Ankylosing spondylitis belongs to a family of the diseases called spondyloarthropathies, this

family includes multiple other conditions in addition to ankylosing spondylitis like reactive
arthritis, psoriatic arthritis, arthritis related to inflammatory bowel disease as well as a
undifferentiated spondyloarthropathy. Ankylosing spondylitis is more common in males
than females and its first symptom usually appear in the third decade of the patient’s age.
Most patient are diagnosed before they reach 40 years of age and the average delay since
the onset of the symptoms till the time of the diagnosis is between 5 and 8 years. Some
causes that might explain that delay in diagnosis is that clinicians are usually not aware of
the condition, that sacroiliitis doesn’t appear in X-rays in the early stages of the disease and
the difficulty in differentiating inflammatory and mechanical back pain.

Aetiology-
As an autoimmune disease, AS develops through complex interactions between genetic
background and environmental factors. Although significant progress has been achieved in
the past decades, the aetiology of AS remains unclear to some extent. To date, studies have
revealed some factors that may be related to the occurrence of AS, including genetic
background, immune reaction, microbial infection, and endocrinal abnormity.

Genetic factors have been acknowledged as crucial in the genesis of AS. The correlation
between AS and genetics has been a perpetual topic since hereditary factors of AS were first
confirmed within families in 1961.
Genetic effects have been identified as pathogenic factors that contribute to over 90% of
the population variance for AS manifestations. One of the most important genetic factors is
major histocompatibility complex (MHC) class I allele HLA-B27.

In addition to the association with the genesis of AS, HLA-B27-positive patients showed a
significantly lower average onset age and a higher prevalence of acute anterior uveitis than
did HLA-B27-negative patients.

In addition, genetic influence is not alone in the development of AS. HLA-B27-transgenic rat
studies on β2 macroglobulin (β2m), a noncovalent part of the MHC-I complex, has proven
that additional β2m reduces HLA-B27 misfolding and promotes arthritis and spondylitis,
implying that B27 misfolding is associated with intestinal inflammation. This result
suggested that abnormal β2m can coordinate with HLA-B27 in AS development, which may
be explained by protein misfolding theories.

AS is related to a series of autoimmune diseases, including IBD, anterior uveitis and

psoriasis, which suggests that they may share a genetic basis and some common
immunological processes. The differences observed in immune cells and cytokines in AS
suggest the role of immunological effects in AS pathogenesis. In the peripheral blood of AS
patients and healthy HLA-B27-positive controls, the levels of T cells secreting tumour
necrosis factor (TNF)-α and interferon (IFN)-γ were reportedly lower. CD8+ T cells in AS
patients tended to secrete more IL-10.
Microbial infection acts as a triggering factor of the host innate immune system and AS
development. The gut microbiome,
including Lachnospiraceae, Veillonellaceae, Prevotellaceae, Porphyromonadaceae,
and Bacteroidaceae, showed significant differences in AS patients compared with that in
healthy controls. Klebsiella pneumoniae acts as an opportunistic pathogen in the normal
human gut, and studies have suggested that it may be an exacerbating agent in the
autoimmune process of AS.

The treatment of AS is mainly composed of pharmacological drug and surgical treatment. In

clinic, NSAIDs and TNF-alpha inhibitors are the main drugs for AS. Moreover, interleukin
receptor blockers and some drugs that inhibit new bone formation have received increased
attention and become the focus of future research, including IL-6 receptor inhibitor
sarilumab and Wnt signal pathway inhibitors.

A more recent theory explaining the pathogenesis of (spondylarthritis) SpA involves the
relationship between the gut microbiome, intestinal inflammation and autoimmune
diseases. The gut microbiome plays a key role in the host’s innate intestinal immune
response and alterations to its composition and dysbiosis are linked to autoimmune and
inflammatory diseases (including those in the spectrum of SpA) through mechanisms such as
increased epithelial permeability, activation of the immune response and molecular
mimicry.

The research regarding the impact of diet in modulating disease activity and symptoms in AS
remains limited. A small number of studies have examined the elimination of various
nutrients from the diet in the management of AS. In a longitudinal observational study,
Appelboom et al. studied the effects of a dairy-free diet on 25 patients with AS. Self-
reported beneficial effects were obtained in 52% of patients after six weeks of follow-up,
out of which 62% could discontinue their treatment with nonsteroidal anti-inflammatory
drugs. Only 24% of studied patients were adherent to this diet after 2 years. When it comes
to the relationship between the impact of the diet and the HLA-B27-positive/negative status
of the included patients, the authors concluded that the effect of the said diet was
independent of the presence or absence of HLA-B27.

The hypothesis that a diet consisting of a high starch intake might be associated with
increased disease activity in AS patients was tested by Ebringer and Wilson by implementing
a low-starch diet for a period of nine months with 36 patients positively diagnosed with AS.
IgA and erythrocyte sedimentation rate (ESR) were monitored both before the
implementation of the low-starch diet and after and revealed that, before the diet, no
reduction in ESR or IgA occurred. However, IgA and ESR significantly decreased over the
nine-month period following the implementation of this type of diet. The so-called “low-
starch diet” consisted of low quantities of carbohydrates, such as bread, potatoes, biscuits,
pasta and cereals, and increased quantities of red and white meat, fish, vegetables and
fruits to compensate for the loss of calories.

Sundström et al. conducted a study in order to assess the relationship between diet, disease
activity and gastrointestinal symptoms in patients diagnosed with AS. Data from 111
participants were analysed based on questionnaires regarding socio-demographic aspects,
dietary habits, including dietary supplements, physical activity, the use of NSAIDs and
gastrointestinal symptoms. Moreover, disease activity and functional capacity were also
measured using the Swedish versions of the Bath Ankylosing Spondylitis Disease Activity
Index (BASDAI) and the Bath Ankylosing Spondylitis Functional Index (BASFI). The study
concluded that 27% of the participants reported gastrointestinal symptoms when
consuming certain types of foods, such as dairy products or foods rich in flour. Although the
study did not find any correlation between diet and disease activity, the high percentage of
patients reporting gastrointestinal symptoms when consuming certain food products
containing starch further demonstrates the impact such products have on the gut
microbiome and, implicitly, on the general wellbeing of patients.

Regarding certain foods that have been incriminated in the aggravation of symptoms in
patients with AS, the effect of fasting on the evolution of the disease was also investigated.
Several studies have analysed the impact that fasting has on the progression or remission of
symptoms in patients suffering from various rheumatic diseases, including AS. A study by
Haugen et al. included 41 patients diagnosed with AS who answered questionnaires
provided regarding different types of diet and fasting. When it came to fasting for an
average period of 7–10 days, more than half of the respondents reported less pain, less
stiffness and less joint-swelling, although the results were similar among all rheumatic
diseases and not specific to patients suffering from AS. Moreover, the patients were
interviewed regarding diet treatments undergone and their effects on the disease, with 47%
reporting less pain, 46% less stiffness and 36% reduced joint swelling, without any
differences regarding the type of rheumatic disease incriminated. No particular diet has
been analysed such that its making a significant improvement to the symptomatology of
patients with AS in comparison with other diets can be concluded.

List of foods that may cause or aggravate inflammation:

- Refined carbohydrates (white bread)
- Fried food
- Red meat
- Margarine
- Artificial sweeteners such as aspartame, saccharine, sucralose, and MSG
- Dairy products- only it is having an interaction with medication
- Caffeine
- Sugar
- Seed oils (rapeseed, sunflower, canola oil)- too much omega-6 (linoleic acid) which
sets the stage for chronic inflammation. Linoleic acid is not inflammatory itself, the
body coverts it to arachidonic acid – building blocks for inflammatory compounds.
- “nightshade” family foods including eggplants, pepper, tomatoes and potatoes
contain solanine which can aggravate inflammation in arthritis.
- Animal based protein such as whey protein ( found in protein shakes) are more
acidic than plant based, which increases the risk of inflammation.

“Good” foods for decreasing inflammations:

- Oils such as EXTRA virgin olive oil and avocado oil
 - Wild caught salmon (salmon contains amino acid leucine, arginine, and methionine
which has an inhibitory effect on cytokines TNF- and IL-1 both of which are
elevated in serum in AS. Leucine enriched amino acids accelerate recovery from
muscle damage by preventing excessive inflammation.
- Spinach, kale
- Whole grains
- Probiotics to restore gut health
- Ginger- (contains gingerol which is a phenol phytochemical in ginger inhibit
prostaglandin and leukotriene biosynthesis through suppression of 5-lipoxygenase or
prostaglandin synthetase. Additionally, they can also inhibit synthesis of pro-
inflammatory cytokines such as IL-1, TNF-α, and IL-8).

Other factors that can contribute to deterioration-

- Stress- rise in stress levels can lead to activation of pro inflammatory cytokines
ultimately causing a flare up.
- Best exercise for people with AS is low impact such as swimming, cycling
- Whole body cryotherapy produces significant improvements in spinal mobility
parameters.

PHD synergy protein shake ingredients:

Vanilla Crème Flavour

PhD Protein Blend [Milk Protein Concentrate (Providing 80% Micellar Casein), Whey
Protein Concentrate (Milk), Hydrolysed Wheat Protein (Providing Peptide Bonded L-
Glutamine)], Maltodextrin, Creatine Monohydrate, Flavourings, Stabiliser (Guar Gum,
Xanthan Gum), Magnesium Oxide, Zinc Oxide, Vitamin B6, Sweetener (Sucralose),
Emulsifier (Sunflower Lecithin).

Therapeutic Benefits of Pinene, Anti-inflammatory and Analgesic Effects – Arthritis

Pinene is one of the dominant terpenes found in cannabis strains known to benefit chronic
pain. Alpha-pinene’s anti-inflammatory and analgesic benefits take place through inhibition
of COX-2, the same system in which NSAIDs like ibuprofen work. Pinene is also anti-
inflammatory via prostaglandin PGE-1 and its antioxidant and anti-inflammatory effects in
human chondrocytes (cartilage cells), suggests potential benefit in arthritis with analgesic
benefits as well.