Quote from Dr. Garrett Smith on November 23, 2018, 12:52 pm

This site is amazing, extremely evidence-based:  The Tanning Blog - How to use UV-exposure for Vitamin D , aka www.thetanningguru.com/

"It seems like daily exposure to sun, even in the north American winter (mostly UVA sun exposure), should decrease skin vitamin A. This in turn should increase the body RBP and push out more vitamin A from the liver and fat. There is a strong emphasis of getting enough UVB on the skin for vitamin D production, but it seems like UVA is helpful too since it will help deplete vitamin A on the skin.

Retinoids and UV exposure

1. Chronic UV exposure (study compared baseline and 3 and 6 months in psoriasis patients) seems to increase serum vitamin A levels; maybe because of the increased RBP and the body wanting to rid vitamin A from liver and fat stores
2. In mice: At the skin retinoids absorb light in the UV wavelength range and degrade.
3. In mice: UVA and UVB deplete dermal skin stores of vitamin A.
4. In mice: UVA temporarily increases RBP at 8h and 24h. An initial dip of RBP at 2h is probably because the body thinks there is less vitamin A since the UVA destroys vitamin A and then starts ramping up RBP once the fat and liver stores push out more vitamin A
5. Topical retinoids increased RBP production.

Photodecomposition and Phototoxicity of Natural Retinoids

Thermal and Photo Stability

It has been shown that RP is much less stable under photoirradiation conditions than is retinol (6). The results shown in Figure 3 confirm that RP (1% in oil-in-water cream) photodecomposed faster than ROH [retinol] under differing doses of UVA radiation. Boehnlein et al. (9) reported that after RP was topically applied in acetone to human skin, about 18% of RP penetrated the skin in 30 hrs. In addition, approximately 44% of the absorbed RP formed are highly dependent on experimental conditions including vehicle, retinoid concentration, dosage and wavelength of the light, photoirradiation time, and the presence of other agents or impurities that can interfere with the photochemical reactions.

The above shows that light can break down Poison/"Vitamin A" in the skin.  As you will read below, this is mostly for worse:

Perspective

Regarding human toxicity, the long-term consequences of using cosmetics containing RP are currently unknown. It has been demonstrated that photoirradiation of RP can result in forming toxic photodecomposition products, generate ROS, induce lipid peroxidation, and cause DNA damage. Also, topically applied RP produces many of the cutaneous changes associated with the use of drug products containing RA which in some instances can enhance photocarcinogenesis. Thus, a study of the photocarcinogenesis of RP, under conditions relevant to the use of RP in cosmetics, is timely and important. As a consequence, RP has recently been nominated by the U.S. FDA and selected by the National Toxicology Program (NTP) as a high priority compound for phototoxicity and photocarcinogenicity studies. The goal of these studies is to provide relevant information necessary for risk assessment of RP in cosmetic creams.

I want you to understand what it says above.  Basically, retinyl palmitate applied to the skin, then applying sunlight to it, would do the following:

• Form toxic breakdown/decomposition products
• Generate reactive oxygen species (ROS), one type of free radicals, which are "a type of unstable molecule that contains oxygen and that easily reacts with other molecules in a cell. A build up of reactive oxygen species in cells may cause damage to DNA, RNA, and proteins, and may cause cell death."
• Induce lipid peroxidation, which is "the process in which free radicals "steal" electrons from the lipids in cell membranes, resulting in cell damage."
• Cause DNA damage
• Produces many changes associated with skin cancer.

What you should be asking yourself, is how could this EVER have been approved to be used in ANY skin product, EVER?!?!  Then, you should go read my other post on how sun allergy and sun poisoning are signs of Poison/"Vitamin A" toxicity (and major detox/dumping into the system).  Humans store Poison/"Vitamin A" in the skin and subcutaneous tissues, so whether it is applied topically, or being stored there from within, it's going to have nasty things happen when the UV light hits it based on the above research.

Photodecomposition and Phototoxicity of Natural Retinoids

Retinoids absorb light in the UVA range (315-400 nm) and thus would be photoexcited by light containing UVA. For instance, RP (retinyl palmitate) has a maximum UV-visible absorption at 326 nm (3) and thus, may be able to absorb UVA light and act as a photosensitizer.

https://search.proquest.com/openview/bac06ba61d772caf24199f71603fbe0e/1?pq-origsite=gscholar&cbl=30729

Topical delivery of retinoids counteracts the UVB-induced epidermal vitamin A depletion in hairless mouse

possible: RBP doesn’t protect ROL from UVB induced depletion.

https://www.karger.com/Article/Abstract/18279

Retinol and Retinyl Ester Epidermal Pools Are Not Identically Sensitive to UVB Irradiation and Anti-Oxidant Protective Effect

Results: A single UVB dose induced a rapid, dose-dependent decrease in both ROL and RE in the epidermis of hairless mice, with partial replenishment after 24 h. The dose-response curve for ROL showed a high sensitivity to UV at doses not exceeding 200 mJ/cm², followed by a plateau, whereas RE underwent a continuous dose-dependent decrease at UVB doses up to 1 J/cm²

https://www.sciencedirect.com/science/article/pii/S037851730700854X

UVA is the major contributor to the photodegradation of tretinoin and isotretinoin: Implications for development of improved pharmaceutical formulations

https://repositorio-aberto.up.pt/bitstream/10216/74426/2/31212.pdf

Narrowband ultraviolet B treatment for psoriasis increases serum vitamin A levels

see page 97.

Vitamin A (retinol) is obtained from diet, stored mainly in liver and adipose tissue and released ‘on demand’. It is primarily transported bound to the adipokine, serum retinol-binding protein-4 (RBP4).1,2 The skin contains retinolmetabolizing enzymes and stores significant amounts of retinol as retinyl esters (RE).2,3

RE account for 85–90% of total epidermal vitamin A. Most are depleted by a single exposure to UVB,4 and are rapidly replaced by retinol uptake from dermal blood vessels.3–5 It was reported that the activity of the enzyme that esterifies retinol in epidermis increased to 167% at 2 days after UVB irradiation, suggesting a rapid influx of unesterified retinol.7 We showed that NB-UVB significantly and persistently increased serum retinol levels while clearing psoriasis."

This site is amazing, extremely evidence-based:  The Tanning Blog - How to use UV-exposure for Vitamin D , aka http://www.thetanningguru.com/

"It seems like daily exposure to sun, even in the north American winter (mostly UVA sun exposure), should decrease skin vitamin A. This in turn should increase the body RBP and push out more vitamin A from the liver and fat. There is a strong emphasis of getting enough UVB on the skin for vitamin D production, but it seems like UVA is helpful too since it will help deplete vitamin A on the skin.

Retinoids and UV exposure

1. Chronic UV exposure (study compared baseline and 3 and 6 months in psoriasis patients) seems to increase serum vitamin A levels; maybe because of the increased RBP and the body wanting to rid vitamin A from liver and fat stores
2. In mice: At the skin retinoids absorb light in the UV wavelength range and degrade.
3. In mice: UVA and UVB deplete dermal skin stores of vitamin A.
4. In mice: UVA temporarily increases RBP at 8h and 24h. An initial dip of RBP at 2h is probably because the body thinks there is less vitamin A since the UVA destroys vitamin A and then starts ramping up RBP once the fat and liver stores push out more vitamin A
5. Topical retinoids increased RBP production.

Thermal and Photo Stability

It has been shown that RP is much less stable under photoirradiation conditions than is retinol (6). The results shown in Figure 3 confirm that RP (1% in oil-in-water cream) photodecomposed faster than ROH [retinol] under differing doses of UVA radiation. Boehnlein et al. (9) reported that after RP was topically applied in acetone to human skin, about 18% of RP penetrated the skin in 30 hrs. In addition, approximately 44% of the absorbed RP formed are highly dependent on experimental conditions including vehicle, retinoid concentration, dosage and wavelength of the light, photoirradiation time, and the presence of other agents or impurities that can interfere with the photochemical reactions.

The above shows that light can break down Poison/"Vitamin A" in the skin.  As you will read below, this is mostly for worse:

Perspective

Regarding human toxicity, the long-term consequences of using cosmetics containing RP are currently unknown. It has been demonstrated that photoirradiation of RP can result in forming toxic photodecomposition products, generate ROS, induce lipid peroxidation, and cause DNA damage. Also, topically applied RP produces many of the cutaneous changes associated with the use of drug products containing RA which in some instances can enhance photocarcinogenesis. Thus, a study of the photocarcinogenesis of RP, under conditions relevant to the use of RP in cosmetics, is timely and important. As a consequence, RP has recently been nominated by the U.S. FDA and selected by the National Toxicology Program (NTP) as a high priority compound for phototoxicity and photocarcinogenicity studies. The goal of these studies is to provide relevant information necessary for risk assessment of RP in cosmetic creams.

I want you to understand what it says above.  Basically, retinyl palmitate applied to the skin, then applying sunlight to it, would do the following:

• Form toxic breakdown/decomposition products
• Generate reactive oxygen species (ROS), one type of free radicals, which are "a type of unstable molecule that contains oxygen and that easily reacts with other molecules in a cell. A build up of reactive oxygen species in cells may cause damage to DNA, RNA, and proteins, and may cause cell death."
• Induce lipid peroxidation, which is "the process in which free radicals "steal" electrons from the lipids in cell membranes, resulting in cell damage."
• Cause DNA damage
• Produces many changes associated with skin cancer.

What you should be asking yourself, is how could this EVER have been approved to be used in ANY skin product, EVER?!?!  Then, you should go read my other post on how sun allergy and sun poisoning are signs of Poison/"Vitamin A" toxicity (and major detox/dumping into the system).  Humans store Poison/"Vitamin A" in the skin and subcutaneous tissues, so whether it is applied topically, or being stored there from within, it's going to have nasty things happen when the UV light hits it based on the above research.

Photodecomposition and Phototoxicity of Natural Retinoids

Retinoids absorb light in the UVA range (315-400 nm) and thus would be photoexcited by light containing UVA. For instance, RP (retinyl palmitate) has a maximum UV-visible absorption at 326 nm (3) and thus, may be able to absorb UVA light and act as a photosensitizer.