Correspondence 527
were probably triggering frequent episodes of herpes simplex
in our patients was simply based on the analogy of viral etiology
put forth by Wolf et al.,1 and we stand by it. In view of the not
yet fully understood pathomechanism of Wolf’s isotopic phen-
omenon, we also discussed various other postulates brought
forth over a period of time for improved comprehension. The
hypothesis of “neuroimmunologic interactions” by Farber2 is
just one and may not necessarily explain the phenomenon
in our cases.
Furthermore, colocalization of herpes simplex infection
over a scrofuloderma scar in our patients owing to general
debility or immunosuppression following some occult tuber-
cular focus, as has been suggested, appears far-fetched. On
the contrary, only a good immunity will produce an occult
focus. Second, herpes simplex infection has been more
frequently observed primarily over muco-cutaneous areas
under circumstances of lowered immunity. Their own case
report of Kaposi’s varicelliform eruptions overlying active
lesions of lupus vulgaris is neither relevant to our report nor
can it be juxtaposed with our cases. The sole critical criterion
for the diagnosis of Wolf’s isotopic phenomenon is occur-
rence of a second unrelated disease over a scar.1 Neither of
Omega-3, omega-6 and psoriasis: a different view
Correspondence
45
A recent commentary in this journal suggested that omega-6
linoleic acid may be protective against psoriasis by way of its
elevation of prostaglandin E2 (PGE2) and subsequent down-
regulation of cellular immunity.1 The commentary connected
the reported low frequency of psoriasis in West Africans with
a nonspecific report of increased dietary maize consumption.
I would like to put forth an alternative hypothesis and comment-
ary on the reported low incidence of psoriasis in West Africa.
Maize is indeed a significant source of the dietary omega-6
fatty acid linoleic acid, and its potential in promoting PGE2
production is well documented.2 However, linoleic acid can
also cause a rise in leukotriene B4 (LTB4), an inflammatory
mediator which has been found elevated in psoriatic scales,
psoriatic epidermis, patient serum and suction blister fluid from
psoriatic plaques.3 In addition, linoleic acid can cause a LTB4-
induced elevation in the same cytokines that PGE2 may sup-
press, i.e. interleukin-1, interferon-gamma and tumor necrosis
factor alpha.2 Thus, LTB4-induced elevation in these cytokines
via dietary linoleic acid may be detrimental in psoriasis.
PGE2 elevation has been observed in psoriasis, with levels
in suction blister being almost 5 times greater than those in
nonpsoriatic controls.4 Research has also shown that those
with psoriasis have elevated levels of adipose arachidonic
acid, the precursor of which is linoleic acid, and lower levels
of the parent omega-3 fatty acid alpha-linoleic acid (ALA).5
Adipose tissue fatty acids are reflective of long-term dietary
© 2004
2005 The International Society of Dermatology
our patients had clinical nor histological evidence of under-
lying active cutaneous tuberculosis, and the scars underneath
the herpetic lesions were starkly obvious.
Last but not the least, according Wolf et al.,1 herpetic infec-
tion as the first disease has perhaps been over-represented in
the reported cases of isotopic response. This may be owing to
easy recall or its striking dermatomal pattern.
In their review, Kaposi’s sarcoma has been observed over
the primary lesions of phlebitis. As a more precise definition
of this very interesting phenomenon has now been provided
by Saraswat et al., we may be seeing reports of nonviral
diseases more often in the future.
Nand Lal Sharma
Department of Dermatology, Indira Gandhi Medical
College, Shimla, India
E-mail: nandlals@hotmail.com
References
1 Wolf R, Brenner S, Rucco V, et al. Isotopic response. Int J
Dermatol 1995; 34: 341– 348.
2 Farber EM. Psychoneuroimmunology and dermatology. Int J
Dermatol 1993: 3293 – 3294.
intake. These findings are difficult to reconcile with a
hypothesis that suggests PGE2 elevation is protective in
psoriasis.
A higher dietary intake of omega-3 fatty acids may be the
protective factor in the low incidence of psoriasis in West
Africa. Although limited, a number of studies have revealed
higher omega-3 levels in those living in West African nations.
Recent research has shown that the breast milk of Congolese
women is particularly high in the parent omega-3 fatty ALA
and its conversion product, docosahexaenoic acid.6 This sup-
ports previous research which shows that Congolese children
have lower levels of linoleic acid and higher levels of omega-
3 fatty acids than North American and European children.7 In
addition, children within Nigeria have exceptionally high
omega-3 fatty acid levels relative to linoleic acid in plasma
lipid fractions when compared to control children living in
Dusseldorf, Germany.8 The Fulani are a nomadic people who
reside throughout Western Africa. Their traditional diet leads
to high ALA and low linoleic acid levels in breast milk in
women compared to Western populations.9 While the relev-
ant data are far from robust and remain equivocal, omega-3
fatty acids, as opposed to linoleic omega-6, have been shown
to be of value in the treatment of psoriasis and as a comple-
ment to standard prescription drug therapy.11 Omega-3 fatty
acids can lower PGE2 levels in humans; however, they are still
capable of diminishing T helper cell 1 (Th1)-type responses.
While the mechanisms remain obscure, the research shows
International Journal of Dermatology 2005, 44, 524
527 – 525
528
528 Correspondence
that omega-3 fatty acids can influence cellular immunity by
means other than prostaglandin synthesis.2
An ideal ratio of omega-6 to omega-3 fatty acids of 1.8 : 1
has been recommended by an international panel of experts
as part of a United States National Institutes of Health
Panel.12 This ratio is close to that found in human history and
close to that found in traditional hunter-gatherer diets. This
essential fatty acid recommendation is a long way from the
current 15–20 : 1 ratio of omega-6 to omega-3 currently con-
sumed in Western diets.12 This skewed ratio is a result of the
large-scale introduction of linoleic-rich oils such as corn, soy-
bean, safflower and sunflower oils into the food supply. The
low frequency of psoriasis among Japanese, Norwegian Lapp
and Eskimo populations10 may be a result of their high intake
of omega-3 fatty acids, particularly from deep, cold-water
fish. In these populations, the dietary intake of linoleic acid is
lower than that in typical Western diets. If linoleic acid were
protective against psoriasis, it should follow that incidence
levels would be extremely low in the United States, where
linoleic acid-derived omega-6 intake is outnumbering omega-
3 by up to 20 : 1. Clearly, that is not the case.
Alan C. Logan, ND, FRSH
New York, USA
Disclosures: The author is a consultant to companies
in the food and dietary supplement industry.
The author makes no direct income on the sales
of dietary supplements containing omega-3 fatty acids.
References
1 Namazi MR. Why is psoriasis uncommon in Africans? The
influence of dietary factors on expression of psoriasis. Int J
Dermatol 2004; 43: 391–392.
Further support for the Protective Effect of Linoleic Acid
Against Psoriasis
I appreciate Dr Logan’s comments, but would like to point
out the following.
1 Elevation of leukotriene B4 (LTB4) is not restricted to pso-
riatic plaques, but is also found in uninvolved skin of patients
with psoriasis.1 Although application of LTB4 and 12-HETE
(12-Hydroxyeicosatetrenoate) to symptomless skin of
psoriatic patients produces enythema and attracts neutrophils,
it does not reproduce the psoriatic lesions. The dramatic
appearance of numerous microabscesses, compared to the
relative paucity of microabscesses in chronic plaques of
psoriasis, suggests that the former dramatic appearance of
numerous microabscesses is an interesting experimental
artifact. This finding, along with the elevation of LTB4 in
both involved and uninvolved skin, implies that an important
piece of the puzzle may be missing.1 Moreover, some well-
International Journal of Dermatology 2005, 44,
44, 528
524 – 529
525
2 Calder PC, Gimble RF. Polyunsaturated fatty acids,
inflammation and immunity. Eur J Clin Nutr 2002; 56:
S14–S19.
3 Ikai K. Psoriasis and the arachidonic acid cascade. J
Dermatol Sci 1999; 21: 135–146.
4 Reilly DM, Parslew R, Sharpe GR, et al. Inflammatory
mediators in normal, sensitive and diseased skin types.
Acta Dermatol Venereol 2000; 80: 171–174.
5 Vahlquist C, Berne B, Boberg M, et al. The fatty-acid
spectrum in plasma and adipose tissue in patients with
psoriasis. Arch Dermatol Res 1985; 278: 114–119.
6 Rocquelin G, Tapsoba S, Dop MC, et al. Lipid content and
essential fatty acid (EFA) composition of mature Congolese
breast milk are influenced by mothers’ nutritional status:
impact on infants’ EFA supply. Eur J Nutr 1998; 52:
164–171.
7 Leichsenring M, Doehring-Schwerdtfeger E, Laryea MD,
et al. Investigation of the nutritional state of children in a
Congolese village. II. Plasma fatty acid composition. Eur J
Pediatr 1988; 148: 159–163.
8 Koletzko B, Abiodun PO, Laryea MD. Comparison of
fatty acid composition of plasma lipid fractions in
well-nourished Nigerian and German infants and
toddlers. J Pediatr Gastroenterol Nutr 1986; 5:
581–585.
9 Schmeits BL, Okolo SN, VanderJagt DJ, et al. Content of
lipid nutrients in the milk of Fulani women. J Hum Lact
1999; 15: 113–120.
10 Giardina E, Sinibaldi C, Novelli G. The psoriasis genetics
as a model of complex disease. Curr Drug Targets Inflamm
Allergy 2004; 3: 129–136.
11 Mayser P, Grimm H, Grimminger F. n−3 fatty acids in
psoriasis. Br J Nutr 2002; 87: S77–S82.
12 Simopoulos AP. The importance of the ratio of omega-6/
omega-3 essential fatty acids. Biomed Pharmacother 2002;
56: 365–379.
Correspondence
45
conducted studies have shown that LTB4 antagonists are
neither effective against psoriasis nor prevent its relapse,
either clinically or at the cellular level, suggesting that further
development of LTB4-modulating drugs for the treatment of
psoriasis is not indicated.2
2 Although linoleic acid can also cause a rise in LTB4,
which can stimulate the production of some T helper cell 1
(Th1)-type cytokines that prostaglandin E2 (PGE2) can sup-
press, on the whole it suppresses the cellular immune response
and the associated Th1 cytokines.3
3 Given the potent inhibitory effect of PGE2 on the cell-
mediated immune response, its elevation in psoriasis may be
a regulatory response rather than part of the pathogenic
process. The frequently reported exacerbation of psoriasis
with nonsteroidal anti-inflammatory agents (NSAIDS),
which decrease PGE2 levels, gives more weight to the former
notion.
2005 The International Society of Dermatology
© 2004