Stretch Mark Therapy and Prevention

What can prevent stretch marks and what needs to be in a product for stretch mark therapy to work?

Stretch marks can be avoided by preventing an immoderate inflammation when our skin is overly stretched, and stretch mark therapy can be effective if scars in the dermis are dissolved while regaining skin’s firmness, strength, suppleness, and thickness.

As it is discussed in the first part of this section about stretch marks removal this can be achieved with the support of the biological immune serum for stretch marks, which contains molecules formed by glycans (complex sugar chains) and peptides, proteins, enzyme, coenzymes and oligoelements that support the innate immune system of the skin and contribute to both dissolve scars in the dermis and organize and regulate proliferation of all the necessary elements of healthy skin: collagen, elastin, proteoglycans and glycosaminoglycans.

What about preventing inflammation with anti-inflammatory drugs?

The answer is this is NOT feasible during pregnancy if attempted with drugs (synthetic steroids or non-steroidal anti-inflammatory drugs) but it can be done with a novel naturally occurring substance that supports the immune system of the skin locally, wherever it is applied topically.

To understand why you cannot use traditional drugs to halt the inflammatory process that leads to stretch marks, we first need to analyze what is inflammation.

Inflammation is a localized protective reaction of tissue to irritation, injury, or infection, characterized by pain, redness, swelling and sometimes loss of function.

The process of inflammation, both vascular and cellular, is orchestrated by an array of molecules produced locally.

These mediators include histamine, leukotrienes, prostaglandins, complement components, kinins, antibodies, and interleukins.

Stretch marks are associated with the release of histamines and other inflammatory mediators by mast cells that reside within the connective tissues when tissues in the area are fragile and overly stretched.

Wherever inflammation occurs there are certain local mechanisms in common, despite differences in the precipitating factors and also in the relative prominence of the four cardinal features: calor (heat), rubor (redness), tumor (swelling and dolor (pain).

They are the manifestations of the body’s defense against injury or against invasion by foreign material or microorganisms, including the means of removal or destruction of the offending agent, restriction of the spread of infection, and preparations for the healing process.

But the immune system that implements vital self-preservation may also sometimes cause inflammation by misdirected attack on some part of the body itself.

Diseases such as rheumatoid arthritis and rheumatic fever may be other examples in which an uncontrolled or misdirected inflammatory response with an autoimmune component is turned against the host. In stretch marks the trigger seems to be the tearing of skin fibers due to overstretching, which unfortunately further injures the tissues before the repair yields scars.

Tissue damage results in the release by cells of various chemical agents, including prostaglandins. Vasodilator substances relax the blood vessels in their vicinity and the resulting increase in blood flow accounts for the redness and heat; swelling follows from increased permeability of blood vessels.

This all enhances the supply of factors normally present in the blood that are important for the inflammatory response, including white blood cells and certain proteins in the plasma. Locally released substances (cytokines), as well as bacterial toxins if there is infection, attract cells of the immune system — macrophages and lymphocytes.

The phenomena of inflammation reflect an appropriate response to infection, or to mechanical damage either by acute injury or prolonged overstretching, pressure or friction. When they occur inappropriately as a reaction against the body’s own tissues the manifestations are similar. Thus conditions that might be called ‘inflammatory’ may refer to chronic infections, or to degenerative processes (as in osteoarthritis), or they may result from congenital abnormalities (as in cystic fibrosis) or autoimmune disease (such as rheumatoid arthritis or regional ileitis (Crohn’s disease)).

It would be inappropriate to attempt by treatment to diminish the body’s responses, in terms of both local and widespread effects, if and when they were entirely appropriate and necessary to contain or cure the condition.

Alleviation of the pain of inflammation by analgesic drugs is clearly beneficial to the sufferer; otherwise the first concern of treatment is if possible to remove the cause (such as treating infection by antibiotics, or removing foreign material).

Other treatments in recent decades have been directed against inflammation itself, in conditions related to injury, ‘wear-and-tear’, and auto-immunity. Many anti-inflammatory drugs that have been developed for serious illness (not for stretch marks) function by preventing the formation of the inflammatory mediators or by blocking their actions on the target cells whose behavior is modified by the mediators.

Imitation and enhancement of the body’s own anti-inflammatory corticosteroids became possible with synthetic steroid preparations, but there are too many undesirable side effects. Topical administration of corticosteroids to pregnant animals can cause abnormalities of fetal development. The relevance of this finding to human beings has not been established; however, the use of topical steroids in pregnancy should be limited because of possible teratogenic effects (can interfere with normal embryonic development or cause malformations to the fetus).

Along with the understanding of the role of prostaglandins in the mediation of inflammation and fever, a whole family of ‘non-steroidal anti-inflammatory drugs’ (NSAIDS) were developed, and they are widely used for a variety of muscle and joint problems, from accidental sprains to widespread arthritis. These drugs inhibit enzymes necessary for formation of prostaglandins, thus diminishing their local and general effects. (aspirin was well known to be useful in this context long before it was known to act by this mechanism).

No evidence has emerged for any positive or negative effect on the progress of the underlying conditions themselves (as opposed to relief of the symptoms), supporting the notion that the body’s inflammatory responses are not always useful. Symptoms may indeed be relieved, but there are side-effects of NSAIDS and they can not be used during pregnancy.

Non-steroidal anti-inflammatory drugs, when given during the latter part of pregnancy, may cause closure of the fetal ductus arteriosus, fetal renal impairment, inhibition of platelet aggregation, and delay labor and birth. Continuous treatment with non-steroidal anti-inflammatory drugs during the last trimester of pregnancy should only be given on sound indications. During the last few days before expected birth, agents with an inhibitory effect on prostaglandin synthesis should be avoided. (See what the Department of Health & Aging of the Australian Government, Therapeutic Goods Administration – safeguarding public health & safety in Australia by regulating medicines, medical devices, blood & tissues; says about this topic in: prescribing medicines in pregnancy). NSAIDS also cause gastrointestinal complications related to the inhibition of prostaglandin synthesis where and when it is normally needed.

Discouraging The Over-Zealous Immune System Response That Attacks Healthy Tissue

Products for scar removal containing a naturally occurring serum that supports the immune system and is created by a mollusk Crystomphalus Aspersa (also known as Helix Aspersa Müller) with soft tissues very similar to human skin tissues can help to prevent and cure stretch marks and get rid of cellulite.

We offer two creams for the prevention and/or treatment of stretch marks.