Causes of acne
Acne is an inflammatory condition of the skin oil glands. Oil glands (also called sebaceous glands) are primarily located on the face, chest, back, and upper arms. The thick, oily material secreted by the oil glands is called sebum. During puberty, hormonal changes can stimulate sebum secretion by the oil glands and also cause their enlargement. As a person approaches adolescence, the oil glands are often further activated. Acne and its associated problems of self-esteem and social inhibition affect up to 80% of adolescents and young adults (Russell 2000). Adults in their 40s are also affected by acne and rosacea. The causes of acne are unknown, and there is still much to be learned about the factors that influence its development. Topical treatment is usually sufficient for most persons with acne. However, systemic treatment is often required for deep acne with nodules and cysts.
The first part of this protocol discusses the various conventional therapies that are used by dermatologists or sold as over-the-counter preparations in pharmacies. The second part deals with natural approaches. You will note that some alternative treatments contradict what mainstream medicine believes.
Types of Acne
The manifestation of acne varies in severity:
- Open comedones (blackheads), dilated follicles with central, dark, solid plugs.
- Closed comedones (whiteheads), inflammatory changes of small follicular papules with or without red papules.
- Nodules (pus deep in the dermis).
- Superficial pustules (pus at follicular openings).
- Cysts (nodules that fail to discharge to the surface of the skin).
- Large deep pustules (nodules that break down, leading to scars).
Usually, acne is diagnosed by the patient. However, a physician will determine if the condition is noninflammatory (open or closed comedones), inflammatory (nodules, pustules, or cysts), or a combination of both (the most common occurrence) and recommend treatment (Russell 2000).
CAUSES AND MANIFESTATIONS OF ACNE
Acne or acne-like lesions can occur in response to a variety of compounds: corticosteroids, halogens, isonicotinic acid, diphenylhydantoin, and some psychotropics. Exposure to various industrial pollutants such as oils, coal tar derivatives, tobacco smoke, and chlorinated hydrocarbons are also possible causes of acne. Other factors that can exacerbate acne include cosmetics, facial creams, overwashing and overly aggressive scrubbing, and repetitive touching or scratching. Generally, however, acne is not caused by poor skin hygiene or by eating chocolate and pizza or by drinking soda. The link to emotional stress is less certain. It may be that it is the acne that is causing emotional stress. In some women, acne worsens before menstruation (Russell 2000).
In acne, plugged oil glands are visible as black (open comedones) or white (closed comedones) dots at the skin surface. The black appearance is caused by the presence of oxygen on the skin oil, not by dirt. When the oil builds up, the swollen gland often appears as a white blemish called a whitehead (closed comedone). The primary problem is that the oil gland openings become plugged by a build-up of oil and skin cells in the tiny orifices that are supposed to conduct oil to the surface. As the irritation increases, red spots are produced that appear as acne blemishes. It is a false notion that acne is infectious. Acne cannot be transmitted to others, and it is not an allergy. While acne itself is not an infection, the combination of the oil from the sebaceous glands (sebum) and desquamated cells provide an excellent environment for the growth of Propionibacterium acnes, the principal organism in inflammatory acne (Russell 2000). (Desquamation is a normal process in which the top layer of the skin comes off or sheds in tiny flakes.) Bacteria can invade the blemishes, causing the oil to be altered and giving rise to an infectious irritation (inflammation) of the wall of the oil gland. Eventually the gland breaks open below the skin.
Acne in young people tends to manifest as small red blemishes (papules), pus-filled yellowish blemishes (pustules), larger hard blemishes (nodules), and sometimes cystic lesions under the skin. Cysts are the most difficult of all acne conditions and pose the greatest threat of scarring. The cysts rupture and are walled off by the skin. A primary reason for treating acne is to prevent scarring.
As the redness due to facial acne blemishes improves, the red blemishes turn a light purplish color as healing begins. Most blemishes will fade with time, perhaps with little scarring or discoloration. Generic or over-the-counter products may be effective in treating less severe acne conditions. However, generic medications can produce unpredictable and inconsistent results, particularly if an infectious condition exists. Therefore, for more severe acne, professional medical treatment that includes prescription drugs and instructions about suitable cosmetics (moisturizers, foundation, and blush) is often required (see the section on Acne Treatments). Avoid the sun. Sun exposure can actually make acne worse and also can cause skin cancer later in life.
Rosacea (also called acne rosacea) is a rash that is often confused with conventional acne. It is a long-term condition seen in adults. The cause is unknown, but it is linked to widened blood vessels in the nose, forehead, and cheeks. Rosacea occurs most frequently in women who have a fair complexion and who are over 30. Symptoms include a swollen red nose, puffy cheeks, and a persistent red blush on other parts of the face. Oral antibiotics such as tetracycline are effective in the treatment. Topical antibiotics such as metronidazole gel are also helpful.
Sex, Hormones, and Acne
Sexual activity has absolutely no connection with the development or remission of acne lesions. However, some women do experience a flare-up of acne symptoms from a few days to as much as a week before the onset of their menstrual periods. This flare-up can often be handled adequately by adjusting the acne treatment regimen, including increasing the dosage of the medicines already being used at that time.
Androgens are male sex hormones. Acne is considered to be an androgen-dependent condition. Therefore, androgen excess, either systemic or local, has been associated with more severe forms of the disease. Androgens control sebaceous gland secretion and exacerbate the development of abnormal follicular epithelium (Takayasu et al. 1980; Pochi 1982; Schiavone et al. 1983).
The endocrine glands, such as the thyroid, adrenal, and pituitary glands, secrete hormones directly into the blood or lymph. Endocrine disorders producing excess androgens are important etiological factors in the onset of acne. These include idiopathic adrenal androgen excess, partial defect in 21-hydroxylase, and polycystic ovarian syndrome. Free testosterone, dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S), and low sex hormone binding globulin (SHBG) levels have all been implicated. The skin of acne patients shows a greater activity of 5-alpha-reductase–the enzyme converting testosterone to the more potent androgen, dihydrotestosterone. This increased activity is independent of systemic levels of androgens and may explain the poor correlation between systemic levels of androgens and the severity of the acne lesions. If a drug test reveals high levels of dihydrotestosterone, ask your doctor for the drug, Propecia. Take one tablet a day.
Stress, Cortisol, and Acne
Although the relationship between emotional stress and acne is debatable (Russell 2000), cortisol–the body’s primary stress hormone–does have several negative side effects, such as increased glucose production, immunosuppression, and neuron damage. Cortisol has been implicated in female adult acne; cortisol is also responsible for most age-related damage to the skin. Cortisol is synthesized using coenzyme A, so an increased demand for cortisol forces the body to slow its fatty acid metabolism, due to the limited supply of pantothenic acid. Reduced fatty acid metabolism leads to acne breakouts (Leung 1997).
Pantothenic Acid Deficiency
Pantothenic acid (vitamin B5) is used to form coenzyme A, one of the most important enzymes in the body. Coenzyme A is vital in both fatty acid metabolism and in the formation of sex hormones. Therefore, Leung (1997) suggested that a dietary deficiency of pantothenic acid could be the main cause of acne. When there is a plentiful supply of pantothenic acid, both of these processes can be carried out, but when the person’s diet does not supply enough panthothenic acid, the body has to adjust accordingly. Fatty acid metabolism may be reduced, causing a sebum buildup in the pores and leading to an acne outbreak. Taking pantothenic acid supplements or applying a topical cream has been shown to quickly and completely clear up acne (Leung 1995; 1997) (refer to the section on Vitamin B5 for additional information on supplementation with pantothenic acid).
As noted earlier, cosmetics such as make-up foundation and rouge may actually block oil glands, exacerbating existing lesions and causing new ones. Night creams and moisturizers can also obstruct oil glands and exacerbate acne. Although the causal relationship between cosmetics and acne may be overstated, hypoallergenic, oil-free, water-based, noncomedogenic foundations, moisturizers, and powder rouges are better products for use on the skin. Use of cosmetics should be minimized. Hair products with oil and suntan lotions can also worsen acne (Russell 2000).
Western medicine no longer considers acne to be a food-related condition. Therefore, physicians seldom ask patients to change their diets as a means of reducing or stopping the outbreaks of acne. We should point out, however, that inflammation has been shown to play a role in acne. Later in this protocol, we discuss dietary changes that may help mitigate acne. Readers may want to refer to the Chronic Inflammation protocol to learn what they can do to inhibit proinflammatory reactions in the body. Following an anti-inflammatory diet could theoretically reduce acne and definitely protect against a host of serious diseases (such as atherosclerosis and cancer).
Also known as:Ach; Acetyl Choline; O-Acetylcholine
Acetylcholine is a type of Neurotransmitter that is the most abundant Neurotransmitter in the Brain. Acetylcholine is also produced in the Intestines.
A Solal Protocol toincrease the level of acetylcholine
Acetyl-l-carnitine - One capsule in the morning
Taurine - One capsule twice a day
Pregnenolone - One tablet in the morning after breakfast
PS - Phosphatidylserine - One capsule in the morning
Multi-B - Two capsules daily
Ginkgo Biloba - One capsule in the morning
Biological Functions of Acetylcholine
Nerve Fibres that release Acetylcholine are described as Cholinergic.
1. Digestive System
Acetylcholine is produced in the Intestines where its function is to enhance the process of peristalsis, thereby helping to prevent Constipation.
It has been hypothesized that Acetylcholine malfunction (especially in its relationship with Nicotinic Receptors) may be an underlying cause of Chronic Fatigue Syndrome (CFS). The rationale is that Acetylcholine malfunction in the Peripheral Nervous System may account for the physical (muscle) Fatigue experienced by CFS patients and that Acetylcholine malfunction in the Central Nervous System may account for the mental Fatigue experienced by CFS patients. Insufficient release of Acetylcholine at the Neuromuscular Junction is an underlying cause of many cases of (muscular) Fatigue.
3. Musculoskeletal System
Acetylcholine is responsible for stimulating Muscles to “move”:
Neuromuscular Junctions at the end of Motor Nerves conduct the release of Acetylcholine from the Axons of Motor Nerves to their target Muscle Fibres and via this process Acetylcholine facilitates the “movement” of Muscles.
Acetylcholine ensures that Mucous Membranes remain lubricated and moist.
Acetylcholine is required for optimal Muscle Tone.
Acetylcholine increases Alertness, Attentions span, controls the Parasympathetic Nervous System (a component of the Autonomic Nervous System) and is widely distributed within the Brain.
Deficiency is implicated in Alzheimer’s Disease.
Acetylcholine improves Concentration ability, Coordination., decreases Dementia and a deficiency is implicated in Depression.
Optimal Acetylcholine levels enhance various aspects of Intelligence and is involved in Learning.
Acetylcholine relays the Nerve Impulses that are involved in Memory and Acetylcholine deficiency has been implicated in Memory loss.
Acetylcholine increases Motivation as well as helps to maintain Sleep.It controls the amount of sensory input that reaches the Brain during Sleep and increases the stimulus barrier (increasing the threshold of sensory inputs before waking occurs) during Sleep.Optimal Acetylcholine allows sleepers to remain asleep through minor noises and other disturbances.Light sleepers are likely to have sub-optimal Acetylcholine:
- Acetylcholine appears to govern Rapid Eye Movement (REM) Sleep.
5. Sexual System
Decreased Sexual Desire in persons aged 40 and over is partly due to low Acetylcholine levels
Acetylcholine is involved in some aspects of Sexual Performance:
- In males, Acetylcholine plays a role in the Corpus Cavernosum of the Penis for the attainment of erections.
Acetylcholine Enhances the Function of these Substances
Acetylcholine stimulates the activity of Nitric Oxide Synthase.
Acetylcholine stimulates the production of Nitric Oxide (by stimulating the activation of Nitric Oxide Synthase).
Acetylcholine is a precursor for the release of Vasopressin.
These Substances Enhance the Function of Acetylcholine
Acetyl-L-Carnitine (ALC) facilitates the synthesis and release of Acetylcholine.
- ALC’s ability to increase the synthesis of Acetylcholine occurs as a result of it “donating” its Acetyl group towards the production of Acetylcholine.
- ALC also mimics the function of Acetylcholine.
- ALS increases Choline Acetylase levels.
Taurine increases Acetylcholine levels in the Hippocampus.
Dehydroepiandrosterone (DHEA) (after its conversion to DHEAS) enhances the release of Acetylcholine from the Hippocampus.
Pregnenolone increases the release of Acetylcholine in the Hippocampus.
Krebs cycle Chemicals
Acetyl Coenzyme A is involved in the endogenous synthesis of Acetylcholine.
Phosphatidylserine facilitates the production and release of Acetylcholine within the Cerebral Cortex and reverses the decline in Acetylcholine release that occurs in tandem with the progression of the Aging Process.
Dimethylaminoethanol (DMAE) increases Acetylcholine levels within the Brain:
- DMAE inhibits the metabolism of Choline in peripheral tissues (permitting “free” Choline to enter the Brain and stimulate the production of Acetylcholine).
Pyroglutamate stimulates the release of Acetylcholine in the Brain (this is believed to occur as a secondary effect from Pyroglutamate stimulating the release of Gamma Aminobutyric Acid (GABA) in the Brain).
Vitamin B1 facilitates the synthesis and presynaptic release of Acetylcholine.
Vitamin B5 is an essential catalyst for the conversion of Choline, Dimethylaminoethanol (DMAE) or Phosphatidylcholine to Acetylcholine.
Vitamin B12 facilitates the production of Acetylcholine.
SOLAL “MULTI B COMPLEX” FOR A COMBINATION OF ALL THE B GROUP VITAMINS
Ginkgo biloba increases the responsiveness to and number of receptors for Acetylcholine (i.e. Muscarinic Receptors) within the Brain.Ginkgo biloba stimulates the uptake of Acetylcholine into the Hippocampus of the Brain.
Last Updated (Friday, 15 April 2011 14:55)