Psoriasis
Psoriasis is a complex disorder involving immune attacks in skin with chronic
inflammation and overgrowth of the upper layers of skin. Psoriatic plaques
are covered with thick silvery scales which shed at an alarming rate - super
dandruff. The disease usually involves the extensor surfaces of the body - the
opposite to eczema which prefers the flexor surfaces. Psoriasis tend to be a
chronic disease lasting years to decades and in some patients follows and
erratic course - flaring and subsiding in cycles lasting many months.
People with extensive psoriasis tend to suffer stoically and are often
unwilling to bare their body in public - swimming pools and beaches are of
limits for some because of embarrassment about the skin lesions which do look
rather menacing to onlookers who are not familiar with the disease. Swimming in
salt water and sun exposure is often helpful. Ultraviolet light treatment has
been used as a standard therapy. For years people have been treated with coal
tar baths followed by ultraviolet light exposure with benefits. Now, of course,
we are warning people against ultraviolet light exposure and have concerns about
the carcinogenic potential of coal tar.
Psoriasis affects 1.5 % to 2.0 % of the population in western countries with
Equal incidence in males and females There is genetic tendency: when one parent
has psoriasis, 8 % of offspring develop psoriasis, and when both parents have
psoriasis, 41 % develop psoriasis. Class I antigens associated with psoriasis
are: HLA-B13, -B17, -Bw57, -CW6.
Little progress has been made in understanding and treating Psoriasis - it is
one of the many immune-mediated diseases that rage-on unchecked. Medical
treatments have not been very helpful and for many years psoriasis has been a
target of dubious marketing practices - numerous creams and lotions have
been offered to treat the disease. Coal tar derivatives and peeling agents have
been the most plausible treatments but offer little relief. Even the steroids -
the all purpose drugs for skin disorders - are disappointing.
Psoriatic plaques tend to be good breeding grounds for bacteria and fungi, so
that secondary infection is almost inevitable. Topical antifungal agents (such
as Nizoral shampoo) may be helpful, but there is little evidence that infection
is the initial cause of the problem.
Even the steroids, the all-purpose drugs for skin disorders, are
disappointing. Synthetic vitamin A analogues can reduce the skin growth
abnormalities in psoriasis. Tazarotene in an aqueous gel has been effective even
on thick plaques on the knees and elbows. The strongest immune-suppressant drugs
such a cyclosporine can control psoriasis but at high risk of developing other,
more serious health problems. When cyclosporine is given to patients who have
received psoralen with UV light therapy, they have, for example, a 7-fold
increase in the incidence of squamous cell skin cancer.
Agents that block tumor necrosis factor have been presented as a breakthrough
in therapy, effective in treating plaque psoriasis and psoriatic arthritis. In
2005, an intense marketing effort persuaded at least half the dermatologist in
the US to use these agents. Unfortunately, behind the hype, there is some bad
news. While anti-TNF antibody is in theory a smart strategy for blocking immune
activation, the proposal to use this treatment long-term incurs high cost
plus complications and serious hazards. Anti-TNF drugs can improve arthritis and
psoriasis but paradoxically, they cause a surprising number of skin diseases,
including psoriasis. Flendrie et al reported that 25% of patients treated with
anti-TNF drugs required consultation with dermatologists. The events recorded
most frequently were skin infections, eczema, and drug-related eruptions. Other
events with a possible relation to TNF-a-blocking therapy included vasculitis,
psoriasis, drug-induced systemic lupus erythematosus, dermatomyositis, and a
lymphomatoid-papulosis-like eruption. An increased incidence of tuberculosis has
been described as well as a growing number of serious infections with fungal,
mycobacterial, and intracellular bacterial pathogens.
Psoriatic arthritis occurs in 5% to 8% of patients with psoriasis.
There are two types:
1. Mild, single joints - involving, asymmetrically, a few distal
interphalangeal joints of the hands and feet: 2. Aggressive psoriatic arthritis
with bone erosion and ankylosis involving the sacroiliac, hip, and
cervical areas with ankylosing spondylitis; seen especially in erythrodermic and
pustular psoriasis.
Nail Abnormalities
Pitting, yellow-brown discoloration and deformation of finger and toe nails
are common; 51.8% of patients suffered from pain-caused by the nail
changes, and a large group of patients was restricted in their daily activities,
housekeeping and/or profession
Skin and nail growth disturbances are secondary to an immune cell
infiltration of the skin and the release of immune mediators (cytokines) which
promote cell growth and inflammation at the same time. Evidence suggests that
T-lymphocytes lead the attack on the skin. Although psoriatic plaques tend
to be good breeding grounds for bacteria and fungi, it is doubtful that
infection is original cause of the problem.
Is Psoriasis Food Allergy?
Trent and Kerdel described the immune activity in psoriatic skin: “The
process begins with the presence of antigens, which cause the maturation of
Langerhans cells and the migration of antigen-presenting cells (APC) to the
lymph node. Once in the lymph node, the APCs interact with T cells,
causing T-cell activation and subsequent T-cell proliferation. Some of these
proliferating T cells are memory T cells, which ultimately migrate to the
inflamed target areas of the skin. When these T cells are activated, they will
release type 1 cytokines (Th1), such as interferon gamma, IL-2 and IL-12, and
TNF. These cytokines are responsible for keratinocyte proliferation and lack of
maturation, and vascular changes characteristic of psoriasis.”
I would edit their description by stating: “the process begins with
the presence of food antigens in the skin.” Food proteins that enter the
body through a leaky digestive tract can make their way into the skin and invite
immune cells to attack. This is a delayed pattern immune response that occurs
slowly and is usually not noticed by psoriasis patients and is not detected by
any office or laboratory test. See
delayed
hypersensitivity mechanisms.
Food antigens may arrive in the skin as immune complexes, attach to skin
cells and/or are presented by resident macrophages which trigger
lymphocytic activity. While this is just a theory, its better than no therapy at
all and can lead to a immediate therapeutic experiment. Psoriasis responds
variably to Diet Revision Therapy. In several remarkable cases, remission of
psoriatic arthritis with clearing of the skin lesions has been achieved by
rigorous application of the Alpha Nutrition
Program.
For moderate to severe psoriasis, we are inclined to start diet revision with
an extended food holiday on Alpha ENF and use mild topical treatment include
daily warm water baths with sea salts to soften the thickened skin and
gentle scrubbing to remove skin scales. Topical Vitamin A gel
applications to the thickest plaques is an option.
Psoriatic skin is badly damaged and takes many weeks to heal. Food
reintroduction must be slow and patient since it is easy to reactivate the
disease with wrong food choices.
NB Skin tests, blood tests for food allergy and rotation diets are not
useful.
