page is under construction
http://www.sunsaferx.com
$1/pill
Notes
Combination of antioxidents, each of which have been independently proven to reduce skin aging and tanning.
Probably start with 2 pills a day for a week or so then 1 pill a day.
After about 2 months it appears to build up to having a Sunscreen Protection Factor (SPF) of about 4
They have sold 1,000’s of bottles in the US and Asia since 2010
They believe that even tiny amount of sun causes damage.
Vitamin D Life suspects that
- There is a threshold affect - that UV damage accumulation only occur above a threshold intensity
- The presence of Vitamin D can reduce the damage to the skin by UV
(as with many other health problems, Vitamin D prevents skin damage far better than it treats skin damage)
Available on US Amazon and their website – where they ship internationally.
Testamonials include people who had been “allergic” to the sun being able to be out in the sunscreen
Website includes lots of studies on each of the ingredients.
Anti-oxidents also shown to reduce macular degeneration
Vitamin D Life is Unaware of any other company which has so many anti-oxidents proven to reduce skin damage – at the amount included in the pill
See also PubMed on skin aging and UV
- Reactive molecule species and antioxidative mechanisms in normal skin and skin aging 2014
- Ultraviolet radiation, aging and the skin: prevention of damage by topical cAMP manipulation PDF is at bottom of this page
- The role of antioxidants in skin cancer prevention and treatment PDF is at bottom of this page
Vitamin D Life wonders if anti-oxidents protect against all of the problems in the following study
MicroRNAs in skin response to UV radiation Sept 2013 PDF at bottom of this page
Solar ultraviolet (UV) radiation, an ubiquitous environmental carcinogen, is classified depending on the wavelength, into three regions; short-wave UVC (200-280 nm), mid-wave UVB (280-320 nm), and long-wave UVA (320- 400 nm). The human skin, constantly exposed to UV radiation, particularly the UVB and UVA components, is vulnerable to its various deleterious effects such as erythema, photoaging, immunosuppression and cancer.
To counteract these and for the maintenance of genomic integrity, cells have developed several protective mechanisms including
- DNA repair,
- cell cycle arrest and
- apoptosis.
The network of damage sensors, signal transducers, mediators, and various effector proteins is regulated through changes in gene expression. MicroRNAs (miRNAs), a group of small non-coding RNAs, act as posttranscriptional regulators through binding to complementary sequences in the 3´-untranslated region of their target genes, resulting in either translational repression or target degradation. Recent studies show that miRNAs add an additional layer of complexity to the intricately controlled cellular responses to UV radiation. This review summarizes our current knowledge of the role of miRNAs in the regulation of the human skin response upon exposure to UV radiation.
PMID: 23834148
From DNA repair to proteome protection: new molecular insights for preventing non-melanoma skin cancers and skin aging March 2014
Non-melanoma skin cancers (NMSC) are the most common human neoplasms and continue to represent an important public health issue with greater than one million cases diagnosed each year. The primary factor contributing to the molecular pathogenesis of NMSC is unprotected skin exposure to ultraviolet (UV) radiation, ie, UVA (wavelength: 315-400 nm) and UVB rays (wavelength: 280-315 nm) with additional albeit less damaging factors of infrared radiation (wavelength: ~750 nm-1 mm) and environmental pollutants. Skin carcinogenesis by DNA damage is the current predominant paradigm of UV toxicity, which may be caused by direct damaging effects of energy deposited by photons or indirect oxidative action of short-lived reactive oxygen species (ROS) formed from water that reacts with biomacromolecules. UV rays are capable to induce direct both DNA damages, mainly consisting in the formation of helix-distorting photoproducts such as cyclobutane pyrimidine dimers ( CPDs), as well as oxidative damage to DNA bases, including the formation of 8 - oxo - 7, 8-dihydro-2'-deoxyguanosine (8OHdG). Growing evidence also suggests that the efficiency of DNA repair after exposure to UV radiation is crucially dependent on the levels of oxidative protein damage, including but not limited to DNA repair proteins. Besides DNA lesions, UV-induced oxidative stress can indeed result in carbonylation of proteins, a major form of irreversible protein damage that inactivates their biological function. Interestingly, microorganisms characterized by extreme resistance to UV rays have an intrinsic capacity to protect their proteome, rather than genome, from radiation-induced damage, suggesting that protein carbonylation (PC) may serve as a reliable and innovative biomarker of UV photodamage. This review discusses the main DNA and protein markers of UV-induced damage (eg, CPDs, 8OHdG, and PC) and their relationship and importance to the current understanding of skin carcinogenesis. The identification of key DNA and protein signatures of photodamage may represent a therapeutic target for translational studies of innovative therapeutic and preventive approaches for reducing both skin aging and the morbidity and mortality associated with NMSC.
Dermal damage promoted by repeated low-level UV-A1 exposure despite tanning response in human skin.
JAMA Dermatol. 2014 Apr;150(4):401-6. doi: 10.1001/jamadermatol.2013.8417.
Wang F1, Smith NR1, Tran BA2, Kang S3, Voorhees JJ1, Fisher GJ1.
IMPORTANCE:Solar UV irradiation causes photoaging, characterized by fragmentation and reduced production of type I collagen fibrils that provide strength to skin. Exposure to UV-B irradiation (280-320 nm) causes these changes by inducing matrix metalloproteinase 1 and suppressing type I collagen synthesis. The role of UV-A irradiation (320-400 nm) in promoting similar molecular alterations is less clear yet important to consider because it is 10 to 100 times more abundant in natural sunlight than UV-B irradiation and penetrates deeper into the dermis than UV-B irradiation. Most (approximately 75%) of solar UV-A irradiation is composed of UV-A1 irradiation (340-400 nm), which is also the primary component of tanning beds.
OBJECTIVE:To evaluate the effects of low levels of UV-A1 irradiation, as might be encountered in daily life, on expression of matrix metalloproteinase 1 and type I procollagen (the precursor of type I collagen).
DESIGN, SETTING, AND PARTICIPANTS:In vivo biochemical analyses were conducted after UV-A1 irradiation of normal human skin at an academic referral center. Participants included 22 healthy individuals without skin disease.
MAIN OUTCOMES AND MEASURES:Skin pigmentation was measured by a color meter (chromometer) under the L* variable (luminescence), which ranges from 0 (black) to 100 (white). Gene expression in skin samples was assessed by real-time polymerase chain reaction.
RESULTS:Lightly pigmented human skin (L* >65) was exposed up to 4 times (1 exposure/d) to UV-A1 irradiation at a low dose (20 J/cm2), mimicking UV-A levels from strong sun exposure lasting approximately 2 hours. A single exposure to low-dose UV-A1 irradiation darkened skin slightly and did not alter matrix metalloproteinase 1 or type I procollagen gene expression. With repeated low-dose UV-A1 irradiation, skin darkened incrementally with each exposure. Despite this darkening, 2 or more exposures to low-dose UV-A1 irradiation significantly induced matrix metalloproteinase 1 gene expression, which increased progressively with successive exposures. Repeated UV-A1 exposures did not suppress type I procollagen expression.
CONCLUSIONS AND RELEVANCE:A limited number of low-dose UV-A1 exposures, as commonly experienced in daily life, potentially promotes photoaging by affecting breakdown, rather than synthesis, of collagen. Progressive skin darkening in response to repeated low-dose UV-A1 exposures in lightly pigmented individuals does not prevent UV-A1-induced collagenolytic changes. Therefore, for optimal protection against skin damage, sunscreen formulations should filter all UV wavelengths, including UV-A1 irradiation.
PMID: 24305962
Protective effects of citrus and rosemary extracts on UV-induced damage in skin cell model and human volunteers, July 2014
Journal of Photochemistry and Photobiology B: Biology
Volume 136, 5 July 2014, Pages 12–18
A. Pérez-Sáncheza, 1, E. Barrajón-Catalána, 1, N. Caturlab, J. Castilloc, e, O. Benavente-Garcíac, e, M. Alcarazd, e, V. Micola, ,
Highlights
• UV radiation is the major cause of skin disorders such as photoaging and melanoma.
• Oral consumption of photoprotective plant compounds may contribute to skin health.
• Citrus and rosemary compounds protect synergistically skin cells from UV radiation.
• Oral ingestion of the combination reduces MED upon UV radiation in human volunteers.
Ultraviolet radiation absorbed by the epidermis is the major cause of various cutaneous disorders, including photoaging and skin cancers. Although topical sunscreens may offer proper skin protection, dietary plant compounds may significantly contribute to lifelong protection of skin health, especially when unconsciously sun UV exposed. A combination of rosemary and citrus bioflavonoids extracts was used to inhibit UV harmful effects on human HaCaT keratinocytes and in human volunteers after oral intake. Survival of HaCaT cells after UVB radiation was higher in treatments using the combination of extracts than in those performed with individual extracts, indicating potential synergic effects. The combination of extracts also decreased UVB-induced intracellular radical oxygen species (ROS) and prevented DNA damage in HaCaT cells by comet assay and decreased chromosomal aberrations in X-irradiated human lymphocytes. The oral daily consumption of 250 mg of the combination by human volunteers revealed a significant minimal erythema dose (MED) increase after eight weeks (34%, p < 0.05). Stronger protection was achieved after 12 weeks (56%, p < 0.01). The combination of citrus flavonoids and rosemary polyphenols and diterpenes may be considered as an ingredient for oral photoprotection. Their mechanism of action may deserve further attention.
Note: Sunscreen in a pill has Vitamin C, not Cirtus
I think that the function may be non-linear.
That is: The UVB photons received at high intensity contribute much more to skin ageing than the low intensity photons.
Over a millions years of evolution seems to have provided a way for most bodies and even cellular creatures to quickly deal with UVB damage - even in the era when the UVB was 10X stronger.
I notice, for example, that small scale DNA skin damage in corrected in < 1 nanosecond.
In the extreme non-linearity implies: Far less likely to have skin ageing (skin cancer, DNA damage, etc) if that portion of skin had never burned.
- Mechanisms of Photoaging and Chronological Skin Aging 2002
This article reviews our current understanding and presents new data about the molecular pathways that mediate skin damage by UV irradiation and by the passage of time. - PATHOPHYSIOLOGY OF PREMATURE SKIN AGING INDUCED BY ULTRAVIOLET LIGHT PDF, not web page
- Mechanisms of Skin Aging PDF not web page, OXIDATIVE STRESS
- UV Photodamage of DNA UV Photodamage of DNA See page 35 of PDF
- Understanding Inflammation: The Root Cause of Skin Aging April 2014
Acute inflammation from: burns; overexposure to UV rays; stress; toxins, such as pollution and smoking; trauma; alcohol; immune reactions; and infection by pathogens and foreign bodies