Pimples (Acne)

Your Acne Treatment is Going in Right Way ?

 1.       Definition of Problem

Acne or pimple is a chronic inflammatory disease of the pilosebaceous unit, which may be due to excess production sebum occur because of excess androgens production and altered keratinization and make a ground to work for the infection of Propionibacterium acnes, in hair follicles on the face, neck, chest, and back which resulted in inflammation. Though, the instigating factor exactly responsible to trigger the acne is yet to be established. However, one can easily have speculation about the role of liver which is responsible for synthesis of Acute Phage Proteins, a vital component of first line of nonspecific defense on surface and inside of body. Thus, the role of diet can’t be overruled. Colonization with P acnes and family history might have important roles in the disease, exactly what triggers acne and how treatment affects the course of the disease remain unclear.

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2.      Some Facts

      ·         Acne appears in all most all people to various extent from in age of 15 to 17 yrs [1, 2, 3]

      ·         Its ranges from moderate to severe in 15-20% in young population [1, 4, 5]

      ·         It is among the top three most prevalent skin conditions in the general population as found in large studies in the U.K., France and the U.S.A.[ 6, 7, 8]

     ·         One of important study in USA showed that severity of acne in boys correlated with pubertal maturation while boys between 10-11 yrs had more than 10 primary acne signs [9], while 78% girls between 8-12yrs had acne [10].

      ·      Importantly, prepubertal girls with severe acne had notably higher dehydroepi-androsterone sulphate levels [9, 10].

      ·         Total cost of treatment and loss in productivity due to acne in US is $3 bn/yr [11].

        3.      Symptoms

Acne appears on the skin as [12]

·         occluded pores ("comedones"), also known as blackheads or whiteheads,

·         tender red bumps also known as pimples or zits,

·         pustules (bumps containing pus),

·         and occasionally as cysts (deep pimples, boils).

        4.      Predisposing Factors

In general alteration in hormonal condition, especially androgen is said to responsible acne, which cause excess production of sebum. However, there are various other components are designated as contributors of acne, [13], including family history, body mass index, and diet may influence the risk of moderate to severe acne. The influence of environmental and dietetic factors in acne should be further explored [14].

a.      Genetic 

The heritability of acne is almost 80% in first-degree relatives [11]. A study by researchers showed that genetic factors explained significant proportions of acne variance contributing to 31–97% of phenotypic appearance [15].

b.      Diet

A study conducted in 2005, revealed that there was no clear, positive evidence that any dietary components increase acne risk [16]. Moreover, no serious correlation could be established between iodine, vitamin A, antioxidants, omega-3 fatty acids and fiber and development of acne. However, there is some evidence regarding benefit with high doses of oral zinc from double-blind, randomized controlled trials has been established [17, 18].  

                                                              i.      Glycaemic Index

Some studies shown that no significant differences in serum glucose, insulin, leptin, GI or glycaemic load between patients with acne and controls [19]. Other concerned factors, including weight loss of participants and the fats and protein consumed needed further explanation to establish what factors might have caused the decreased lesion count, or if it was a combination of various factors [20].

Nevertheless, while discussion is about infection or immunity, a basic correlation with liver can’t be overlooked. As the liver is an organ with predominant innate immunity, playing an important role in host defenses against invading microorganisms [21]. Connectively, one more line of research is needed to looked into as sebum is stimulated by androgens, a possible mechanism for an association between a high-GI diet. The acne is hyperinsulinaemic state which leads to increased androgen along with insulin-like growth factor (IGF)-1 and altered retinoid signaling [22,23,24]. 

                                                           ii.      Dairy

The evidence suggesting an association between dairy food intake and acne is currently weak and needs to be tested in an experimental fashion.

                                                         iii.      Chocolate

Workers reported that chocolate causes or exacerbates acne, particularly among adolescents [25, 26]. More recently, a small, nonrandomized, uncontrolled study of 10 people Recently, a significant increase is reported in acneiform lesions upon consumption of chocolate made up of 100% cocoa [27]. Moreover, its really very rear occurrence to find any such correlations as it would be against benefits of corporate sectors.

c.       Sunlight

Various authors have debated whether ultraviolet radiation or visible light worsens, improves or has no effect upon acne. A Cochrane systematic review of clinical trials of light therapy published up to 2008 found evidence for some benefit of light therapy, in the short term at least, and therapy with blue, blue/red or infrared is of more benefit than yellow, red or green light. Sample sizes were often small and of variable quality [28]. Though the applicability of various type of photodynamic treatments are being questioned because of prospective adverse impacts [29].

d.      Hygiene

Though, prima facia it seems that poor levels of hygiene lead to the development or exacerbation of acne vulgaris [30, 31]. Some researchers have claimed that sweat can trigger or exacerbate acne [32]. However, researchers failed to provide clear advice for or against washing as a means of helping acne, and there is certainly no robust evidence that acne is caused or propelled by a lack of hygiene [11]. Nevertheless, such conclusion usually contradicts the basic theories of infections and therefore, such facts should be considered with cautions.

e.      Smoking

Recently, researchers provide an unethical but statistically significant correlation between acne prevalence and the number of cigarettes smoked per day and a dose-dependent relationship between consumption and severity (not affected by age, sex or social class) [33]. Though such recommendations can’t be put forth due to other health issues.

f.       Stress and Picking

Early retrospective study professed to be a major trigger factor in exacerbating acne [34]. Stress is responsible to induces the local expression of neuropeptides which may pose as a pathogenic step in acne exacerbated or caused by stress [35]. Recent studies found that stressful circumstances exacerbate acne [36, 37, 38, 39,  40]. Also, observational study showed that picking at acne lesions worsened the inflammation and pustules [41]. It is likely that picking will ultimately affect the healing process and increase the likelihood of scarring.

g.      Infection

The exact role of bacteria such as Propionibacterium acnes in the pathogenesis of acne vulgaris is subject now a matter of debate as in case of any external wound. This was first postulated in 1896 and further supported by a study in 1909 [42]. Even after such reports worker at present assume as P. acnes was a secondary colonizer of the anaerobic lipid-rich environment, rather than a primary pathogen [43, 44, 45]. Though some researches, in recent in vitro studies revealed direct involvement of P. acnes is in acne pathogenesis [46, 47]. Conclusively, perhaps P. acnes plays more of a role than an innocent bystander after all [11].

Fig. 1: mode of pathogenesis & various points to adopt check for acne development

 5.      Pathogenesis

The pathogenesis of acne is complex and dependent on the interplay of multiple factors and all contribute to the development of acne vulgaris [48], which occur due to blockages in the skin's hair follicles. This blockage is supposed to be outcome of following abnormal consecutive processes [49]:

Fig. 2: Steps in pathogenesis 

Dihydrotestosterone (DHT) [50] and DHEA-S are the couple of agents responsible for androgen-induced sebum production. DHEA-S are secreted during adrenarche (a stage of puberty), and this leads to an increase in sebum synthesis, which provides environment good for commensalism for P. acnes. This cause instigation of immune response [1]. Consequently, inflammation in acne takes place by increasing the production of several pro-inflammatory chemical signals (such as IL-1α, IL-8, TNF-α, and LTB4); IL-1α is known to be essential to comedone formation, especially IL-1α [51, 52].

Fig. 3: Steps in pathogenesis 

 P. acnes has ability to bind TLR-2 and TLR-4, resulted in the activation of later and followed by release of various inflammatory signals in form of increased secretion of IL-8, TNF-α, and IL-1α. This ultimately cause inflammation. Parallel to this sebaceous gland cells also produce more antimicrobial peptides, such as HBD1 and HBD2, in response to binding of TLR2 and TLR4 [51].

Fig. 4: Steps in pathogenesis 

Additional capability of P. acnes to aggravate skin inflammation is by the alteration of sebum's fatty composition, mainly squalene, which in turn activates NF-κB and consequently increases IL-1α levels [34]. Moreover, squalene oxidation also cause raise in activity of the 5-lipoxygenase enzyme responsible for conversion of arachidonic acid to leukotriene B4 (LTB4) [51]. LTB4 promotes skin inflammation by acting on peroxisome proliferator-activated receptor alpha (PPARα) [51]. PPARα increases activity of activator protein-1 (AP-1) and NF-κB, thereby leading to the recruitment of inflammatory T-cells [51]. The inflammatory properties of P. acnes can be further explained by the bacterium's ability to convert sebum triglycerides to pro-inflammatory free fatty acids via secretion of the enzyme lipase. These free fatty acids spur production of cathelicidin, HBD1, and HBD2, thus leading to further inflammation [51].

6.      Prevention & Treatment

Isotretinoin, arguably the most effective acne treatment, normalizes ductal hyperproliferation, greatly diminishes sebum production and sebocyte terminal differentiation, and manifests decreased numbers of P acnes organisms. 

There is no ideal treatment for acne, although a suitable regimen for reducing lesions can be found for most patients. Good quality evidence on comparative effectiveness of common topical and systemic acne therapies is scarce.

Topical therapies including benzoyl peroxide, retinoids, and antibiotics when used in combination usually improve control of mild to moderate acne.

Treatment of acne depends upon multiple lines, cleaning of skin pores, based on reduction of bacterial loads (antibiotics), reduction in inflammation (anti-inflammatory effects); hormonal manipulation, which includes, α-hydroxy acid, (anti-androgen medications), antiseborrheic medications, (azelaic acid, benzoyl peroxide), hormonal treatments (keratolytic soaps, nicotinamide, retinoids, and salicylic acid) [52]. Commonly used medical treatments include topical therapies such as antibiotics, benzoyl peroxide, and retinoids, and systemic therapies including antibiotics, hormonal agents, and oral retinoids [53, 54].

Top 10 acne treatment cream available in market (consumption wise) and their claimed mode of action: (for details please visit the site)

a.       Himalaya Acne-N-Pimple Cream: 

b.       Jovees Anti Acne & Pimple Cream:

c.       Shahnaz Hussain Sha Derm:

d.       Garnier Skin Naturals Pure Pimple Control Pen: 

e.       Biotique Chlorophyll Oil Free Anti Acne Gel Ecopack:

f.        Avene Diacneal Treatment Care for Acne Prone Skin: 

g.       Lotus Herbals Acne Gel Tea Tree Anti-Pimple & Acne Gel: 

h.       Clearasil

i.        Shahnaz Husain Shaclear – Anti Pimple Lotion: 

j.         Shahnaz Husain Shaclove – Cream for Pimples:

        7.      Author’s Recommendation

There are some facts which should be considered before planning of treatment:

Worry about acne should be in accordance with its severity. Don’t be panic as it will not be going to be a cancer. As stress affects immune response adversely, and disease is manifested in terms of inflammation, thus stress should be reduced.

Fig 5: stress & pimples (a.b, c & d)

Overload on liver should be avoided as it is site for synthesis for acute phage proteins, which is responsible for first line of nonspecific immune response. Though there are much clinical data to support the fact but certainly can’t be ruled out. Take fibrous diet, Assure all required micro-nutrients and take some natural source of anti-oxidents +Vit B5

Fig 6: liver & acne (e, f, g)

Under normal circumstances, the pH of skin is on acidic side in order protect from infection, thus any fruits or apple cider vinegar, can be apply superficially. Moreover, vitamin C has a vital role to play in any infection, thus its routine use in feed should be assured. 

Try to keep skin pores open by application of stem or cleansing agents, as the P acne is anaerobic bacterium. Excess of oils on skins should be remove by using appropriate soaps. Antibacterial and anti-inflammatory creams can be applied superficially. However, a researcher has claimed that the effect of hormonal factors in this disease entity becomes secondary to that of the availability of pantothenic acid. A complete cure of this condition is effected by a very liberal replacement therapy with the vitamin [55].