A
concerned consumer wrote (my bolding & italics):
I would like to know why you decided to include artificial
ingredients like paraffin in your cosmetics.
Paraffin is developed out of oil. You can pollute
soil and water with this, needing only very little. How does it
work in our skin? Why don´t you
regard it as dangerous there? Why didn´t
you use plant oils like other companies
do?
Please tell me about your aims
when developing your cosmetic line. What was your purpose?
Why do you think your products are superior
to others? Why are they unique? Would
you regard them as totally harmless? When
yes, why?
For me, cosmetics should be "skin
food", you should be able to eat
them, and this should not endanger your
health. We "eat"
anyway through our skin, we don´t
only eliminate through it. And therefore, only the
best is good enough. I am just testing
skin oil produced by a competitor that you are asked to put in your
salad as well. This sounds great for me! Your products,
you are not supposed to eat, because this might be harmful.
Please explain this to me, thanks! For me, it´s a contradiction,
when your aim is to produce natural skin
products totally harmless and beneficial.
The Director, Stuart Thomson responds as follows:
Fair questions, I would have, indeed had asked these same
questions 15 years ago at the height of my environmental activism
(when I started and chaired a regional branch of Earthlife Africa).
My main evolving research interest at the time was botanical pesticides,
ie evolutionary defensive natural chemicals in plants to control
their pests (since I was growing most of my own food at the time).
I was (and remain) committed to natural alternatives and being a
herb farmer at that time, I decided it was safest for me to make
my own agronomic, household and personal care products. It was out
of this activity that my product range arose and grew spontaneously
with no intention other than to meet my own needs and eventually
also as a means of funding my research institute.
Concurrently, my toxicology interests were shifting from a decade
of studying toxic synthetics to the even more fascinating study
of the natural defensive toxicants intrinsic to foods and other
plants themselves, an important and fascinating field that even
today few researchers have adequately explored, a rather odd state
of affairs, considering that natural substances are at least as
toxic and as widely used as synthetics. As a result of this rather
fortuitous research direction, I found myself studying comparative
toxicology, and eventually, having discarded the shackles of philosophical
prejudice, unusally straight unbiased toxicology. On re-evaluating
my crude plant oil/herb/vitamin-based natural home-made products, I was shocked
at their hidden toxic nature. You should be too.
Your overall comments appear to bear testimony to your being
locked an artificial, yet widely held man-made is toxic and nature
is begin dichotomy. As romantic as this widely held notion might
be, it simply cannot be reconciled in accordance with the facts.
If you think about it for just a moment, even restricting yourself
to the plant kingdom, you will have to admit that at least half
of it is toxic to humans, whether ingested or applied topically,
at concentrations that commonly occur in nature. “But”, you
might reply, “with ‘natural’ product selection, we have identified
and rejected the worst toxins, so man-made chemicals are far more
toxic than natural chemicals”. Partially correct, but only up
to a point, since human discernment falls short on both sides, natural
and manmade.
When the Soviets chose a poison to eliminate dissidents in the West,
they did not concoct a deadly man-made toxin, but used the castor
bean (Ricinus communis) to extract Ricin, a super-toxin,
so richly concentrated in the seed, which toxin is lethal in quantities
measured in just a few hundred millionths of a gram (size of a grain
of salt) (New Scientist, 16 July 1987). Ricin has also been
considered, indeed prepared as a biological warfare agent
(D Sifton and G Kelly, Eds, Biological
Agents, in PDR Guide to Biological and Chemical Warfare Response,
Physicians' Desk Reference, Thomson, NJ, 2002).
Carefully ‘processed’ by humans however, castor oil
has high utility and quality and can be safely used as a very effective
cathartic, purgative, laxative, personal lubricant and skin emollient
(W color:'>Lewis and
M Elvin-Lewis, Medical Botany: Plants Affecting Man's Health, John
Wiley & Sons, NY, 1977)
Industrially the oil is used in paints, varnishes and textiles and
in the production of nylon and motor oil. The seedcake is used as
an organic fertiliser and the ricin as a chemotherapeutic anti-tumour
agent (monoclonal antibody production) (M
Windholz et al, Eds, The Merck Index: An Encyclopedia of Chemicals,
Drugs and Biologicals. Merck & Co, NJ, 1983).
Jojoba seed (Simmondsia chinensis) yields jojoba
oil, a high quality polyunsaturated liquid wax/oil (two
unsaturated bonds) that is used similarly to castor oil, as a treatment
for skin disorders, as an antifoam agent in antibiotics production
as well as for candles, plasticisers, detergents, fire retardants,
industrial lubricants and transformer oil (National Research Council, Jojoba: New Crop for
Arid Lands, New Raw Material for Industry. National Academy Press,
Washington, DC, 1985). Jojoba contains spanproteolytic and protease
inhibitory anti-physiological factors (Simmondsin) and toxic cyanogenic
glucosides and must be ‘treated’
to eliminate these toxins (Wantke
F et al, Contact Dermatitis, 34(1), 1996); (Perez-Gil F et al, Arch
Latinoam Nutr, 39(4), 1989); (Cokelaere M et al, Food Chem Toxicol,
36(1), 1998); (Shrestha M et al, J Agric Food Chem, 50(20), 2002).
'Purified' cottonseed oil
from the cotton plant (Gossypium species) is used similarly. The
relatively crude oil is widely used for cooking in developing countries.
Gossypol, a major toxin, causes pathological changes in
human testes and male sterility (L
Bernardi and L Goldblatt, in “Toxic Constituents of Plant Foodstuffs”,
I Lerner, Ed, Acad Press, NY, 1980)
and is a potent initiator and promoter of skin carcinogenesis
(Haroz R, Thomasson J, Toxicol
Lett, Suppl 6(72), 1980).
Crude unrefined oil contains up to 750mg/100ml of gossypol and its
toxic actions are due to its oxidative production of free radicals
(Coburn M et al, Biol
Bull, Woods Hole Mass, 159(468), 1980).
Clearly nature is not always benign.
She can, in fact, be as deadly as she is nurturing and useful.
Against the background of these three examples, how do you
reconcile acceptance of these ‘natural’ and ‘treated’ oils for human
usage, with your expressed concern and rejection of the use of supposedly
‘artificial’ mineral oil for similar purposes? (We use the word
paraffin in South Africa to denote illuminating oil and hence I
differentiate the food/cosmetic grade by the name ‘white mineral
oil’) At what point - after how much and what kind of processing
(and why) – do castor, jojoba, cottonseed and mineral oil change
from ‘natural’ to ‘unnatural’, and from ‘dangerous’ to ‘totally
harmless’ and ‘beneficial’? Which of the above applications are
artificial/unnatural and hence legitimate or illegitimate, according
to your ‘dangerous man-made vs safe natural’ criteria?
I will add briefly to my previous data on this subject
(see my article “Internet Health Scares”: “Natural & Synthetic
Carcinogens: A Rational Perspective Of Relative Toxicity & Risk”,
where I pointed out that naturally occurring chemicals, known to
be potent carcinogens, are routinely produced during the preparation
of food). The degree of
exposure to carcinogens, ingested unnecessarily from browned material
produced during cooking is several million orders of magnitude greater
than from topical white mineral oil preparations, the highest quantities being measured in fried/grilled meats
and other heat-baked/browned protein-rich foods (Ames B, Science, 18 May, 1984); (Coultate T, Food: The Chemistry
of It’s Components, Royal Soc Chem, Lond, 1986); (Ames B et al,
Science, 17 April 1987); (Gold L et al, Science, 9 Oct, 1992).
Please note that the illogically offensive word “paraffin”
is derived from the Latin words “parum”, meaning “not much” and
“affinis”, meaning “affinity”, in reference to its chemical un-reactivity,
rendering it the ideal oil, vastly “superior” to all contemporary
plant oils for our purpose as a deliberately inert spreading/carrier
agent and protective barrier. Bearing testimony to this property
is the fact that whereas distilled water is routinely used as a
vehicle for water soluble substances in allergic contact patch testing,
white mineral oil is similarly used as the vehicle for oil soluble
test substances, due to its reliable non-sensitising and non-irritating
properties (Kang H et al, J
Dermatol, 31(5), 2004); (Torres M et al, Allergy, 59(2), 2004).
The other equally illogically offensive word “petroleum”
is derived from the Latin words “petrus”, meaning “rock” and “oleum”,
meaning “oil”, which is why we correctly refer to it as “mineral
oil”. Being refined from crude petroleum oil (hence the term “oil
refineries”), mineral oil is not at all synthetic. Synthetic oils
are entirely manmade from various sources, including vegetable oils.
Petroleum crude oil is our planet’s richest repository of pure
organic material, sourced from natural ancient algal/plant deposits
that pre-date modern synthetic human activity and its attendant
anthropogenic toxins, in fact rendering crude oil intrinsically
purer than contemporary plant oils. White mineral oil is a highly
refined fraction thereof.
On the question of ecology, there is no intrinsic
reason why the utilisation of crude oil as a raw material resource
should be any less sound than using current crops for similar purposes.
Indeed, being several orders of magnitude more concentrated, crude
oil is a far superior option, freeing scarce arable land from having
to be planted for alternatives resources. Toxic by-products, and
in particular, emissions of aromatic hydrocarbons and related chemicals
that are harmful to humans, are no worse when the crude mineral
and plant oils are processed/combusted and compared (Zou L, Atkinson S, Environ Technol, 24(10), 2003), without even considering that the former, ironically,
is likely to be relied on to process the latter. Mineral
oil does take longer to biodegrade, but then it is either considerably
purer or more concentrated and would be expected to degrade more
slowly. Under
ideal conditions, mineral hydrocarbons are completely decomposed
to carbon dioxide and water, with some biomass production (Muratovba A, Turkovskaia O, Prikl Biokhim Mikrobiol, 37(2), 2001); (Cloesen C, Kabuya A, Physical
and chemical properties of environment friendly lubricants, Research
RW No 2174, Univ Liege); (Plohl K et al, Acta Chim Slov, 49:279, 2002).
Petroleum mineral oils are used extensively in several food industries
as machine lubricants and as food separator coatings. Due to its
self-limiting laxative effect, there are no extraordinary toxicological
problems associated with its use, only possible nutritional implications
from reduced uptake of fat-soluble vitamins
(Seventeenth Report of the Joint FAO/WHO Expert Committee on
Food Additives, World Health Org Tech Rep Ser No 539, 1974); (FAO
Nutrition Meetings Report Ser No 53, 1974). In many respects,
plant oils are likely to be inferior even in these applications.
Furthermore, all so-called “toxic oil syndromes”, eg over
2500 deaths in Spain, have been from processed crop oils, not mineral
oils (Hard G, Hum Exp Toxicol, 19(3),
2000); (Closa D et al, Lipids, 36(10), 2001); (Posada de la Paz
M, Epidemiol Rev, 23(2), 2001); (Posada de la Paz M, Environ Health
Perspect, 111(10), 2003); (Sanchez-Porro Valades P et al, J Clin
Epidemiol, 56(7), 2003).
Mineral oils are manufactured from crude oils by vacuum distillation to produce
a residual oil that is further refined. The related petroleum jelly is a purified mixture of
semi-solid, saturated hydrocarbons obtained from the residue of
distillation left in the still after all the oil has been vaporised.
Paraffin wax is a crystalline substance obtained by distillation
and purified by sweating. Similar purification principles applicable
to white oil apply to food/cosmetic grades of these items. Aromatic
compounds, including alkylated heterocyclic
and polycyclic hydrocarbons are the only seriously undesirable constituents of these
crude oil petroleum products, based on their carcinogenic potential following chronic industrial exposure to poorly refined oils. ‘White mineral’ oils/paraffins, petrolatums/petroleum
jellies and paraffin waxes produced from crude oils that have undergone
appropriate treatment, are not toxic or carcinogenic to humans (Mineral Oils, IARC Monograph,
Vol 33, 1984); (Mineral Oils, IARC Monograph, Suppl.7, 1987/1998).
Eliminating the alkylated 3-7-ring renders these various end products
totally non-carcinogenic
(Mackerer C, et al, Appl Occup Environ Hyg, 18(11), 2003).
It is remarkable that there is only one potentially
seriously harmful compound in the un-purified material, making concern
over this non-existent substance in the finished products totally
irrational. Widespread prejudice against topical application of
the appropriate food/cosmetic grade of these innocuous natural-sourced
substances is based on foolish and stubborn belief systems rather
than on reasoned facts. The reality is that any more than an assimilable
quantity of topically applied plant oil, represents the real hazard.
Emollients and moisturizing creams are used to break the dry skin cycle and to maintain
the smoothness of the skin. The term 'moisturizer' is often used
synonymously with emollient, but moisturizers often contain humectants
in order to hydrate the stratum corneum. Dryness is frequently linked
to an impaired barrier function. Mineral oil has an immediate
barrier-repairing effect in de-lipidised stratum corneum (Loden
M, Am J Clin Dermatol, 4(11), 2003) and like sebum, does
not represent a substrate for bacteria and free radical attack as
non-fossilised plant oils do. White mineral oils additionally even
possess moderate UV-A and UV-B photo-protective effects at relatively
low viscosities (Lebwohl M et al,
J Am Acad Dermatol, 32(3), 1995); (Boyvat A et al, Photodermatol
Photoimmunol Photomed, 16(4), 2000); (Fetil E et al, Eur J Dermatol,
12(2), 2002).
Mineral oil has been ignorantly criticised as ‘smothering the skin’ and isolating
it from oxygen. Under highly ‘oxidative susceptible’ conditions,
this is precisely what sebum and anti-oxidants are intended to do.
To quote an expert: “The only way to stop harmful oxidation,
is to stop the oxygen supply” (J
Loliger, Natural Antioxidants, In: J Allen and R Hamilton, Rancidity
in Foods, Applied Science Publishers, Lond, 1983). Smothering is one of the main functions of sebum,
which is invariably stripped from the skin by the artificial practice
of washing. Plant oil also smothers the skin, but unfortunately
rather than protecting it from oxygen, actually provides a chemical
substrate for the formation of the worst forms of oxygen - reactive
oxygen species, including free radicals.
This brings me to the main reason for selecting mineral
oil above all for the formulation of our spreading/carrier cream
fractions, namely the remarkably close similarity between mineral
oil and sebum and also associated, its superior resistance
to oxidation, compared with all plant oils of suitable
viscosity. Unlike the nearly fully saturated fatty acids of animal
fats that are solid at room temperature, plant fatty
acids are typically unsaturated and liquid at room temperature.
Relatively saturated plant fats/oils such as jojoba, olive or coconut
are simply too sticky to be used without the addition of highly
unsaturated oil. Even minimally unsaturated fats exposed
to skin warmth and atmospheric oxygen (21%)
will quickly become toxic. It has been well-stated that “the polyunsaturated oils from seeds
are recommended for use in paints and varnishes (significantly
better than mineral oils), but skin contact with these substances
(polyunsaturated seed oils) should be avoided” (Raymond Peat, PhD, Unsaturated Vegetable Oils: Toxic, referencing Lynch R, "Utilization
of polyunsaturated fatty acids by human diploid cells aging in vitro,"
Lipids 15(6), 1967).
Plant oil fatty acids may be saturated (single carbon bonds), mono-unsaturated (one
double carbon bond) or polyunsaturated (two or more double carbon
bonds), the degree of saturation determining the degree to which
each type resists oxidation. Highly reactive carbon fragments
arise from the breakdown of fatty acids as hydrogen splits from
carbon in the unsaturated fatty acid group. These unstable fragments
with their unpaired electrons - free radicals (superoxide
anions, hydroxyl radicals, peroxyl radicals, hydrogen peroxide,
hydroperoxides and peroxinitrite anions) - are powerful oxidisers
and serve as strong initiators and promoters of further oxidation
by extracting hydrogen from other organic, natural plant oil and
animal fat molecules to trigger a chain-reaction of reactive
oxygen species that ‘on the skin’ are not controlled by cellular anti-oxidative
enzymes. These oxidations
form reactive oxygen intermediates, which
form smaller chain organic compounds such as aldehydes, ketones,
alcohols and acids that ultimately destroy the biological
integrity of cellular essential fatty acids and damage cellular
membranes and macromolecules, in particular proteins and more critically,
microstructures such as DNA, leading to premature visible aging,
inflammatory skin disorders and skin cancers.
Lipid hydroperoxides are primary products of the
oxidation of oils and fats, including free fatty acids, triacylglycerols,
phospholipids and sterols. One type of free radical likely to be
formed on and in the skin is the fatty acid hydroperoxide,
which is formed through three different mechanisms, namely autoxidation,
photo-oxidation and enzymatic oxidation. Under mild reaction conditions,
hydroperoxides are formed through autoxidation, a free radical
chain reaction between unsaturated lipids and oxygen to form hydroperoxides,
which then undergo further reactions with or without the participation
of other compounds. The formation of hydroperoxides from unsaturated
fatty acids is accelerated by exposure to light, either by direct
photo-oxidation or by photosensitised oxidation of unsaturated fatty
acids. Photo-oxidation is the oxidation under light in the
absence of photosensitisers. Polyunsaturated
fatty acids, important components of membranes serving cells and
cellular organelles, if attacked by oxygen, can form lipid peroxyl
radicals.
Enzymatic oxidation results from hydrolytic reactions
catalysed by lipases from plant cells. Most plants contain enzymes
capable of catalysing the direct oxidation of lipids with molecular
oxygen. Crushing, macerating or pressing these tissues, as
is standard practice during the preparation of crude “natural cosmetics”,
initiates lipid-oxidising lipolysis via the enzymes lipoxygenase
and cyclooxygenase, which are widely distributed throughout the plant and animal kingdoms
and have affinity for especially free fatty acids, but also for
triglycerides and are able to catalyse co-oxidation reactions, capable
of initiating oxidation of other compounds that can interact
with oxidisable substrate such as carotenoids, chlorophyll,
vitamins C and E, thiols, proteins or other lipids.
(Spiteller G, Exp Gerontol, 36:1425, 2001) The lipid peroxidation of biomembranes, mediated by reactive oxygen
species and free radicals, is one of the major causes
of cellular damage induced by UV radiation and toxins. (Kalka K et al, Skin Pharm Appl Skin Physiol 13:143, 2000)
Lipid hydroperoxides are, enzymatic oxidation end products that are extremely
unstable in the presence of transition metal ions or vitamin
C, breaking down to alkoxy free radicals that decompose
to form cytotoxic and genotoxic oxidation products - aldehydes,
polymers, alcohols and hydrocarbons capable of substantially
damaging cell membranes and DNA and initiating
mutagenesis and carcinogenesis (R Hamilton, The Chemistry of Rancidity in Foods, In:
Allen J and R Hamilton, Rancidity in Foods, Applied Science Publishers,
Lond, 1983); (Erasmus U, Fats that Heal…Fats that Kill: The Complete
Guide to Fats, Oils, Cholesterol and Human Health, Alive Books,
BC Canada, 1993); (Burcham P, Mutagenesis,
13:287, 1998); (Marnett
L, Carcinogenesis, 21:361, 2000);
(Hwa Lee S et al, Science, 192,
15 June, 2001). (Bhasin G
et al, Cancer Lett, 183(2), 2002); (Udilova N et al, Food Chem Toxicol,
41(11), 2003).
Photosensitised oxidation of lipids is an important
pathway for the formation of hydroperoxides from unsaturated
fatty acids, with hydroperoxides being formed in the presence
of oxygen, light energy and a photosensitiser. Vegetable oils
may contain natural photosensitisers such as chlorophyll that yields
singlet oxygen and free radicals in the presence of visible light
and can severely oxidize lipids, producing several cytotoxins in
oils and fats that may harm the skin (Frankel E, Prog Lipid Res, 19:1, 1980); (Fakourelis N et
al, J Food Sci, 52:234, 1987); (Lee E, Min D, J Food Sci, 53(6),
1988); (Frankel E, Lipid Oxidation, The Oily Press Ltd, Dundee,
1998). Even a trace of chlorophyll
can catalyse the destructive processes (Krinsky N, Pure
Appl Chem, 51:649,1979); (Krinsky N, Free
Rad Biol Med, 7:617, 1989); (Bradley
D, Min D, Crit Rev Food Sci Nutr, 31:211, 1992), even after bleaching (Gunstone F, J Am Oil Chem Soc, 61:441, 1984).
One of the most important characteristics
of chlorophyll is the absorption of visible light
between 400-500 nm and 600-700nm. Singlet oxygen and free radicals
generated from triplet oxygen by such light excited photosensitisers play important roles in the formation of toxic volatile compounds
in organic materials, with eg total yield in lard with 5 ppm chlorophyll
added under natural light for 48 hours being 19 times greater than
without chlorophyll (Lee J-H, Photo-oxidation and Photosensitized Oxidation of Linoleic
Acid, Milk, and Lard, Dissertation, Ohio State Univ, 2002); (Lee
J, Min D, Photoxidation and Chlorophyll Photosensitized Oxidation
of the Volatile Compound Formation from Lard. IFT, Chicago, 2003). Given that this experiment used a mere 5ppm of chlorophyll added to lard, one of the most saturated
fats, one can appreciate the magnitude of the problem with eg fresh olive oil, containing up to 10 ppm chlorophyll and
which is considerably less saturated than most oils routinely constituting
the bulk of the majority of so-called natural products.
Phyto-pro-oxidants are produced naturally
in plants. Photosensitisation
results from absorption of light energy and formation of toxic oxyradicals
that disrupt living systems by reacting with proteins, nucleic acids,
lipids and other biomolecules critical to cell function.
Excited state sensitisers can even interact with biomolecules
directly, causing damage without the need for oxygen. Over
200 furanocoumarins (including psoralens,
thiophenes, polyacetylenes, citral, quinoline alkaloids, isoquinoline
alkaloids, beta-carbolene alkaloids, benzophenanthrene alkaloids
and hydroxycinnamic acid derivatives) have been identified in
natural plant sources. In the presence
of light, these compounds form excited states that can react directly
with and damage DNA as well as crosslink. (Berenbaum
M, in: Oxidative Stress and Anti-oxidant Defences in Biology, Ahmed
S, ed, Chapman & Hall, NY, 1995)
Such damage can also arise from similar reactions with unsaturated
lipids (Specht
K et al, Photochem Photobiol, 47:537, 1988).
Additionally, furanocoumarins are capable of interacting
with oxygen to produce singlet oxygen, superoxide anion radicals
and hydroxyl radicals (Larson
R, Marley K, In: Oxidants in the Environment, Environ Sci Tech,
J Nriagu and M Simmons, Eds, John Wiley & Sons, NY, 1994).
Organic compounds possessing photosensitisers cannot be detoxified
in plant oils that themselves contain or in which such sensitisers
have dissolved, where such oils remain on the skin, unable to be
absorbed due to excess and hence are unable to be detoxified by
the body’s mechanisms. Plant food photosensitisers include,
but are certainly not limited to the following: angelica,
anise, buckwheat, carrots, celery, citrus fruit (esp limes), dill,
fennel, fig, parsley, parsnip. Plant food contact
allergens include: allspice, artichokes, bay (laurel),
cardamon, cayenne pepper, chicory, cinnamon, cloves, garlic, horseradish,
lettuce, mango, nutmeg, pineapple, onion, potato, radish, rocket,
thyme, tumeric, vanilla. (Marzulli F, Maibach H, J Soc Cosmet Chem, 21:695, 1970); (Magnus
A, Dermatological Photobiology, Blackwell Scientific Publications,
Oxf, 1976); (A Rook et al, Eds, Textbook of Dermatology, Blackwell
Sci Publ, 1988); (Pathak M, Clin Dermatol, 4:102, 1990); (J Guin,
Ed, Practical Contact Dermatitis, McGraw-Hill, NY, 1995); (I Kocheva,
In: Photoimmunology, J Krutmann, C Elmets, Blackwell Science, Oxf,
1995) Skin foods?
Protein oxidation is an important area of gerontological and oncological concern
that is disproportionately overshadowed by lipid oxidation (Vladimirov I et al, Biofizika, 11(2), 1966); (Vladimirov I et
al, Biofizika, 15(2), 1970); (Vladimirov Y et al, Photochem Photobiol,
11(4), 1970); (Roshchupkin D et al, Biofizika, 18(1), 1973); (Starke-Reed
P, Oliver C, Arch Biochem Biophys, 275(2), 1989); (Stadtman E, Science,
28:257, 1992); (Grune T, Biogerontol, 1(1), 2000); (Friguet B, et
al, Ann N Y Acad Sci, 908:143, 2000); (Merker K, Grune T, Exp Gerontol,
35(6-7), 2000); (Grune T et al, The Journals of Gerontology
Series A: Biological Sciences and Medical Sciences, 56:B459-B467
(2001); (Stolzing A, Grune T, Clin Exp Dermatol, 26(7), 2001); (Rogers
K et al, Free Radic Biol Med, 32(8), 2002); (Shringarpure R, Davies
K, Free Radic Biol Med, 32(11), 2002); (Wondrak G, J Investig
Dermatol, 121(3), 2003); (Poppek D, Grune T, Gerontol Geriatr,
37(3), 2004). Mineral oil, being a hydrocarbon,
has no penetrative affinity for proteins (Rele
A, Mohile R, J Cosmet Sci, 54(2), 2003) and
cannot oxidise and transfer reactive oxygen species to cells
like plant oils.
Pro-oxidants are
the opposit of antioxidants and since many anti-oxidants can paradoxically
function as pro-oxidants under varying conditions, exogenous
anti-oxidants applied topically cannot be relied upon to quench
the destructive oxidative chain reactions accompanying lipid oxidation.
In particular many anti-oxidant vitamins
[and even anti-oxidative enzymes (Morliere P, Santus R, Eur J Biochem, 256,
184, 1998); (Heck D et al,
J Biol Chem, 278(25), 2003)] can function as pro-oxidants, especially under extracellular conditions
(eg on the skin) (Rice-Evans
C, The Role of Antioxidants in Biological Systems, In: Advances
in Applied Lipid Research, JAI Press, 1996); (Frankel E, Lipid Oxidation, The Oily Press Ltd, Dundee, 1998). Clearly, the more plant oils are applied
to the skin, the more reactive oxygen species are generated and
the greater is the degree of oxyradical dermal cell, collagen and
elastin damage, especially since exogenous lipids lack the benefit
of cellular anti-oxidative enzyme controlled oxidation protection.
Vitamin C in
excess of normal cellular concentrations can act as a
pro-oxidant, capable of inducing free radical damage,
including cell death, nuclear fragmentation
and internucleosomal DNA cleavage, mainly in the presence of even traces of iron (a ubiquitous pollutant, especially
in urban air and hence constantly depositing on exposed skin) or
alcohol (produced during the breakdown of plant
oils and found in very high concentrations in some cosmetics as
a ‘natural preservative’ and itself also a recognised carcinogen)
(Yamamoto K et al, Chem Lett, 1149, 1987); (Laudicina D, Marnett L, Arch Biochem Biophys, 278:73,1990); (Stadtman E, Am J Clin Nutr, 1125S, 1991); (Trommer
H et al, Pharm Res, 19(7), 2002); (Kaneko T et al, Arch Biochem Biophysics, 304(1), 1993);
(Porter W, Toxicol Ind Health, 9:93,1993); (Frankel E et al, J Agric Food
Chem,42:1054, 1994); (Frankel E, Lipid Tech, 7:77, 1995); (Buettner G, Jurkiewicz B, Radiat Res 145:532, 1996);
(Almass R et al, Eur J Pediat, 156(6), 1997); (Podmore I et
al, Nature, 392(6676), 1998); (Carr A, Frei B, FASEB J, 13(9), 1999);
(Paolini
M et al, Life Sci, 64(23), 1999);
(B Halliwel, J Gutteridge, Free
Radicals in Biology and Medicine, Oxford University Press, NY, 2000);
(Lee S, Science, 292(5524), 2001); (Fisher A, Med Hypotheses, 61(5-6),
2003).
Vitamin E in excess of normal cellular concentrations
makes lipoproteins more reactive towards radical oxidants and oxidative
conditions eg exposure to light and this can result in pro-oxidant
activity (Jung M, Min D, J Food Sci 55:
1464, 1990); (Kagan V et
al, Free Radic Res Commun, 16(1), 1992); (Bowry V et al, Biochem
J, 288:341, 1992); (Neuzil J et al, Free Rad Biol Med, 22(1-2),
1997); (Walke M et al, Photochem Photobiol, 68(4), 1998); (Podmore I et al, Nature, 392(6676), 1998); (Upston J et al, FASEB J, 13(9),
1999). When topical vitamin E was evaluated in cultured human normal fibroblasts exposed
to natural ultraviolet A radiation, pre-treatment of cells
with all topical forms of vitamin E resulted in an increased
susceptibility to cytotoxic photo-induction of DNA single-strand
breaks and longer persistence of damage, and hence increased mutagenic/carcinogenic
risk (Nocentini S et al, J Photochem Photobiol, 73(4), 2001).
Beta-carotene (& other carotenoids eg lycopene) in excess of normal cellular concentrations, especially
with other antioxidants and UV, acts as a pro-oxidant,
via formation and decomposition of lipid hydroperoxides,
increasing production of
reactive oxygen species and toxins, promoting
cellular and tissue damage and exacerbating pre-existing skin cancers (Terao J et al, J Food Process
Preserv, 4:79,1980); (Faria J, Mukai M, J Am Oil Chem Soc 60:77, 1983);
(Burton G, Ingold K, Science, 244:569, 1984); (Warner
K, Frankel E, J Am Oil Chem Soc, 64:213, 1987); ( Suzuki T et al, J Jph Oil
Chem Soc, 38: 486, 1989)(; (Kigoshi M, Niki E, In: K Yagi et al,
Eds, Oxygen Radicals, Elsevier
Science Publ, Amsterdam, 1992); (Palozza
P et al, Free Rad Biol Med, 19:887, 1995); (Palozza P et al, Free Radic
Biol Med, 22(6), 1997); (Zhang P, Omaye S, Toxicol, 146(1), 2000); (Obermüller-Jevic
U et al, FEBS Lett, 509(2), 2001); (Zhang P, Omaye S, Toxicol Vitro,
15(1), 2001); (Palozza P et al, Free Radic Biol Med, 30(9), 2001).
Selenium in excess
of normal cellular levels is also capable of pro-oxidant cytotoxicity
(especially to DNA) and this action results from the
pro-oxidant catalytic activity of the selenide anions, including
reaction with thiols, such as glutathione (which can also
act as a pro-oxidant), producing oxidative-stress inducing super
oxide anions, hydrogen peroxide and other reactive oxygen species,
especially when intracellular methylation reactions and antioxidant
defenses are exceeded (Xu H et
al, Huzahong Longong Daxue Xuebar, 19:13, 1991); (Chaudiere J et
al, Arch Biochem. Biophys, 296:328, 1992); (Spallholz J, Free Radic Biol Med, 17(1), 1994); (Ursini F, In: Oxidative Processes
and Antioxidants, R Paoletti, Ed, Raven Press, NY, 1994); (Spallholz
J, Biomed Environ Sci, 10(2-3), 1997); (Wirth T, Molecules, 3:164, 1998); (Shen C et al, Proc Am Assoc Cancer Res, 40:360, 1999);
(Barceloux D, Clin Toxicol, 37:145,1999); (Stewart M et al, Free
Radic Biol Med, 26:42, 1999); (Shen H, Free Radic Biol Med, 28(7),
2000); (Shen C et al, Cancer Epidemiol Biomarkers Prev, 10(4), 2001); (Shen H et al, Free Radic Biol Med, 28(7), 2000); (Chen W, Biochem J, 370(Pt 3), 2003); (Wycherly B et al, Nutr
Cancer, 48(1), 2004).
Confirming my own pioneering concerns regarding the
problems of plant oil lipid peroxidation and in particular, the
associated anti-oxidant pro-oxidation, recent clinical and experimental
data confirms that supplementation of the complex and ‘intricately
balanced natural antioxidant defence system’ with anti-oxidants
demands due caution (Young
A, Lowe G, Arch Biochem Biophys, 385(1), 2001); (Bondet V et al, J Am Oil Chem Soc, 77:813,
2000); (Black H, Front Biosci,
7:d1044, 2002) The
old adage “prevention is better than cure” must surely apply here
regarding the application to the skin of anything but traces of
fixed plant oils (as opposed to volatile, eg essential oils, which
are not unsaturated, do not oxidise and being volatile, progressively
evaporate relatively quickly, quickly reducing their risk and are
therefore safer than fixed oils) which clearly represent unacceptable
oxidation rates and oxyradical risks. Not only do oxyradicals and
their products damage and age the skin and underlying tissues, they
far more seriously represent considerable carcinogenic risk. (a
phenomenon so well accepted that I am not even going to reference
it)
The phenomenon of oxidised lipids causing cancer remains pertinent.
A considerable number of lipid hydroperoxides, endoperoxides, enals,
epoxides and aldehydes produced from the oxidation of unsaturated
oils and saturated fats, even during refrigeration, have been shown
to be mutagens and carcinogens
(making concern over one carcinogen already removed from mineral
oil absurd) (M Simic and M Karel,
Eds, Autoxidation in Food and Biological Systems, Plenum, NY, 1980);
(Petrakis N et al, Cancer Res, 41:2563, 1981); (Levin D et al, Proc
Natl Acad Sci, USA, 79:7445, 1982); (Bird R et al, Mutat Res, 101:237,
1982); (W Pryor, Ed, Free Radicals in Biology, Academic Press, NY,
1982); (Cambell M, Fantel A, Life Sci, 32:2641, 1983); (Ames B,
Science, 224, 18 May, 1984); (Marnett L et al, Mutat Res, 148:25,
1985); (International Agency for Research on Cancer, IARC Monograph
on Evaluation of the Carcinogenic Risk of Chemicals to Humans, Vol,
39, IARC, Lyon Fr, 1985); (Ames B et al, Science 236, 17 April,
1987).
Besides lipid peroxidation, many atoms
in the organic molecules of biological systems can become free radicals,
including sulphur, carbon, halogens, nitrogen and phosphorus (Gulumian M, Spec Med, April 1994). Even the pro-oxidant production of reactive oxygen species by eg sterols, (exogenously & endogenously)
can be significant in the cell damaging and tumour promoting
action of UV-A light on skin (Albro P et al, Photochem Photobiol, 66(3), 1997); (Lasch J et al,
Biochim Biophys Acta, 1349(2), 1997). For the sake of brevity, I have limited discussion to lipids and oxygen.
Not only do the use of antioxidants carry risk of pro-oxidative
damage; they also carry specific risks of tumour promotion. Vitamin E acts as a tumour promoter at high concentrations.
Vitamin C at high concentrations further amplifies the promoting
effect of high concentrations of tocopherols. The process whereby tumour promotion by vitamin E
occurs is simply as a result of alpha-tocopherol acting as a free
radical scavenger, with the formation and transfer of the alpha-tocopherol
free radical center to the surrounding lipids, resulting in lipid
oxidations (Mitchel R, McCann R, Cancer Detect Prev, 27(2), 2003), clearly a vicious circle and not rendering vitamin
E as a viable solution to lipid oxidation and carcinogenesis.
There is of course, considerable research attesting to the
protective and other beneficial effects of the main paradoxical
pro-oxidant antioxidants, but these are unfortunately always tests
on animals or laboratory tests of substances in isolation from a
full complement of the ingredients in a topical product formula.
Human testing for carcinogenesis is of course unethical (as is that
or any experiments on animals), yet animal and human trials, as
with drugs, would be the only way to establish the risk versus benefit
profile to consumers, which is simply unaffordable for cosmetics.
It is clearly impossible to anti-oxidise plant oils
over and above the proportion of these that are assimilable and
hence relatively quickly isolated from unlimited oxygen, chemicals
and light, in the skin, within the first 15 minutes or so following
application. After approximately 15 minutes, fatty acid degradation
and chain reaction oxidation begins to build exponentially in a
chain reaction of destructive hyperoxidation and the production
of ever-increasing toxins, first on the skin and shortly thereafter,
within the skin and eventually the underlying tissues and the circulation
in the body itself. Gaia’s creams are formulated in such a way as
to ensure that the bio-active components in the formula will be
fully assimilated within the critical first 15 minutes, after which,
given the heat radiating from the body, solar heat, ambient warmth
and the 21% atmospheric oxygen, any unsaturated vegetable lipid
molecules, other botanical and organic components and nutrients,
including anti-oxidants, become actively involved in reactive
oxygen processes as pro-oxidants, free radical initiators, donors,
substrates, catalysts, promoters and synergists of oxidative damage,
a situation which our selection of inert
spreading/carrier agents is specifically designed to avert.
Manufacturers of
products using plant oils in the formulation of their base cream
are hard pressed to stabilise and preserve these lipids even in
the cool and oxygen limiting jar/tube/bottle, let alone the several
hours that such products will remain in contact with the skin and
air. Why do you think the world's major houses use mineral
oils, if they could use unsaturated plant oils instead? Personally, I
doubt that manufacturers using mineral oil in the formulation of
their spreading/carrier agents were particularly mindful of plant
oil-caused reactive oxygen species posing pro-aging and skin cancer
risks to consumers, as much as they had commercial concerns over
rancidity and spoilage. Most manufacturers still add significant
or token amounts of plant oils out of ignorance or as marketing
hype, so the mere use of mineral oil is not a guarantee that the
product is not toxic or will not become toxic on the skin. Gaia
Research uses plant oils and antioxidants in its topical products,
but only as cell-targeted actives, not in base spreading/carrier
components, where cream formulations are used. These actives and
all other ingredients are formulated in an informed and calculated
minimalist, yet optimising approach, based on abovementioned considerations,
ensuring that Gaia’s products are earth, people and animal friendly,
by dedicated intention and design.
From the perspective
of the possibility of the use of inappropriate grades of mineral
oil and other cosmetic ingredients, avoiding cheap products or moderately-priced
products with big advertising campaigns and avoiding products not
having prominent company profiles and ready accountable accessibility,
can go a long way to protecting consumers, but does not provide
the science-based certainty attendant to requesting and evaluating
progressive research documents such as this and applying the challenging
concepts therein to products under consideration. It can confidently
be stated that the order of potential toxicity of ingredients in
Gaia products are from highest to lowest risk as follows: fixed
plant oils, anti-oxidative vitamins, volatile essential oils, herbal/yeast
extracts, other plant-based speciality ingredients (cleansers),
other nutrients and co-factors, petroleum inerts and benzoate preservatives.
I am no more of an apologist for the existence or abuse of manmade
petroleum-based products than for the existence of toxic plants
or for mankind’s abuse thereof.
The
notion of cosmetics being “skin-foods” and also “capable
of being eaten to be harmless”, is certainly romantic, but nevertheless
silly, if not actually deleterious, as attested to above. I could
have no objection to macerating fruit and or vegetable salads with
a salad oil dressing in a food processor and applying this as a
masque for a short period, away from the sun and strong light. Trying
to preserve even a fraction of this in a container, be it a bottle,
jar or even ampule, would be futile, let alone actually stopping
it from decomposing on and otherwise harming the skin. The skin
in no way approximates the digestive tract in terms of the absence
of light or relative absence of oxygen and in the absence of digestive
secretions is clearly unable to process nutrients. The skin
can absorb small molecules, but like the digestive system, is not
selective regarding beneficial and harmful substances, the digestive
tract at least having the liver to filter and neutralise some toxins.
Assimilated skin toxins bypass the liver, potentially causing significant
toxicity and immunological ramifications. Several foods contain toxicants, including antivitamins
(to eg A, B6, D, E, K); enzyme inhibitors (to eg cholinesterase,
glucose-6-phosphate dehydrogenase); physiological disorganisers
and disrupters (eg hemagglutinins, saponins, lathrogens, nitrates,
oxalates, phytates, cyanogenic glycosides, irritants, allergens,
photosensitisers); hormonal disrupters (eg estrogens); antimetabolites
(especially amino acids, eg canavanine); numerous alkaloids
(eg solanine); numerous mycotoxins (eg aflatoxins), as well
as numerous other toxins produced by plants, mainly as defensive
chemicals (allelochemicals) against predators and competitors (Yamaguchi M, World Vegetables, AVI Publ, 1983); (M Rechgcigl,
Ed, Handbook of Naturally Occurring Food Toxicants, CRC, 1983);
(Ames B, Science, 221:1256, 1983); (Ames B et al, Proc Natl
Acad Sci, 87:7777, 1990); (S Colegate, P Dorling, Plant-Associated
Toxins: Agricultural, Phytochemical & Ecological Aspects, CAB Intl, 1994); (J Harborne, B Baxter,
Eds, Dictionary of Plant Toxins, Wiley, 1996).
The greatest risks to the skin, for the reasons mentioned, are
oxidising or oxygen–rich products. The latter do have potential, mainly for infection control and
wound healing, in particular if based on dissolved oxygen rather
than reactive oxygen compounds. An interesting cliché is that “the
skin must breath”. Although the skin has greater similarity
to the lungs than the digestive system and oxygen is indeed taken up by the epidermis, this is exclusive
only for the uppermost layers to a depth
of between 0.25-0.40mm
that is without vasculature and is ‘almost’ exclusively supplied by atmospheric oxygen, much of
this (0.15mm), is dead and dying cells without oxygen consumption
and the remaining layers are served by blood transfer in healthy
individuals. (Stücker M et al, J.
Physiol, 538(3), 2002) Topical oxidising plant oil is a far
more inflexible barrier than mineral oil, rendering reactively toxic
all oxygen afforded opportunity to come into contact with the skin
as atmospheric oxygen dissolves in the water fraction of the cream
emulsion and migrates to the skin.
Sincerely
Stuart Thomson, Director, Gaia Research
|