Lecture 19
ECZEMA-29 October 2010
IMPACT OF DIET
Vitamin A
Allergy
Nickel
Breast feeding
Preventative dietary therapy for children to prevent atopic dermatitis
Dietary Deficiencies (elimination or reduction causing dermatitis
Riboflavin
Biotin
Essential fatty acids
VITAMIN A
Dose issue in food-more on vitamin A in the next lecture
Issue of dermaceuticals
ALLERGY
This refers to atopic dermatitis and point up the problem with functional foods
Diet allergens interact with IgE antibodies bound to mast cells the mast cells release IL-4,5,6 and TNF-a (early response)
These cytokines are pro-inflammatory and act accordingly through the IgE mediated late response
Leukocytes are attracted and stimulated to release their own pro-inflammatory cytokines
Allergy-Nickel
Nickel sensitivity or allergy found in fasting persons given 600 mG nickel in water
-likely atopic dermatitis
also in nickel rich foods like chocolate, nuts, beans, porridge oats
Allergy- Breast feeding
Various proteins can lead to atopic dermatitis
Elimination therapy by infant or mother
Infants with recent atopic dermatitis-breast milk with higher ratios of linoleic to the total of gamma-linolenic, dihomogammalinolenic , and arachidonic acids-this is consistent with the concept of lowered gamma-linolenic and dihomogammalinolenic acids in atopic dermatitis patients-lowered PgE1 allows for IL-4 driven IGE synthesis
The fatty acid ratios may explain why breast feeding does not always prevent atopic dermatitis
Preventative dietary therapy for children to prevent atopic dermatitis
Prevalence and incidence of atopic dermatitis down in children if:
Kids prolonged breast feeding is anti-allergenic
-avoidance of cows milk
-immunoprotective factors in breast milk
a diet free of cows milk and eggs to nursing mothers
supplementation of soya formula containing sucrose when breast milk is not available
Cooking and other technological advancements
In meat based baby foods
Reduction of severity of response to skin prick antigen (meat) test in atopic dermatitis infants fed milled or freeze dried meats in comparison to steam cooked meat
Dietary deficiency
Riboflavin
Deficiencies of riboflavin lead to dermatitis
Via conversion of
vitamin B6 to its coenzyme (necessary for elongation of gamma linolenic acid to arachidonic acid)-
consequently there is less DGLA formed
OR
Curtailed conversion of tryptophan to niacin-role of niacin in atopic dermatitis is unclear
Biotin deficiency
Mechanism is unclear but as linoleic acid is elevated and dihomogammalinolenic acid is decreased it is suggested that an interference with delta 6 desaturase and or the elongase that follows
Essential fatty acids
Omega 6
Gamma-linolenic acid is low in the skin and therefore dihomogammalinolenic acid is low in the skin in atopic dermatitis
This deficiency of gamma linolenic acid and its sequelae particularly comes up in parenteral nutrition that is deficient in lipids
This raises the issue of whether linolenic acid is essential as opposed to linoleic acid being essential
Omega 3
Issue of alpha-linolenic fatty acid versus eicosapentaenoic acid essentiality
Recall that eicosapentaenoic acid is anti-inflammatory
Fish protein can cause allergy so source of eicosapentaenoic acid is important
ECZEMA
FUNCTIONAL FOODS AND NUTRACEUTICALS
Such foods are really only functional by elimination or by meeting dietary deficiencies and that is not really a definition of functional foods
Designer functional foods
Use of fish- fish protein allergy is an issue for some
DERMACEUTICALS
Retinoic acid-skin creams reduces seborrhoeic dermatitis skin flakiness by inhibiting oil gland activity but it stimulates the inflammation of atopic dermatitis
ATOPIC DERMATITIS
EVENING PRIMROSE OIL
Plasma PGE1 AND PGE2 profiles are identical between atopic dermatitis and healthy controls
What is the significance of this observation
FIOCCHI fed 3 g/day of GLA in the form of evening primrose oil for 4 weeks to children with infantile atopic dermatitis
A significant decrease in sleep interruption and itching requiring anti-histamine or corticosteroid therapy
Uncontrolled and short duration failed to account for cyclical nature of atopic dermatitis
BIAGI- fed children with atopic dermatitis a supplement of 22.5 mg GLA /kg body weight/day in the form of a 50/50 min (olive oil/evening primrose oil) or 45 mg GLA/kg bodyweight per day (pure evening primrose oil) for 8 weeks
Only 45 mg dose produced clinical improvement
ISSUES
WHITTAKER- no improvement in atopic dermatitis patients taking 600 mg GLA/day for 16 weeks in the form of evening primrose oil-complicated by the use of emollient and corticosteroidal cream
DOSE
IS NOT AN ISSUE ?? DURATION OF TREATMENT NOT AN ISSUE??
HEDEROS- saw improvement with evening primrose oil in atopic dermatitis patients but used an analogue scale up to 100 (worst ever seen by physician) and reports of child itch by parents
ISSUES
LEHMAN- atopic dermatitis patients-decreases in LTB4 (pro-inflammatory) from leukocytes from patients on evening primrose oil (540 mg GLA/day for 12 weeks
The rise in leukocyte DGLA and DGLA/AA ratio may explain this decrease
BAHMER- atopic dermatitis patients-a positive study used only one patient
ANDREASSI- atopic dermatitis patients fed 548 mg GLA/day in the form of borage oil for 12 weeks-clinical improvement compared to placebo
HENZ- saw improvements only in those who had significant rises in erythrocyte DGLA levels-however this was only a small percentagew of the the patients-suggests borage oil was only effective in a select group
COMPARE TO EVENING PRIMROSE OIL
BORAGE OIL
TOLLESON AND FRITZ- topically applied GLA (0.05 mg/kg body weight) topically applied GLA in the form of borage oil in the nappy area of children with infantile seborrhoeic dermatitis and age matched healthy controls twice a date for 4 weeks-improvements in terms of loss of lesions
TOLLESON AND FRITZ- topically applied GLA (0.05 mg/kg body weight) topically applied GLA in the form of borage oil in the nappy area of children with infantile seborrhoeic dermatitis and age matched healthy controls twice a date for 4 weeks-improvements in terms of loss of lesions -however there was no control group
Nothing done
Nothing done
FISH OIL
Widespread success-why omega 3 superior?
Brings omega 3 to omega 6 ratio closer to ideal?
Other reasons?