itching
  • Lack of sweating
  • Temperature dysregulation
  • Dryness

How to diagnose small fiber neuropathy?

The first step to diagnose small fiber neuropathy is taking a care history, reviewing risk factors, and performing a detailed physical examination.  On physical exam, deep tendon reflexes (e.g., knee jerk reflex) are normal and there’s no loss of strength.  If there is a suspicion for SFN your doctor may send you for electrodiagnostic tests (EMGs).  These are colloquially called nerve conduction tests.

Small fiber neuropathy affects small myelinated A-delta and unmyelinated C fibers, NOT large fibers.  This means that EMGs are typically negative because these are good for looking for problems affecting large fibers like carpal tunnel syndrome.

One way to diagnose small fiber neuropathy is with a skin biopsy, more specifically epidermal nerve fiber density testing (ENFD).  This technique allows direct visualization, quantification, and morphologic assessment of small sensory fibers innervating the skin.  This technique has a sensitivity of 88% and a specificity of 95 – 97%.  In layman’s terms, the test will miss 12% of cases of small fiber neuropathy, but if the test is positive, there’s a 3 – 5% chance that it’s a mistake (false positive).   These are actually pretty good values.    A report by the European Federation of Neurological Societies states that ENFD is a reliable and efficient tool to assess for SFN.

How is epidermal fiber density testing done?

Epidermal fiber density testing is done by taking 2-4 three mm punch biopsies.  This test happens in clinic.  It’s quick and safe.  Your doctor can only do these in areas that have been validated: near the ankle, upper thigh, the foot, near the wrist, and the upper arm.

The biopsy is then sent to a specialized pathologist and stained with anti-protein gene product 9.5 antibody (PGP 9.5), which stains all the axons.  The pathologist can then painstakingly count all the nerves and calculate the density.  The density is then compared to age and sex matched control values to decide whether it’s abnormal.

Common causes of small fiber neuropathy

Once your doctor makes a diagnosis of small fiber neuropathy, then the question is whether there is an underlying cause.  About 50% of small fiber neuropathy cases are idiopathic, meaning that doctors can’t find an underlying cause.  As a result that leaves us with the other 50%.  Of those cases, the most common cause is diabetes mellitus.  In fact, autoimmune diseases make a relatively small proportion of cases, so it’s important to look for other causes first.  There are MANY other causes but these are some of the more common conditions that can cause small fiber neuropathy.

Non-autoimmune causes

  • Diabetes mellitus
  • Lyme disease
  • Hepatitis C infection
  • HIV
  • Celiac disease
  • Chronic kidney disease
  • Hypo/hyperthyroidism
  • Alcohol abuse
  • Medications, especially chemotherapy
  • Vitamin B12, B6, B1 deficiency
  • Paraneoplastic syndromes
  • Amyloidosis
  • Exposure to heavy metals

Autoimmune causes

  • Sjögren’s syndrome
  • Systemic lupus erythematosus
  • Sarcoidosis
  • Rheumatoid arthritis
  • Scleroderma
  • Inflammatory bowel disease (Crohn’s disease and ulcerative colitis)
  • Vasculitis
  • Psoriasis and psoriatic arthritis

Some genetic conditions can also cause small fiber neuropathy, like Fabry’s, but these are very rare.

Treatment

I won’t talk too much about treatment because it really depends on the underlying cause.  If you’re dealing with an autoimmune disease… treat it.  Sometimes symptomatic treatment is also necessarily. The following are some medications that are often used:

  • Tricyclic antidepressants
  • Serotonin norephinephrine re-uptake inhibitors (SNRIs)
  • Pregabalin
  • Gabapentin
  • Topical lidocaine
  • Topical capsaicin

Doctors sometimes use intravenous immunoglobulin (IVIG) in extreme situation, particularly in situations where an autoimmune disease is the culprit. The evidence supporting this type of treatment isn’t great.  Sometimes it works, sometimes it doesn’t.  Moreover, there are no large randomized controlled studies looking at IVIG treatment for small fiber neuropathy.

Ultimately, we’re going to need to understand why and how small fiber neuropathy happens to come up with effective treatments.

Conclusion

I hope this helps explain how small fiber neuropathy (SFN) mimics fibromyalgia and why it’s important to distinguish between both.  For those who want to learn more about small fiber neuropathy and how to live with it, I’ve included a link to a great YouTube video.

Please leave your comments below!

References

Lauria G, Devigili G. Skin biopsy as a diagnostic tool in peripheral neuropathy. Nature Clinical Practice Neurology. 2007 Oct 3;3(10):546-57.

Devigili G, Tugnoli V, Penza P, Camozzi F Lombordi R, Milli G, Broglio , Granieri E, Lauria G. The diagnostic criteria for small fibre neuropathy : from symptoms to neuropathology. Brain 2008; 131; 1912-19.

Lauria G, Hsieh ST, Johansson O, Kennedy WR, Leger JM, Mellgren SI, Nolano M, Merkies IS, Polydefkis M, Smith AG, Sommer C, Valls-Sole J. European Federation of Neurological Societies/Peripheral Nerve Society Guideline on he use of skin biopsy in the diagnosis of small fiber neuropathy. Report of a joint task force of the European Federation of Neurological Societies and the peripheral nerve society. J Peripher Nerv Syst. 2010 Jun;15(2):79-92.

Giannoccaro MP, DonadioV, Incensi A, Avoni P, Liguori R. Small nerve fiber involvement in patients referred for fibromyalgia. Muscle Nerve. 2014 May;49(5):757-9.

Kosmidis ML, Koutsogeorgopoulou L, Alexopoulos H, Mamali I, Vlachoyiannopoulos PG, Voulgarelis M, Moutsopoulos HM, Tzioufas AG, Dalakas MC. Reduction of intraepidermal nerve fiber density (IENFD) in the skin biopsies of patients with fibromyalgia: a controlled study. J Neurol Sci. 2014 Dec 15;347(1-2):143-7.

Chan AC, Wilder-Smith EP. Small fiber neuropathy: getting bigger! Muscle Nerve. 2016 Feb 13. [Epub ahead of print]

UpToDate 2017

Uceyler N, Zeller D, Kahn AK, Kewenig S, Kittel-Schneider A, Casanova-Molla J, Reiners K, Sommer C. Small fibre pathology in patients with fibromyalgia syndrome. Brain. 2013 Jun;136(Pt 6):1857-67.

Medical Disclaimer

This information is offered to educate the general public. The information posted on this website does not replace professional medical advice, but for general information purposes only. There is no Doctor – Patient relationship established. We strongly advised you to speak with your medical professional if you have questions concerning your symptoms, diagnosis and treatment.

Diseases and Conditions Overcoming Inflammation

Can UV light trigger lupus flares?

July 12, 2017
Can UV light trigger lupus flares?

Now that summer is finally in full swing, I’d like to remind everyone to use broad spectrum sunscreen while enjoying the sun!  This is especially important for people living with systemic lupus erythematosus (SLE). Ultraviolet (UV) light is a known trigger of SLE flares BOTH involving the skin and major organs.  Many people also report joint pain, weakness, and headaches.  These flares can be very serious.

Although we know UV light is a trigger for SLE flares, we still don’t fully know how it happens.  This is what we do know.

  • UV light directly damages the DNA of skin cells.
  • The cells release inflammatory cytokines, most notably interleukin-1α and tumor necrosis factor-α.
  • UV light also increases interferon-α signaling. People with high levels of interferon-α signaling often develop fevers, fatigue, and low white cell count (leukopenia).  Interferon-α signaling is thought to be an important part in the development of SLE.

Take home points

So while you’re enjoying the sun remember to:

  1. Avoid the sun when UV light is strongest, between 10 AM and 3 PM. If you use IFTTT, check out this app.  You will get a notification on your phone when the UV index is high… and it’s free!
  2. Use broad spectrum UVA/UVB sunscreen.  Try to aim for a SPF higher than 30.
  3. Try wearing clothing that have vivid colors and a tight weave. The Skin Cancer Foundation has a great article regarding this topic: “What is Sun-Safe Clothing?”
  4. Wear a broad-brimmed hat when spending time in the sun.

Be safe and please leave your comments below!

References

 Fernandez D, Kirou KA. What causes lupus flares?  2016 Mar;18(3):14. doi: 10.1007/s11926-016-0562-3.

Medical Disclaimer

This information is offered to educate the general public. The information posted on this website does not replace professional medical advice, but for general information purposes only. There is no Doctor – Patient relationship established. We strongly advised you to speak with your medical professional if you have questions concerning your symptoms, diagnosis and treatment.

Diseases and Conditions Featured

Guide to living with rheumatoid arthritis: Part 1

July 5, 2017
Have you recently been diagnosed with rheumatoid arthritis? RheumDoctor presents a guide to living with rheumatoid arthritis

Rheumatoid arthritis…  Your rheumatologist diagnosed you with rheumatoid arthritis and you have a lot questions.  What’s rheumatoid arthritis?  Can I get rid of it or will I live with this disease for the rest of my life?  What should I expect?  How do I fight it?  This week I’ll present to you Part 1 of a Guide to living with rheumatoid arthritis.  I’m going to present this as a three-part series.  Part 1 will cover the basics: what is rheumatoid arthritis, the cause, symptoms, diagnosis, treatment, etc.  In Part 2 I’ll cover prognosis, what to expect, diet and exercise.  In Part 3, I’ll be covering the financial side of rheumatoid arthritis: How to get access to medications and how to deal with insurance companies.

I hope you find this information useful.  Be strong, be brave, and know that you’re not alone.

What is rheumatoid arthritis?

Rheumatoid arthritis is an autoimmune disease that causes inflammation throughout the body but mainly affect joints. Without treatment, rheumatoid arthritis can eventually lead to permanent joint destruction.  Autoimmune diseases occur when the immune system loses “tolerance to self”.  What this means is that the immune system can no longer distinguish between healthy cells and cells that don’t belong like bacteria or cancerous cells.

According to the CDC, about 1% of people living in the US suffer from rheumatoid arthritis.  It tends to occur 2-3 times more often in women and tends to start in your sixties but it can start at any age.  [1]

Some common signs and symptoms include:

  • Pain and swelling in the joints. Particularly small joints like the knuckles, wrists, and toes.
  • Morning stiffness that lasts more than one hours
  • Having difficulty opening jars. Weakness in the hands.
  • Fatigue, fevers, unintentional weight loss.

What causes rheumatoid arthritis?

We’re actually unsure.  We do know that in certain cases there is a genetic link. People that have a certain HLA class II genotype (shared epitope) tend to get rheumatoid arthritis more often.  Especially, if they smoke cigarettes.  Moreover, we know that rheumatoid arthritis tends to run in families.  However, most cases of RA happen spontaneously and not everyone who has a genetic risk factor develops RA.

There’s still a lot of work that needs to be done to fully understand what causes rheumatoid arthritis.  Like most autoimmune diseases, our best guess is that people who have RA probably were born with some sort of genetic predisposition for the disease.  Then they get exposed to something in the environment like a virus, trauma, stress, hormonal change, which then triggers the disease to come online.

What are the symptoms of rheumatoid arthritis?

Usually rheumatoid arthritis presents with pain, swelling, and prolonged stiffness involving small joints, like the ones in your hands or feet.  When I mean prolonged, I mean more than one hour.  But RA can present in many ways. These can be divided into typical (90% of cases) and atypical presentations (10% of cases).

Typical

Insidious (55% – 65%): People develop pain, swelling, and prolonged stiffness mainly involving small joints like the toes and knuckles. This progressively worsens over months.

Subacute (15% – 20%): Again small joints are painful, swollen, and stiff but the this develops over weeks. Usually people experience some fatigue.

Acute (10%): Joints suddenly become swollen and tender over days. Some people have a fever, drenching night sweats, and sometimes can lose weight without trying.

Atypical (10% of cases)

Palindromic pattern: This type of presentation isn’t technically considered rheumatoid arthritis. It’s just that 33% to 50% of people with this type of presentation progress to full-blown rheumatoid arthritis. Typically, one joint is involved. It becomes tender and swollen for a few days then gets better on its own. Then a few weeks to a few months later it happens again. The flare can happen in the same joint but not necessarily. Treatment with hydroxychloroquine can decrease the risk of developing full-blown rheumatoid arthritis, so it’s important to start treatment as this stage.

Insidious onset of the elderly: As the name suggests this type of presentation occurs in the elderly, so people aged greater than 65 years. People experience extreme pain and stiffness shoulders and the hips. Sometimes you can see whole hand or foot swelling. Sometimes it’s very difficult to differentiate from polymyalgia rheumatica or remitting seronegative symmetrical synovitis with pitting edema (RS3PE).  People with polymyalgia rheumatica and RS3PE typically do NOT have any positive antibodies.

Rheumatoid nodulosis: Rheumatoid arthritis can cause nodules and bone cysts on radiographs. Usually people also have joint pain and swelling but sometimes all they have are nodules.

Arthritis robustus: This is rather rare. I’ve only seen it once. It typically occurs in men. Essentially the person develops horrible rheumatoid arthritis hand deformities but experiences little or no pain.  I know it’s hard to believe, but it’s possible!

Untreated rheumatoid arthritis

By James Heilman, MD (Own work) [CC BY-SA 3.0 (http://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons

How is rheumatoid arthritis diagnosed?

The diagnosis of rheumatoid arthritis, contrary to popular belief, is primarily a clinical diagnosis. Having a positive antibodies like a rheumatoid factor (RF) does not necessarily mean that you have rheumatoid arthritis because MANY conditions can have a positive rheumatoid factor. Some of these include:

Rheumatoid arthritis, mixed cryoglobulinemia types II and III, sarcoidosis, and other autoimmune diseases like Sjogren’s syndrome. Other non-rheumatology diseases that can cause someone to have a positive rheumatoid factor include infections most notably hepatitis C, tuberculosis, syphilis, HIV, and endocarditis. People suffering from cancer and people with chronic pulmonary and liver diseases, can also have a positive rheumatoid factor.

It’s also important to mention that about 5 – 25% of people aged 60 years and older have a positive rheumatoid factor without any underlying causative disease.

This is why my job as a rheumatologist is so interesting 🙂

The American College of Rheumatology classification criteria for rheumatoid arthritis is as follows:

The 2010 American College of Rheumatology/European League Against Rheumatism classification criteria for rheumatoid arthritis[2]

Who to test?

  • People that have at least 1 joint with definite swelling.
  • And the swelling cannot be better explained by another disease.

Classification criteria for RA (a score of ≥ 6/10 is needed for someone to have definite RA)

Category   Score
A Joint involvement

1 large joint

2 – 10 large joints

1 – 3 small joints

4 – 10 small joints

> 10 joints (at least one small joint)

 

0

1

2

3

5

B Antibodies

Negative RF and negative CCP antibodies

Low positive RF or low positive CCP antibodies *

High-positive RF or high positive CCP antibodies #

 

0

2

3

C Inflammation markers

Normal CRP and normal ESR

Abnormal CRP or abnormal ESR

 

0

1

D Duration of symptoms

< 6 weeks

≥ 6 weeks

 

0

1

* Low positive antibodies means any value that is above normal but less than 3 standard deviations above the upper limit of normal.

# High positive antibodies means any value that is 3 standard deviations above the upper limit of normal.

It’s important to note that these criteria were NOT meant for clinical practice but rather, were really meant for research trials. Sometimes, rheumatologists do deviate. Other conditions should be ruled out and let’s face it, not everyone fits perfectly into the mold. The criteria also does not account for musculoskeletal ultrasound testing. This imaging test can detect very subtle inflammation of a joint.[3]

Positive antibodies without RA

Now sometimes the workup is completely negative including x-rays. This is not uncommon. It can mean many things. It could mean that the rheumatoid factor is not clinically significant. 5–25% of the population can have a positive rheumatoid factor without any underlying condition or any symptoms. Typically the rheumatoid factor levels are low. It could also mean that you will develop rheumatoid arthritis in the future. Studies have shown that antibodies associated with rheumatoid arthritis can be present over a decade before onset of clinical disease. [4]Unfortunately, we don’t have the tools to precisely determine who will convert and who will not. In this situation, your rheumatologist can help you watch for any change in your condition.

How is rheumatoid arthritis treated?

We treat rheumatoid arthritis with medications called disease modifying anti-rheumatic drugs (DMARDs).  These medications slow down or stop the natural progression of rheumatoid arthritis.

Except for a few special situations, EVERYONE should with rheumatoid arthritis should be treated with a DMARD as soon as possible because permanent joint damage can happen in as little as 3 months after symptoms start.[5]

The following are the medications used to treat rheumatoid arthritis in the United States.  It’s important to work closely with your rheumatologist because they all have possible risks and what may be good for your neighbor may not be safe for you.

I’ve broken them down into conventional DMARDs, biologic DMARDs, and pipeline medications that have not been approved as of yet.

Conventional

  • Methotrexate
  • Leflunomide
  • Sulfasalazine
  • Hydroyxchloroquine

Biologics

  • Etanercept, TNF inhibitor
  • Adalimumab, TNF inhibitor
  • Golimumab, TNF inhibitor
  • Certolizumab pegol, TNF inhibitor
  • Infliximab, TNF inhibitor
  • Abatacept, Co-stimulation inhibitor
  • Tocilizumab, IL-6 inhibitor
  • Sarilumab, IL-6 inhibitor
  • Tofacitinib – JAK inhibitor
  • Rituximab – B cell depletion

Pipeline

  • ABT 494, a new JAK inhibitor
  • Baricitinib, another JAK inhibitor
  • Sirukumab, another IL-6 inhibitor

Biosimilars

It’s also important to note that we are starting to see biosimilar medications in the States. These are medications that are sort of copied from existing biologic medications.  They are NOT generic medications. The problem with biosimilars is that because of their complexity, it literally is impossible to exactly copy a biologic medication. If you want to learn more about biosimilar medications, please check this article.

Supplements

If you’re interested in supplementing, there is some research that suggests high dose turmeric/curcuma and high dose fish oil/omega-3 fatty acids may also be helpful.[6][7] However, supplementation should be used in combination with FDA approved medications that I listed above.

Is there a cure for rheumatoid arthritis?

I honestly wish I had better news for you. Unfortunately there is no cure for rheumatoid arthritis. Treatment primarily focuses on arresting the natural progression of the disease with the use of disease modifying anti-rheumatic agents (DMARDs). Conventional DMARDs such as methotrexate, leflunomide, sulfasalazine, and hydroxychloroquine, modulate the immune system to decrease rheumatoid arthritis activity.  Biologic medications like etanercept use a targeted approach, i.e., suppress a specific cytokine.

The goal of treatment is to put rheumatoid arthritis into remission and decrease the frequency of flares.

This may seem very pessimistic, but recent advances have really improved the prognosis of people living with rheumatoid arthritis.

Nevertheless, DMARDs do not cure rheumatoid arthritis.

How do we win the war against rheumatoid arthritis? Before we can win the war and find a cure, we need to know exactly what causes rheumatoid arthritis in the first place and we need to understand its exact pathophysiology. Believe it or not, despite all our advances, we still cannot answer these two questions. Don’t despair, researchers are actively trying to answer these questions.

Can rheumatoid arthritis become fatal?

Rheumatoid arthritis is a systemic autoimmune mediated disease that primarily affect the joints. Note the primarily bit. It can affect a host of different organs including the eyes, lungs, heart, skin, and bone marrow to name a few.

Untreated or poorly controlled rheumatoid arthritis can cause serious conditions such as interstitial lung disease (i.e., inflammation of the lungs), pericarditis (i.e., inflammation of the “sac” surrounding the heart), as well as something called Felty’s syndrome (i.e., a hematologic condition that can cause white cells to dramatically decrease and causes the spleen to enlarge). These severe manifestations of rheumatoid arthritis that can lead to death are hardly ever seen anymore mainly because we have many highly effective medications called disease modifying anti-rheumatic medications (DMARDs). These medications have completely changed people’s prognosis.

Cardiovascular disease and infection

The most common cause of death in people with rheumatoid arthritis these days includes cardiovascular disease and infection – primarily from medications.[8]

Rheumatoid arthritis increases cardiovascular risk via the interplay of inflammation and lipid metabolism. Studies have shown that people who receive treatment with methotrexate and or tumor necrosis factor inhibitors reduce their cardiovascular risk.[9] A British study also demonstrated that cardiovascular was not increased regardless of the choice of DMARD provided that rheumatoid arthritis was well controlled.[10]

Infection remains an ever-present problem in the world of rheumatology. To treat autoimmunity you need to suppress the immune system. Not too much, not too little, but just right. In some cases this has the unfortunate result in causing serious infections that can lead to death in extreme cases.

Rheumatoid arthritis can become fatal in many other ways, however, for the most part it is medication induced – although the pharmaceutical companies don’t really want you to know that. Just read a package insert. They’re terrifying.

However, I’ve been talking about rheumatoid arthritis fatalities. Untreated or undertreated rheumatoid arthritis is HIGHLY debilitating leading to a significant drop in your quality of life. Early treatment with a DMARD is the best way to improve your odds. You have to fight fire with fire!

Can I stop my medications if I’m feeling better?

No. Rheumatoid arthritis is a life-long disease.  If you’re feeling better, great!  However, it’s probably your medications that are keeping you that way.  If you stop your medications the rheumatoid arthritis will come back.  Maybe not now but soon.  Rheumatoid arthritis subsides spontaneously in a VERY small subset of people.

If your medication is making you feel sick, talk to your rheumatologist.  They’re there to make you feel better and they want to find the perfect treatment plan tailored for you.

Do not stop your medications without consulting your rheumatologist.

Next steps

We’ve covered a lot of material today and there’s a lot more coming your way!  Stay tuned for Part 2.  I’ll be covering topics such as what to expect, what to eat, how to exercise, and strategies on how to reduce stress.  Please leave your comments below.

References

[1] https://www.cdc.gov/arthritis/basics/rheumatoid-arthritis.html

[2] https://www.rheumatology.org/Portals/0/Files/2010_revised_criteria_classification_ra.pdf

[3] Horton SC, et al. Ultrasound-detectable grey scale synovitis predicts future fulfilment of the 2010 ACR/EULAR RA classification criteria in patients with new-onset undifferentiated arthritis. RMD Open. 2017 Mar 30;3(1):e000394. doi: 10.1136/rmdopen-2016-000394. eCollection 2017.

[4] Brink M, et al. Rheumatoid factor isotypes in relation to antibodies against citrullinated peptides and carbamylated proteins before the onset of rheumatoid arthritis. Arthritis Res Ther. 2016 Feb 9;18:43. doi: 10.1186/s13075-016-0940-2.

[5] Raza K, et al. Treating very early rheumatoid arthritis. Best Pract Res Clin Rheumatol. 2006 Oct;20(5):849-63.

[6] van der Tempel H, et al. Effects of fish oil supplementation in rheumatoid arthritis. Ann Rheum Dis. 1990 Feb; 49(2): 76–80.

[7] Ramadan G Al-Kahtani MA, El-Sayed WM. Anti-inflammatory and anti-oxidant properties of Curcuma longa (turmeric) versus Zingiber officiale (ginger) rhizomes in rat adjuvant-induced arthritis. Inflammation. 2011 Aug;34(4):291-301. doi: 10.1007/s10753-010-9278-0.

[8] https://www-ncbi-nlm-nih-gov.elibrary.amc.edu/pubmed/26472415

[9] https://www-ncbi-nlm-nih-gov.elibrary.amc.edu/pubmed/28455580

[10] https://www-ncbi-nlm-nih-gov.elibrary.amc.edu/pubmed/28160488

Medical Disclaimer

This information is offered to educate the general public. The information posted on this website does not replace professional medical advice, but for general information purposes only. There is no Doctor – Patient relationship established. We strongly advised you to speak with your medical professional if you have questions concerning your symptoms, diagnosis and treatment.

Recipes

Buckwheat pancake: galettes de sarrasin

June 28, 2017
A picture of the moulin Legare the oldest functional water powered mill in North America. The mill produces 4 tons of wheat and buckwheat flour annually.

Last weekend I took some much needed time off and spent it celebrating la Fête de la Saint-Jean-Baptiste with my family up in my hometown of Saint-Eustache, Quebec.  This is akin to the 4th of July for French Canadians.  Saint-Eustache was founded in 1770 and boasts two famous historical sites: the church and the buckwheat water mill.

Historical Sites

The church gained notoriety for its significance during the battle of the Lower Canada Rebellion on December 14th, 1837.  After rebelling against the English following multiple failures at political reform, seventy rebels were shot or burnt alive inside the church while the English bombarded its facade.  The English then pillaged the city and burnt the majority of the city to the ground.  Many see the rebellion of the Patriotes Canadiens as an example of what could have happened in the United States had the American Revolutionary War failed.

Canon ball from the battle of Lower Canada 1837

By Vincent Poirier (Own work) [CC BY-SA 3.0 (http://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons

Every June 24th the entire province gathers to celebrate our independence and express our gratitude for those who made the ultimate sacrifice.

Now the second famous historical site in Saint-Eustache is the moulin Légaré.  It was built in 1762 and has been in constant operation since then.  In fact, it’s the oldest functional water-powered mill in North America.  The mill, to this day, produces about 40 tons of wheat and buckwheat flour annually!

A picture of the moulin Legare the oldest functional water powered mill in North America

What’s buckwheat and how do I use it?

Contrary to popular belief, buckwheat is NOT a grain.  It just has grain-like seeds which are milled into a flour.  That being said, buckwheat flour is gluten-free and has many trace minerals as well as vitamin B6, pantothenic acid, niacin, folate, thiamine, and choline. Moreover, you will find 4 grams of soluble fiber, 8 grams of protein, and 15% of your daily iron requirements in 1/3 of a cup of buckwheat flour.  Needless to say buckwheat is very healthy and should be part of your diet.

In Quebec, we use buckwheat in our traditional cooking. This is probably because we have a shorter growing season.  Buckwheat likes cold weather, acidic and low fertility soil.

One of the most popular ways to use buckwheat flour is to make pancakes.  We call them galettes de sarrasin.  Essentially it’s a thin pancake, more like a Parisian crêpe. It’s cooked on a sizzling hot cast iron pan and then drizzled with molasses or maple syrup.  But really you can dress it with almost anything: swiss cheese, a fried egg, bechamel, etc.  Sweet or savory, whatever you fancy.

 

Buckwheat Pancake – Galette de sarrasin

Adapted from Recettes de la famille Légaré

2 cups of buckwheat flour

1 tsp of baking powder

1/2 tsp of salt

2 cups of water

Butter

Instructions

  1. In a large bowl, whisk together the water, buckwheat flour, baking powder, and salt.
  2. Heat a cast iron pan on medium heat.  When hot, add about 1/2 tsp of butter.  If you want to be ultra traditional, use lard.
  3. Ladle a spoonful of batter onto the sizzling hot pan.  Flip the pancake once you see holes forming but only for a few seconds. Serve immediately.
Featured Overcoming Inflammation

What is the best diet for autoimmune diseases

June 21, 2017
What are some foods have anti-inflammatory properties?

In recent years there’s been a lot of talk about the autoimmune diet. But what exactly is an autoimmune diet and which foods have anti-inflammatory properties?  These are some of the most common questions my patients ask me in clinic.  Essentially, what foods help autoimmune diseases?  In certain cases, it’s pretty cut and dry.  If you have celiac disease, avoid gluten.  If you have ankylosing spondylitis, Crohn’s disease, or ulcerative colitis, try to follow the FODMAP diet.  There already exists evidence-based research that supports these interventions.

But what about other autoimmune diseases like rheumatoid arthritis, lupus, Sjogren’s syndrome?  What should you be eating if you have any of these?  Do they have their own autoimmune diet?  Should you avoid nightshades, dairy, gluten, eggs, etc.  In recent rears a myriad of “anti-inflammatory diets” have surfaced on the web.  For the most part, they are supported by little if any evidence-based research.  This is unsurprising.  Good quality research requires money.  Lot’s of money… pharma money.  It simply does not make any business sense for these companies to fund large and expensive studies that have no commercial potential.  Believe me, I am not defending big pharma, I’m simply stating reality.

What is epigenetics?

Even though we do not have great scientific evidence supporting a particular autoimmune diet or foods to prevent, cure, or lessen autoimmune diseases, it’s kind of obvious that some lifestyle practices lead to better health outcomes.  Take smoking.  People that smoke tend to get lung cancer and develop heart disease compared to those that don’t smoke.  But how does that work exactly?

Everyone is born with genes.  Some of these genes are active and some remain dormant.  Your genotype is the entire makeup of your genes.  Your phenotype is the result of how your genetic material is expressed.  For example, you may have the genes for blue eyes and brown eyes.  If the genetic material for brown eyes is dominant, you’ll have brown eyes.

This is where it gets really interesting.  Over the course of your lifetime, some of your genes are turned on and off.  This is influenced by factors like aging, the environment, and lifestyle.  Epigenetics is the study of how genes are turned on and off based on external influences.

Epigenetic changes can be good but can also cause harm.  We think that some of these changes can result in autoimmune diseases.  It’s important to remember that epigenetics is in its infancy.  Researchers still are not 100% sure how this happens, let alone, how to specifically manipulate the environment to cause favorable epigenetic change.

Autoimmune diet: what foods should I eat?

This simple answer to this question is, “I don’t know”.  One day, when researchers crack the epigenetic code, I may be able to answer this questions more accurately.  I may be able to tell you, if you follow the rheumatoid arthritis autoimmune diet, this should help control your inflammation.  Unfortunately, I am unable to say that yet.

But like I was saying at the beginning of this post, some people who adhere to certain lifestyle practices tend to be healthier.  Given we don’t really have actionable epigenetic data to guide lifestyle choices, the goal when it comes to nutrition and lifestyle is to adopt habits that have a tendency to result in overall general health to live happier, healthier, and longer.

The Blue Zones®

The Blue Zones® are 5 regions in the world where people statistically people tend to live to 100 years AND who tend to reach this age in health.  The project spawned from the National Geographic Society.  The goal was to find “hot spots of longevity” around the world.  The researchers identified 5 zones and circled them in blue ink.  These regions are as follows:

  • Ikaria, Greece
  • Okinawa, Japan
  • Ogliastra region, Sardinia
  • Loma Linda, California
  • Nicoya Peninsula, Costa Rica

One would think that there are no similarities between people living in Japan versus people in Greece.  What the researchers identified was a core list of lifestyle practices and environmental factors that shared between all the different regions.

The Power 9®

Move Naturally

People that live to 100 years don’t necessarily run marathons or go the gym.  They are always on the go and they move naturally.  For example, they tend a garden, they walk to the market, they use stairs instead of the elevator.

Purpose

People that live in the Blue Zones live with purpose.  They wake up every morning, and they know “why I wake up in the morning”.  Having a clear purpose in life can add an extra 7 years of life expectancy.

Down Shift

We all know that stress can cause inflammation.  I often see people in my clinic who’s rheumatoid arthritis was in perfect control until something really bad happened, like a divorce, job loss, or a death in the family.  Chronic stress leads to chronic inflammation.  People in the Blue Zones develop daily habits to help reduce stress.

80% Rule

The Japanese have a saying “Hara hachi bu”.  This is a mantra that Okinawans say before every meal, reminding them to stop eating when they feel about 80% full.  There is a delay between feeling full and actually being full.  When you feel 80% full, you are actually full.  So if you stop eating when you feel full, you are overeating.  People living in the Blue Zones tend to eat their largest meal at breakfast and their smallest meal at dinner.

Plant Slant

Although not all regions of the Blue Zones eat meat, their diets all mainly consists of fresh veg and beans.  Lot’s of beans: fava, soy, lentils, etc.  They eat meat very sparingly and servings are small, “about the size of a deck of cards”.

Wine @ 5

Thank goodness for this one!  People in the Blue Zones, expect for Adventists, drink alcohol moderately and regularly.  Typically, they drink 1-2 glasses of wine per day with friends and family at the end of the work day.  They found that people who drink regularly and moderately tend to live longer than those who don’t.

Belong

Almost all people who live until 100 tend to belong to some sort of faith-based community.  They found that attending a service 4 times a month can add up to 4 – 14 years of life expectancy.

Loved Ones First

People living in Blue Zones tend to live close to their families.  It’s common to have children, parents, and grandparents living under the same roof.  They also tend to commit to a life partner.

Right Tribe

People in the Blue Zones keep strong social networks.  Not only are these social strong, but they also foster healthy behaviors.  Women in Okinawa create “moais” early on in life.  These are groups of 5 friends that are completely committed to each other for life.


The true beauty in the Blue Zones Project® is that you don’t need to live in a Blue Zone to reap the benefits.  By living the Power 9® you can set yourself up to live with vitality to a ripe old age.

Conclusion

Medications certainly have made a huge difference in the prognosis of many autoimmune diseases like rheumatoid arthritis and lupus but it’s not enough.  By integrating healthy habits we can potentially turn on an and off genes that contribute to ongoing autoimmunity and inflammation.  Although we still don’t know exactly what the perfect autoimmune diet is, by adopting healthy habits set forth by the Power 9®, you can increase your odds to live a long, happy and healthy life.

Recipes

Chive Blossom Butter

June 14, 2017
Chive blossom butter

My mom is what you would call a busy body.  Always out and about: gardening, cooking, cleaning… running a business.  She also happens to be an amazing cook.  This Saturday morning as I was doing my errands, she texted me images of her latest creation.

Beautiful chive blossom's from my mom's garden

Very pretty.  Why aren’t mine like that?

Chive blossoms and lemons

Interesting, show me more.

Unformed chive blossom butter

This does not look appetizing.

Chive blossom butter

Yum!

I can see this tasting great with mashed potatoes, toasted bread, or on a steak.  Although this is not the healthiest recipe, something like this should definitely be shared.

Chive Blossom Butter

Adapted from Popayan www.recettes.qc.ca

50 – 60      Chive flowers with ½ inch of the stem attached, finely minced

1 lb              Unsalted butter, room temperature

1 ½             Lemons, juiced

¼ cup        Extra-virgin olive oil

Salt as desired

  1. In a large bowl, mix the butter, lemon juice, and the olive oil together with a wooden spoon. Then, add the minced chive blossoms.
  2. At this point you can either fill ramequins with the butter-chive blossom mixture or you can mold them into individual sized portions as seen above.

Individual sized portions

  1. Mold the butter-chive blossom mixture into a roll and wrap in wax paper and then in plastic wrapping.
  2. Place in the freezer.
  3. When the mixture has hardened, unwrap, and cut into individual sized portions

 

Makes one pound of butter.

 

Bon appetit!

Subscribe

Enter your email address to receive notifications of new posts.