Deep breathing exercises for Ankylosing Spondylitis

During normal breathing, ribs move up & down to expand the chest cavity. This movement occurs where they join the vertebrae (costovertebral joint). In ankylosing spondylitis, these joint get inflamed & fused. Once fused, the rib movement gets restricted. This leads to ‘strapped-in’ feeling & breathlessness while doing day today activities.

Just as back exercises keep your spine flexible, so also can deep breathing exercises keep the chest wall elastic & preserve one’s ability to take a deep breath.

Here are a few ‘deep breathing exercises’ to help you keep the chest wall elastic & prevent fusion of the costovertebral joints.


  • Rib cage exercises- standing arm exercise, exercise with the ribcage band, lying down & arm stretch exercises ( first three exercises in the video) help exercise the ribcage muscles & prevent fusion at the costovertebral joints.
  • The next two exercises help exercise the diaphragm. During inspiration, the diaphragm moves downwards & expands the chest cavity. These exercises will help you with a more effective breathing particularly if you already have restriction in rib cage movements.
  • The last exercise will help you understand the ‘rib cage breathing’ & ‘diaphragmatic breathing’ & use both more effectively.

Perform these exercises every day; 10 times at a time, at least twice a day.


One can also use an incentive spirometer to exercise the respiratory muscle.

It is a medical device used to improve the function of the lungs & is generally used after a thoracic surgery. However we can also use it to improve the function of the ribcage muscles.

Here is a video to help you understand how to use it–


Take 15- 20 breaths with the spirometer at least twice a day.

Don’t forget to continue your back exercises. They surely complement these exercises & help you preserve your breathing despite ankylosing spondylitis.

Why is breathing difficult & at times, painful in Ankylosing spondylitis?

The mechanical apparatus for breathing consists of the ribs, intercostals muscles, costochondral junctions & the diaphragm. Diaphragm is a muscle located at the base of the chest wall cavity. The ribs move at the joint formed by them with the vertebrae (costovetebral joint). The intercostals muscles are attached to the ribs & are responsible for the movements of the ribs during respiration.

costovetebral joint

During inspiration, the diaphragm moves downwards & expands the chest cavity. At the same time, the ribs move up & out to expand the thoracic cavity. This movement is akin to a bucket handle (moving up). The movement of the ribs is brought about by the contraction of the intercostal muscles.



In Ankylosing spondylitis, there is inflammation of the costovertebral joint. Later, as AS progresses, the joint may also get fused. This inflammation/ fusion then restricts the movement at the joint & consequently the chest expansion. Physically, this manifests as restricted chest expansion.

Ankylosing spondylitis also leads to inflammation at insertion of intercostal muscles to the ribs (enthesitis). This leads to pain in the rib cage area & also further difficulty in taking a deep breath.

Sneezing involves a rapid & high intensity contraction of the intercostal muscles. It is very painful due to the enthesitis & is almost felt like a ‘catch’

Tight control of AS with NSAIDs/ DMARDs/ biologics/ diet & deep breathing exercises are helpful in reducing this chest pain.


How does ankylosing spondylitis cause osteoarthritis of the hip? — the Pacman game

I’m sure all of you know that Ankylosing spondylitis (AS) is an autoimmune disease, which means that the body’s immune system considers its own joints as foreign & attacks them. We have not been able to pinpoint the exact reason for this.
If this immune attack is not controlled in time, it ends up destroying the joints; especially the hips. This is known as osteoarthritis of the hips. Ankylosing spondylitis is a unique disease as it causes destruction of the bones in the hip & at the same time it leads to excessive bone formation in the spine (syndesmophytes). So what starts as backache can well end up as deformities & disability.

But then, how does AS cause destruction of the hips?
Hip joint is lined by a thin membrane called the synovial membrane from the inside. The immune attack is targeted towards the synovial membrane. The synovial membrane swells up due to the attack. This inflamed synovium is like the pacman. Remember the pacman game?… pacman eats away all the dots. In a similar fashion, the pannus eats the cartilage & the bones around it. When it eats the bones, the same is known as erosion. Apart from the hips, these erosions are also seen in the sacroiliac joints. Destruction of the cartilage & the bone ultimately leads to osteoarthritis.





The Pacman game.. Pacman keeps eating the dots…just like the inflamed synovium keeps eating the cartilage & the bones. Note how the AS Pacman has destroyed the hip bones (above) & the sacroiliac joint (SI joint) (below).



Can the hip osteoarthritis be prevented?
Yes, very much so. Seeing a Rheumatologist at the earliest & starting definitive treatment at the earliest can definitely tame this pacman & prevent osteoarthritis.

Low Starch Diet for Ankylosing Spondylitis: Part 2 – The Scientific Evidence

We have already seen (in the last blog) the theoretical possibility of a ‘Low starch diet’ being beneficial for Ankylosing Spondylitis. Let us now see whether it really works in real life & whether there is sound medical evidence to support it.

Today’s medicine works on the basis of evidence. If a new medicine/ intervention is thought to be useful, it is tested in clinical trials. A group of patients is given the standard treatment & placebo (an inert substance that has no effect on disease activity) while another comparable group is given the standard treatment & the experimental therapy/ intervention. A ‘double blinded study’ that ensures that neither the investigator nor the patient knows whether he is taking the experimental drug or placebo is ideal to avoid any bias; both on the investigator or the patient front. This is not possible for studies with dietary modifications as blinding is not possible & bias tends to creep in.

As against medicines, it is very difficult to keep an exact track of the diet of any patient for obvious reasons. It is extremely difficult to ensure that a patient sticks to a particular diet in the long run throughout the study period.

These two factors make studies based on dietary interventions difficult to conduct as well as interpret.

For the reasons mentioned, there are hardly any studies about ‘low starch diet’ in Ankylosing spondylitis. In 1996, Dr. Ebringer discussed the disease activity trend of one of his patients following the diet for a long period (1983- 1995). His ESR showed a continuously decreasing trend. In another study (mentioned widely on the internet with no reliable data available on any of the medical literature sites) 36 patients received Dr. Ebringer’s diet & showed considerable improvement in symptoms. These two studies would be highly inadequate for any definite conclusions.

So, as we have seen, the utility of ‘low starch diet’ in Ankylosing spondylitis is not yet proven scientifically.

One way of looking at things would be to give it a try & see whether it works. However it has to be weighed against the risks involved in pursuing such a diet.

In the next blogpost, let us look at what a ‘low starch diet’ includes/ excludes & the possible health hazards of such a diet.

“Low starch diet’ for ankylosing Spondylitis

Many patients keep asking me about the role of ‘Low starch diet’ to control Ankylosing Spondylitis. This has been a hot topic of discussion on most Ankylosing spondylitis groups on social media & many confirming the good results of a low starch diet.

The original idea of a ‘low starch diet for Ankylosing Spondylitis’ comes from Dr. Alan Ebringer, Prof of Immunology at King’s College London. He found high levels of a gut pathogen called Klebsiella Pneumoniae in stool samples of patients with Ankylosing spondylitis. He also found high levels of antibodies to klebsiella in the blood of patients with Ankylosing spondylitis. These findings indicated the presence of the bacteria in the gut of patients with Ankylosing spondylitis & the body’s immune reaction to it.

These findings evoked further research & Dr. Alan’s further research showed that K. pneumoniae was isolated more frequently during the active phase of Ankylosing Spondylitis & clinical relapse was preceded by appearance of the bacteria in fecal samples. This meant that Klebsiella Pnemoniae was somehow related to inflammation of Ankylosing Spondylitis.

Dr. Alan’s research continued & he went on to show that there are similarities in structure of the HLA-B27 molecule & enzyme Pullulanase produced by the Klebsiella bacteria. There is also similarity between the enzyme & type I, III & IV collagens found in joints & other organs. This gave rise to the ‘Molecular mimicry theory’. The human immunity recognizes Klebsiella as foreign & attacks it. However, since HLA-B27 & collagens have similar structure, they get attacked to. This may be responsible for the inflammation in joints & other structures like the eyes in Ankylosing spondylitis.

One can infer from the proposed ‘molecular mimicry theory’ that by reducing the klebsiella bacteria in the gut, one can reduce the inflammation associated with Ankylosing spondylitis.

Various studies have shown that the gut bacteria including klebsiella grow on undigested starch in the gut. Hence a reduction in starch in the diet may help reduce the klebsiella bacteria in the gut. Klebsiella bacteria is well adapted to the human gut & produces the Pullulanase enzyme that can break down the starch, derive nutrition & thrive in the gut.

The rationale of the ‘low starch diet’ is to cut down on the starch, make life difficult for the klebsiella bacteria. This may indirectly help control the Ankylosing spondylitis.

This is the exact basis of the ‘low starch diet’ for Ankylosing Spondylitis.

Now that we know the basis of the theory, we also need to look at the following points—
1. What is a ‘low starch diet’?
2. Are there any studies conducted in patients with Ankylosing spondylitis to prove the benefits of ‘low starch diet’?
3. If the concept looks so convincing, why do Rheumatologists not recommend it on a regular basis?

I would be answering these questions in the subsequent blog posts. These posts are coming soon & follow my blog so that you don’t miss out on any of those useful posts.

References: Erbinger A, Wilson C. J Med Microbiol 2000; 49: 305-311

How does Ankylosing Spondylitis progress?

Whenever one speaks about Ankylosing spondylitis, I’m sure picture of a man with a hunchback & restricted mobility comes to your mind. This famous photograph from the ACR library clearly describes what a patient with Ankylosing spondylitis goes through in his life. Ever wondered what really happens behind the curtain?

Ankylosing spondylitis is a chronic inflammatory arthritis affecting the sacroiliac joints (joints beneath the buttocks), vertebral joints & the hips. The joints get inflamed & persistent inflammation in the long run leads to formation of new bone.

The inflammation is responsible for the pain & the bone formation leads to restriction in movements of the spine.

Let us have a look at a simple example to understand this. The spine is similar to multiple matchboxes hung by a set of flexible threads. The flexibility of the threads is responsible for the movements of the spine. However, if you put wax on the threads & let it set, the threads do not bend. This is exactly what happens with Ankylosing Spondylitis. The threads are akin to the ligaments of the vertebrae & the matchboxes to individual vertebrae. Once the threads become hardened by inflammation (wax) the mobility is lost.

final box

The hardened ligaments give the typical tram track or bamboo spine appearance on the X-Ray.

Ankylosing spondylitis progression xray 2

Ankylosing spondylitis progression xray final 1

Help me help this lady with Ankylosing spondylitis

It was a nice Wednesday afternoon. Saw this young lady with Ankylosing Spondylitis.

Reminded me of the typical Indian #rheum story.

She had been having symptoms since last 5 years. She had consulted an orthopedic surgeon for the same. She was diagnosed to have Ankylosing Spondylitis & was started on Sulphasalazine. She was 27 years old & the parents were eager to get her married. They found a groom in her hometown (Uttar Pradesh). It was a typical Indian village.

The parents did not reveal anything about the illness, medicines to the groom. The lady had a tough time after marriage. She had to manage household work with all the pain; more so since she was in a rural Indian setup where the newlywed is supposed to take care of all the work. Taking medicines daily was a big problem as the illness was never declared.

There was another major problem for her. The marriage plan was never discussed with any Doctor & they had never consulted a Rheumatologist. She was not even sure whether Sulphasalazine was safe in pregnancy. Contraception is never in the hands of rural women in India & she was no exception.

As days passed, the pain started becoming unbearable for her & started showing up in day-to-day life. The in laws & the husband soon realised that something was amiss. Due to the workload & stress, she was soon on the bed. The in laws felt cheated & sent her back to her parents.

And that is how they reached me, with anxiety & stress clearly showing in their face. This was some 3 months back. She saw me again this week. Ankylosing Spondylitis was now controlled, backache significantly reduced.

The next was the big question- what to do next? Should she go back to her in laws? If yes, what are they to be told…This caught me unprepared. Apart from the medical management, they also wanted me to help them reach a decision. ‘You must be seeing so many patients with such a problem- you help us take a decision’ they quipped.
Ankylosing Spondylitis being a chronic ailment, this decision is a tricky one.
• She is prone to have ups & downs, down the line. Would her family accept the future pain/ regular medicines?
• One thought was to call her husband/ in laws & counsel them about the disease. However, I was wondering whether they would really come all the way to discuss about her ailment.
• The other thought was to ask her to carry on with her life, concentrate on her health for the time being rather than the stress of going back to the in-laws, working hard in a hostile environment.
• At her in-laws’, she would be under pressure with regards to pregnancy & may find it tough to manage it with Ankylosing Spondylitis presently.
This patient has really caught me unprepared on the decision front. I thought I should be asking the #rheum community to help me out reach a solution for her & guide her.
• What is the best possible solution for her right now?
• What should the parents do prior to marriage as in this case.
Please post your opinion & help me help this lady!

Is HLA-B27 the only gene responsible for Ankylosing spondylitis?

We have already seen in the previous posts that HLA-B27 is the most common gene associated with Ankylosing spondylitis (AS). However, HLA-B27 does not seem to be the only gene associated with AS.

Strong indicators of this fact include-
1. AS can occur in individuals who do not carry HLA-B27 gene.
2. Amongst the HLA-B 27 individuals, only about 1-5% individuals develop AS.
3. HLA-B27 positive relatives of AS patients have a risk of developing AS that is 5.6 to 15 times that of HLA-B27 positive individuals in general population. This would mean that there are other non HLA-B27 familial genetic factors involved in causation of AS.

There has been some major work by the Wellcome trust case Control Consortium
& Australo-Anglo-American Spondyloarthritis Consortium to look into the genetics of AS. These (& other) studies have revealed that there are other genes & genetic loci responsible for Ankylosing spondylitis as well—
1. HLA-B60 seen in HLA-B27 positive as well as negative AS patients.
2. HLA-B 39 seen in HLA-B27 negative patients
3. ERAP-1— endoplasmic reticulum aminopeptidase-1
4. Interleukin-23 receptor gene—IL-23R
5. RUNX3
6. KIF21B
7. 2p15
8. IL12B
10. 21q22
11. ANTXR2
12. PTGER4
13. CARD9
14. TBKBP1

Out of these genes, ERAP-1 & IL-23 R have generated maximum interest. The researchers have found that some variants of ERAP1 protect against the development of Ankylosing spondylitis. For individuals who carry HLA-B27, their risk of developing Ankylosing spondylitis decreases by a factor of four if they carry two copies of the protective variant of ERAP1.

HLA-B27 presents the pathogen antigen to the immune cells. The ERAP-1 gene interacts with HLA-B27 to affect how these peptides are presented to the immune system. The researchers have found that some variants of ERAP1 protect against the development of Ankylosing spondylitis by reducing the amount of peptide available to HLA-B27 within cells. This could prove to be a target for treatment in the future.

Tests for these genetic markers are not available routinely as of now. But, then, if they are found to be clinically useful; tests should be available in the future.

1. Investigating the genetic association between ERAP1 and ankylosing spondylitis. Harvey D & colleagues. Hum Mol Genet. 2009 Nov 1;18(21):4204-12.
2. Progress in the genetics of ankylosing spondylitis. Matthew A brown. Briefings in Functional Genomics (2011) 10 (5): 249-257.
3. Interaction between ERAP1 and HLA-B27 in ankylosing spondylitis implicates peptide handling in the mechanism for HLA-B27 in disease susceptibility. The Australo-Anglo-American Spondyloarthritis Consortium (TASC), the Wellcome Trust Case Control Consortium 2 (WTCCC2), Nature Genetics 43, 761–767 (2011)

Ankylosing Spondylitis: Have you missed your diagnosis, as you were HLA-B27 negative?

Doctors as well as patients have equated ankylosing spondylitis with HLA-B27 since a long time. In fact, many of the patients call Ankylosing spondylitis ‘HLA-B27 disease’

This is good as far as awareness is concerned. But, on the flip side, many patients have missed the diagnosis, as they were HLA-B27 negative. This is particularly important, as the average delay in the diagnosis of Ankylosing spondylitis is 8- 11 yrs. The delay for women is even more than that of men. This is quite unacceptable as the first 10 years are the most important for a patient as the treatment can be initiated before permanent limitations of spinal mobility and deformity has set in.

Although HLA-B27 gene is the most important gene predisposing to Ankylosing spondylitis, studies have shown that it contributes only 20-30% of the total genetic risk. No doubt HLA-B27 is a strong risk factor for the development of Ankylosing spondylitis, but that does not mean that it is a must for diagnosis.

So, then how important is HLA-B27 for a diagnosis of Ankylosing spondylitis?
Only about 80-90% of the patients with AS have the HLA-B27 gene. That means that the rest could miss the diagnosis if one would totally depend on HLA-b27 for a diagnosis.
The converse of this is also interesting. Only 1% of people with HLA-B27 develop the disease. So, HLA-B 27 alone cannot be equated with AS in somebody with backache.

Low back pain is a relatively common symptom that may be associated with a variety of conditions other than AS. The single most important feature that raises the suspicion of AS is inflammatory backache. The characteristics of inflammatory backache are –(1) morning stiffness of > 30 minutes, (2) improvement in back pain with exercise but not with rest, (3) awakening because of back pain during the second half of the night only, and (4) alternating buttock pain.

Role of MRI
MRI of the sacroiliac joints is one of the best investigations for a definitive & early diagnosis of AS. HLA-B27 is not diagnostic of AS, but can only guide us towards a diagnosis. MRI of the SI joints can give a definite diagnosis by actually showing the inflamed SI joints. Though, MRI is a costly, time-consuming investigation; its utility in confirming the diagnosis in a particular individual cannot be understated.

All in all, let us not diagnose AS with HLA-B27 alone. Definitive history of inflammatory backache/ other features & MRI of the sacroiliac joints can be the best guide for the diagnosis.

1. Brown MA, Kennedy LG, MacGregor AJ, et al. Susceptibility to ankylosing spondylitis in twins: the role of genes, HLA, and the environment. Arthritis Rheum 1997; 40: 1823–28.
2. Feldtkeller E, Khan MA, van der Heijde D, van der Linden S, Braun J. Age at disease onset and diagnosis delay in HLA-B27negative vs. positive patients with Ankylosing spondylitis. Rheumatol Int 2003; 23:61–6.
3. Blum U, Buitrago-Tellez C, Mundinger A, et al. Magnetic resonance imaging (MRI) for detection of active sacroiliitis – a prospective study comparing conventional radiography, scintigraphy, and contrast enhanced MRI. J Rheumatol 1996; 23:2107–2115.

Do have a look at this video to understand this better–

How does HLA-B27 lead to ankylosing spondylitis?

HLA-B27 gene is closely related to Ankylosing spondylitis. It is found in almost 70-90% of patients with Ankylosing spondylitis.

HLA B27 stands for Human Leukocyte Antigen 27. The HLAB 27 gene produces the HLA B27 molecule, which belongs to the family of MHC class I molecules. The function of this family of molecules is to present antigenic peptides to the T cells.

Let us understand this process of antigen presentation further. Whenever a pathogen (bacterium/ virus) enters the body, body’s immunity recognizes these as foreign. The next step is to inform the other immune cells about these pathogens & provide them with sufficient information about the pathogens. With this information, immune cells then launch an attack against these pathogens. This information about the pathogens consists of parts of the pathogen (called antigens) & is presented by the antigen presenting cells to the T cells. These parts are the signatures of these particular virus/ bacteria. The T cells can trace the location of these pathogens based on the signature antigens they have & launch an attack on them.

Now, let us focus on what happens inside these antigen presenting cells. The signature antigens are given final touches in a structure called proteosomes. The final antigens are carried to another structure called the Endoplasmic reticulum where they are mounted onto the MHC class I molecule. The MHC molecule folds & is then taken to the surface of the cell. This complex is presented to the T cells, which then recognize it & mount an attack on the pathogen. The T cells do not recognize the antigens in absence of the HLA molecule.

A few pathogens have antigens that are similar to proteins in our joints. When such pathogens (eg. Yersinia, Chlamydia) enter the body (generally the gut & cause loose motions), their antigens are picked up by the antigen presenting cells. It is hypothesized that HLA-B27 tends to pick up the particular antigens in the pathogen that are similar to the joint proteins & present them to the T cells. T cells recognize these as foreign & attack any structure with these proteins. The pathogen is definitely taken care of; but as I said, T cells also start considering our joints as foreign & attack them as well. This is precisely what happens in reactive arthritis (ankylosing spondylitis & reactive arthritis belong to the same group of arthritis). In reactive arthritis, one has loose motions followed by joint inflammation. This is called the ‘Arthritogenic peptide hypothesis’

There is an alternative hypothesis to explain the cause of joint inflammation. This is called the HLA-B27 folding hypothesis. The difference between HLA-B27 & the other HLA molecules is that B27 has a slower rate of folding & is prone to misfolding. When this happens on a large scale, the endoplasmic reticulum malfunctions & triggers generation of cytokines (TNF-α, IL-1, IL-6). These cytokines attack the joint & cause inflammation. This sequence of events has been shown in cells of the synovial fluid in patients.

This is how the HLA-B27 positivity; in the presence of infections/ environmental factors translates into inflammation of the joints (spine & other joints) & ultimately manifests as ankylosing spondilytis/ reactive arthritis.

Mear JP, Schreiber KL, Munz C, Zhu X, Stevanovic S, Rammensee HG, et al: Misfolding of HLA-B27 as a result of its B pocket suggests a novel mechanism for its role in susceptibility to spondyloarthropathies. J Immunol 163:6665–6670, 1999

Smith JA, Märker-Hermann E, Colbert RA: Pathogenesis of Ankylosing spondylitis: current concepts. Best Pract Res Clin Rheumatol 20:571–591, 2006

Turner MJ, Sowders DP, DeLay ML, Mohapatra R, Bai S, Smith JA, et al: HLA-B27 misfolding in transgenic rats is associated with activation of the unfolded protein response. J Immunol 175: 2438–2448, 2005

Robert A., Monica L., Erin I.: From HLA-B27 to spondyloarthritis: a journey through the ER Immunol Rev. 2010 January ; 233(1): 181–202

Benjamin R, Parham P. Guilt by association: HLA-B27 and ankylosing spondylitis. Immunol Today 1990: 11: 137–42.