Editorial Note:

The following article, adapted directly from a reply of mine to a letter from a well-known health author in Germany, Barbara Simonsohn, who questioned my sanity for formulating natural cosmetics using mineral oil, remains unchanged except for the introduction and abstract of her letter. Barbara was initially very hostile in encountering the list of ingredients on one of my product labels in Europe and took my German client to task for what she, with her limited knowledge, but strong conviction, considered to be sacrilege and worthy of speaking out about.

An updating of my research notes on the subject resulted in the creation of this document, arguably the most extensive and only treatise of its kind ever undertaken on this subject. As a result of this effort, Barbara Simonsohn withdrew her objections and undertook to research the European market with a view to warning consumers about the dangers hidden attendant to so-called natural cosmetics utilising plant oils as carrier formulation oils, based on my free-radical inducing research and exposé over the indiscriminate use of such oils and several other synergistic cellular toxicants classified as “natural”.


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.


Stuart Thomson, Director, Gaia Research

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