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You want your skin to look good and be healthy.
But many highly-advertised products do damage skin.

 

For years, liquid silicone was injected into women's faces and their breasts. In time, the silicone ended up running down the body, often leading to serious infections.

Then bovine collagen (supposedly non-immunogenic) started to be used as a facial filler. But also in time, the individual's immune system would recognize the foreign material and turn it into hard, ball-like tissues.

NOTE: It is important to remember that it may take years for the immune system start manifesting problems with a particular compound.

On a similar list of problem ingredients is hyaluronic acid.

 

Hyaluronic acid (scientifically named "hyaluronan") is a sugar-like molecule that can bind huge amounts of water (1000-fold its own weight).

When applied to the surface of human skin, it feels smooth and sensuous but will slowly wet the skin's outer protective proteins and damage the skin barrier. This can temporarily improve the look of your skin but does not help skin health. The outer layer of skin (what we actually see) is composed of keratinocytes. The signal that causes the skin to send new keratinocytes to the surface is the dryness of the outer layers. Hydrating (wetting) the outer proteins slows, or even stops, the normal flow of keratinocytes to the surface. If the skin is constantly kept wet, such as by using hyaluronan, skin renewal is slowed and skin ends up looking older.

Skin-damaging cosmetic moisturizers are designed to push water into the skin and wet the outer skin proteins in order to puff it up. Various detergents (although they may not be called "detergents" in the ingredient list) along with water-holding molecules (such as hyaluronic acid) are often used to loosen outer skin proteins so water can interact with them. But this weakens the skin barrier and lets in viruses, bacteria, and allergens. This also means that the skin is replaced at a slower rate and damage remains longer.

The best example of this is the "cold creams" that women applied in the 1930s and 1940s. You may have even seen these in old movies. The skin was kept moist, but many of these women ended up with horrible wrinkles.

Around 1997, studies in Denmark found that oil/water skin moisturizers broke down the skin barrier. The concern was that this could increase infection in hospital patients.


Various polymers of hyaluronan are now used as skin injectable skin fillers. The injectable form of hyaluronic acid is advertised as "not-from-animals", but what they don't tell you is that the source is pathogenic bacteria. The FDA warns that the material contains small amounts of bacterial protein and this can produce allergic responses in time.


Hyaluronic acid in tissues speeds the spread of cancer cells.

Anti-cancer therapies are now being developed to lower hyaluronic acid in tissue in order to stop cancer growth.

Go to: www.ncbi.nlm.nih.gov/pubmed/ and type in "hyaluronic acid cancer" - You'll get 3,484 references as of June 11, 2018. Or type in "hyaluronic acid cancer metastasis", and you will get 332 references. Here's an example of what you'll find:

Fragments of hyaluronan "teach" cancer cells to evade the immune system and grow better. J Immunol. 2008 Sep 1;181(5):3089-98.

Tumor-educated tolerogenic dendritic cells induce CD3epsilon down-regulation and apoptosis of T cells through oxygen-dependent pathways.

Kuang DM, Zhao Q, Xu J, Yun JP, Wu C, Zheng L. State Key Laboratory of Biocontrol, Sun Yat-Sen University, Guangzhou, People's Republic of China.

Defects in the CD3/TCR complex and impairment of T cell function are necessary for tumor evasion, but the underlying mechanisms are incompletely understood. We found that culture supernatants from several types of solid tumor cell lines drove human monocytes to become tolerogenic semimature dendritic cells (TDCs). Upon encountering T cells, the TDCs triggered rapid down-regulation of CD3epsilon and TCR-alpha/beta and subsequent apoptosis in autologous T cells. Consistent with these results, accumulation of immunosuppressive DCs coincided with CD3epsilon down-regulation and T cell deletion in cancer nests of human tumors. The impaired T cell function was mediated by factor(s) released by live TDCs after direct interaction with lymphocytes. Also, the TDC-induced effect on T cells was markedly reduced by blocking of NADPH oxidase but not by inhibition of arginase, inducible NO synthase (iNOS), IDO, or IFN-gamma.

Moreover, we found that hyaluronan fragments constituted a common factor produced by a variety of human tumor cell lines to induce formation of TDCs.

These observations indicate that tumor microenvironments, including hyaluronan fragments derived from cancer cells, educate DCs to adopt a semimature phenotype, which in turn aids tumor immune escape by causing defects in the CD3/TCR complex and deletion of T cells.
2011;6(7):e22836. Epub 2011 Jul 28.


Upregulation of HYAL1 expression in breast cancer promoted tumor cell proliferation, migration, invasion and angiogenesis.
Tan JX, Wang XY, Su XL, Li HY, Shi Y, Wang L, Ren GS.

Department of Endocrine and Breast Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.


ABSTRACT:
Hyaluronic acid (HA) is a component of the Extra-cellular matrix (ECM), it is closely correlated with tumor cell growth, proliferation, metastasis and angiogenesis, etc. Hyaluronidase (HAase) is a HA-degrading endoglycosidase, levels of HAase are elevated in many cancers. Hyaluronidase-1 (HYAL1) is the major tumor-derived HAase.

We previously demonstrated that HYAL1 were overexpression in human breast cancer. Breast cancer cells with higher HAase expression, exhibited significantly higher invasion ability through matrigel than those cells with lower HAase expression, and knockdown of HYAL1 expression in breast cancer cells resulted in decreased cell growth, adhesion, invasion and angiogenesis. Here, to further elucidate the function of HYAL1 in breast cancer, we investigated the consequences of forcing HYAL1 expression in breast cancer cells by transfection of expression plasmid.

Compared with control, HYAL1 up-regulated cells showed increased the HAase activity, and reduced the expression of HA in vitro. Meantime, upregulation of HYAL1 promoted the cell growth, migration, invasion and angiogenesis in vitro. Moreover, in nude mice model, forcing HYAL1 expression induced breast cancer cell xenograft tumor growth and angiogenesis. Interestingly, the HA expression was upregulated by forcing HYAL1 expression in vivo. These findings suggested that HYAL1-HA system is correlated with the malignant behavior of breast cancer.

 


Cosmetic Cigarettes Stop Wasting Your Money


Do you know what is in your cosmetic products? You could be purchasing cosmetic cigarettes without your knowledge!

Cosmetic Cigarettes - What Is In Your Cosmetics?There are many so-called "scientifically-proven" cosmeceuticals that emphasize use of foreign compounds or "new ingredients" designed to "renew genes", "repair DNA", or employ "new technology that reverses cell aging".

However, similar to the hundreds of foreign agents in cigarettes, these "revolutionary products" containing "new" artificial compounds that your body has no background of being able to assimilate, the danger lies in what these ingredients are actually doing over the long term in your body.


Request a free online skincare consultation (or call 1-800-405-1912) to be directed to anti-aging cosmetics from Skin Biology that are healthy, effective, safe for long-term use.