PEER-REVIEW | DERMATOLOGY | Impact on quality of life
Acne on the face is very visible and cannot be covered by clothes; therefore, it is understandable that Sulzberger et al came to the conclusion that: ‘There is no single disease which causes more psychic trauma, more maladjustment between parents and children, more general insecurity and feelings of inferiority and greater sums of psychic suffering than does acne vulgaris’.18 Acne is not a self-limiting cosmetic , and impact at a social,
disorder19
psychological, and emotional level is similar to asthma, arthritis, epilepsy, and diabetes20
— serious diseases with a high
negative impact on overall health. The presence of acne in adult women increases
the risk of anxiety, depression, and suicidal ideation21 and has a negative effect on work or eductional performance. It is more than likely that the media’s
portrayal of flawless skin as an ideal is the leading cause of psychological morbidity in females22
. Acne pathogenesis is
Causes and trigger factors Acne pathogenesis is connected with excess sebum production by the sebaceous glands, follicular occlusion, hyperproliferation of Propionibacterium acnes (P. acnes), and inflammation23 Genetic factors play an important role, so acne occurs
.
earlier and is more severe in those with a positive family history24, 25
.
P. acnes was first implicated in acne pathogenesis in and individuals with active acne had higher densities of P. acnes when compared to normal controls27
189626 .
It was also discovered that antibiotic resistance was associated with treatment failure28–30
.
Androgens, such as dihydrotestosterone (DHT) and dehydroepiandrosterone sulphate (DHEAS)31, 32
, as well as cholesterol33, 34
oestrogen, growth hormones, insulin, insulin growth factor-1 (IGF-1), corticotropin-releasing hormone (CRF), adrenocorticotropic hormone (ACTH), melanocortins, and glucocorticoids are all strongly connected with acne and sebaceous secretion. The skin produces hormones de novo from and have all of the necessary enzymes
required for the conversion from cholesterol to steroids. IGF-1 is correlated with acne35
and women
with acne present higher levels of IGF-1 compared with women without acne36–38 IGF-1 stimulate adrenal androgen
.
synthesis and inhibit the production of hepatic sex hormone-binding globulin (SHBG) with the increase of free androgen39
,
and may mediate some of the effects of androgens, growth hormone, and glucocorticoids40
42 .
Milk consumption is linked to acne because milk is an insulinotropic nutrient and has a high insulinaemic index41
serum insulin and IGF-1 levels42–45
which would increase . Human and
bovine IGF-1 share the same amino acid sequences46
the human IGF receptor47, 48
and both are able to bind to . A study in
1949 reported an association between frequent milk consumption and acne severity49
and it is possible that
upregulation of insulin secretion and the long lasting increase in serum IGF-1 levels50, 51
could be the culprits for acne
development. Milk induces an increase in IGF-1 levels, especially skimmed milk intake, which causes a break-out and/or worsening of acne53, 54 It also contains oestrogen, progesterone, androgen
.
precursors, and 5-reductase-dependent steroids, which are implicated in comedogenesis54 The studies of Adebamowo52, 53, 55
. are the first
connected with excess sebum production by the sebaceous glands, follicular occlusion, hyperproliferation of
Propionibacterium acnes (P. acnes), and inflammation.
to provide direct clinical evidence on the association between milk/dairy consumption and acne. Yoghurt consumption was not correlated
with acne vulgaris occurrence and is consistent with the findings of a number of studies52, 53, 55
and lactoferrin-enriched lactoferrin and its ability to suppress microbial growth56–58
fermented milk decreases acne severity owing to the anti-inflammatory effects of .
An intake of polyunsaturated fatty acids (omega-6 and omega-3) modulates the skin’s inflammatory response59 and omega-3 fatty acids may decrease acne by decreasing insulin60
increasing IGFBP-3 concentrations62
and IGF-1 concentrations61 .
, and Chocolate is rich in biologically active compounds
(caffeine, theobromine and serotonin), which increases secretion of insulin and its peripheral resistance63, 64
.
Chocolate has an effect on the pathophysiological processes involved in the development of acne lesions, especially related to carbohydrate metabolism, and certain individuals eating chocolate may present with the development or worsening of acne lesions. Some cosmetics can contain comedogenic agents that
A study in 1949 reported an
block follicular structures and induce comedonal disease on the cheeks of females, such as isopropyl myristate. However, because the majority of cosmetic products are now noncomedogenic, cosmetics are an uncommon cause65–68
.
association between frequent milk consumption and acne severity and it is possible that upregulation of insulin secretion and the long lasting increase in serum IGF-1
levels could be the culprits for acne development.
July/August 2014 |
prime-journal.com
Stress is a major factor in acne development69–71
, involved both as a trigger
factor and exacerbating factor. Stress induces both neuroendocrine changes that are involved in the appearance of acne lesions and can lead to trauma of the lesions, as well as use of empirical treatments that cause worsening or development of acne lesions. Smoking is associated with skin diseases, inclusively skin cancer72
and practitioners
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