Acne Treatment Program

Acne vulgaris is a chronic inflammatory disorder of the pilosebaceous unit characterized by the formation of comedones (blackheads and whiteheads) and inflammatory lesions (papules, pustules, nodules, and cysts). The development of acne is a complex process involving several key factors: 

1. Excess Sebum Production: Androgens, primarily testosterone, stimulate sebaceous glands to produce sebum (oil). In acne-prone individuals, there's often an overproduction of sebum, creating a favorable environment for bacterial growth. 
2. Follicular Hyperkeratinization:  Abnormal shedding of skin cells within the hair follicle leads to blockage and the formation of comedones. The accumulation of sebum within the follicle further contributes to the comedonal plug. 
3. Cutibacterium acnes (C. acnes) Proliferation: This anaerobic bacterium colonizes the pilosebaceous unit. In the presence of excess sebum, C. acnes proliferates, breaking down sebum triglycerides into pro-inflammatory fatty acids. 
4. Inflammation: The release of fatty acids, along with bacterial factors, triggers an inflammatory response. This leads to the formation of inflammatory lesions and the recruitment of immune cells, perpetuating the cycle. 

• Genetics: A family history of acne increases susceptibility due to variations in sebum production, follicular keratinization, and inflammatory responses.
• Hormones: Hormonal fluctuations, such as those during puberty or menstruation, can exacerbate acne by increasing sebum production.
• Medications: Certain drugs, including corticosteroids and androgens, can induce or worsen acne.  
• Diet: Emerging evidence suggests a link between high glycemic load diets and dairy consumption with acne severity.
• Stress: Stress can indirectly worsen acne through its effects on hormone levels and immune function.