In Part 1 we reviewed the research into diet and the various ways in which ones diet can impact on one’s health and the development of diseases such as psoriasis and arthritis.

Part 2 will concentrate on certain foods that can have a positive impact on one’s health and assist in the repair/healing processes.

It is known that throughout life, environmental conditions and dietary compounds influence gene expression. Only recently it has been observed that exposure to specific phytochemicals can affect gene expression via reversible epigenetic mechanisms and gets recorded in our “epigenome” through life. Epigenetics refers to heritable phenotypical differences or changes in gene expression that are not attributable to changes in DNA sequence, but rather depend on variations in DNA methylation, chromatin structure or microRNA profiles. As such, our dietary epigenetic imprint superposed on our genome may rewire gene expression patterns in the body and the host immune system, and protect against inflammatory disorders, cancer and ageing. 1

It has also been found that the metabolism of nutrients may vary person to person and ultimately result in different health status depending on the genotype of an individual. Nutrigenomic trends towards individualizing/personalizing foods (both to avoid and to consume) and nutritional supplementation, that leads to individual strategies to not only maintain good health but, more importantly, to assist in repair processes.

Phytochemicals/ phytonutrients/ phytonutriceuticals are organic compounds derived from plants that have health protective effects. Besides the common nutrients such as carbohydrates, amino acids and protein, there are certain non- nutrient phytochemicals in vegetables that have biological activity against chronic diseases. They are low in fat and like all plant products, contain no cholesterol. Most phytochemicals are found in relatively small quantities in vegetable crops. However, when consumed in sufficient quantities, phytochemicals contribute significantly towards protecting living cells against chronic diseases. 2

Cruciferous vegetables are vegetables of the family Brassicaceae (also called Cruciferae) which includes vegetable, such as kale, red and white cabbage, broccoli, brussels sprouts, cauliflower, turnip, Chinese cabbage and pak choi. This group of vegetables contains well-known antioxidants, such as vitamins C, E, carotenoids and antioxidant enzymes such as catalase, superoxide dismutase (SOD) and peroxidase, which are found in fresh vegetables. these vegetables are also rich in beneficial plant’s metabolites, which include sulfur containing glucosinolates, anthocyanins, flavonoids, terpenes, S-methylcysteine sulfoxide, coumarins and other minor compounds.4,5 Studies have also identified many compounds that have been isolated from Brassica vegetables and the pharmacological studies in vitro or in vivo have shown that they have a large spectrum of biological activities, including antiinflammatory, antibacterial, antifungal, antitumor, antimutagenic, neuroprotective and antioxidative properties. 4,5

The health potential of Brassica vegetables are partially attributed to their intricate fusion of phytochemicals and their antioxidant activity. Recently, considerable research has been aimed at the detection of plant derived natural antioxidants which can be utilized for human consumption for prevention of non-transmissible chronic diseases and promotion of health. Phytochemicals from Brassica vegetables may act on different and complementary levels. They prevent oxidative stress, induce detoxification enzymes and stimulate the immune system. Reactive oxygen species (ROS) in the body can cause lipid and protein oxidation, DNA damage, base modification and modulation of gene expression. 4,5

Antioxidants counteract, or neutralize, the harmful effects of free radicals. These antioxidants act as scavengers for these tree radicals and reactive oxygen species, thereby preventing them from disrupting the chemical stability of the cells. A variety of external factors such as inflammation, cigarette smoke, air pollutants, radiation (X-rays and ultra-violet rays) can promote free radical formation in our body. Consequently, individuals exposed to these sources of oxidants would require a greater supply of dietary antioxidants. 2 Skin is a major target of oxidative stress due to reactive oxygen species (ROS). Antioxidants attenuate the damaging effects of ROS and can impair and/or reverse many of the events that contribute to excessive growth and reproduction of skin cells. Increased ROS production in patients of psoriasis and decreased concentration of antioxidants leads to oxidative stress, which indicates lipid peroxidation. This may lead to cell damage by continuous chain reactions damaging the cell membranes and tissues. 3 Imbalance between ROS and antioxidants causes oxidative stress. Oxidative stress may be caused by antioxidant deficiency in the diets or increased production of free radicals caused by stress, smoking, environmental contaminations. Antioxidants and other bioactive compounds detoxify ROS and prevent damage to cellular macromolecules and organelles through multi-mechanisms. In human body, several mechanisms are known to defend from free radicals (for example antioxidant enzymes), however in some cases there is a need more substances to overcome their impact. Consumption of vegetables including Brassica species has been strongly associated with the reduced risk of chronic diseases, such as cardiovascular disease, diabetes, and age-related functional decline. 4,5 Antioxidants are also effective in reducing free radical damage of collagen and elastin, the fibers that support the skin structure.6

Carotenoids are yellow, red and orange pigments present in many fruits and vegetables. In the diet they act as powerful antioxidants and are believed to protect the body against free radical attack. Several studies on the bioavailability of B -carotene from vegetables in the human diet have shown that in broccoli it ranges from 22- 24%, in carrots 19-34%, and in leafy vegetables it ranges from 3-6%. Flavonols include quercetin, kaempferol, fisetin, and myricetin. Quercetin is the most important flavonoid in vegetables. It has been detected in onion. Kaempferol, myricetin, and fisetin have also been detected in onion as well as lettuce, and endive.

Anthocyanins give vegetable leaves and fruits their purple and or/red colour, such as in purple cabbage, purple broccoli, purple sweet potato, rhubarb, purple radish and onion. Anthocyanins have also been shown to protect mammalian cell lipoproteins from damage by free radicals. 2

Constant inflammation plays an essential role in many human illnesses and isothiocyanates (ITCs) slow down the activity of many inflammation mechanisms, restrain cyclooxygenase 2, and permanently inactivate the macrophage migration inhibitory factor. Studies have attributed ITCs with  anti-inflammatory abilities . They have been shown to reduce carrageenan-induced rat paw oedema, lessen ear oedema formation and induce leukocyte clearance in inflamed mouse skin and in studies using Human skin organ culture, has been shown to  reduce the expression and secretion of proinflammatory cytokines in human monocytes, macrophage-like cells and inflamed skin.7

As with anything diet should be balanced and any changes should be discussed with your Practitioner.



  • Vanden Berghe W. and Haegeman G.; Epigenetic Remedies by Dietary Phytochemicals Against Inflammatory Skin Disorders: Myth or Reality?; Curr Drug Metab.2010 Jun 1;11(5):436-50.
  • Pradeep Kumar Singh and K. Mallikarjuna Rao (2012): “Phytochemicals in Vegetables and their Health Benefits”, Asian Journal of Agriculture and Rural Development, Vol. 2, No. 2, pp. 177-183
  • Priya R. et al.; Oxidative stress in psoriasis.; Biomedical Research 2013; 25 (1): 132-134
  • Kapusta-Duch J. et al.; The beneficial effects of Brassica vegetables on human health; Rocz Panstw Zakl Hig 2012, 63, Nr 4, 389 – 395
  • Priya Sharma, Sonia Kapoor; Biopharmaceutical aspects of Brassica vegetables; Journal of Pharmacognosy and Phytochemistry 2015; 4(1): 140-147
  • Basavaraj, K H, C Seemanthini, and R Rashmi. “DIET IN DERMATOLOGY: PRESENT PERSPECTIVES.”Indian Journal of Dermatology 3 (2010): 205–210. PMC. Web. 16 Feb. 2016.
  • Yehuda H. et al.; Isothiocyanates inhibit psoriasis-related proinflammatory factors in human skin; Inflamm. Res. (2012) 61:735–742 DOI 10.1007/s00011-012-0465-3



Human beings are continuously exposed to environmental pollutants. Because of its critical location, the skin is a major interface between the body and the environment and provides a biological barrier against an array of chemical and physical environmental pollutants. The skin can be defined as our first defense against the environment because of its constant exposure to oxidants, including ultraviolet (UV) radiation and other environmental pollutants such as diesel fuel exhaust, cigarette smoke (CS), halogenated hydrocarbons, heavy metals, and ozone (O3). The exposure to environmental pro-oxidant agents leads to the formation of reactive oxygen species (ROS) and the generation of bioactive molecules that can damage skin cells.1

 The skin is a potential target for oxidative injury, as it is continuously exposed to UV radiation and other environmental stresses generating reactive oxygen species (ROS). ROS mediated oxidative damage involves a vast number of biological molecules since it causes lipid peroxidation, DNA modification, and secretion of inflammatory cytokines.2 ROS induced oxidation of polyunsaturated fatty acids results in the metabolization of the lipid peroxidation into malondialdehyde (MDA). Lipids are structural components of cell membranes, critical in the formation of the permeability barrier of cells, whilst MDA is used as a biomarker of lipid peroxidation.2,3


Alterations that disturb the skin barrier function in either stratum corneum lipid metabolism or protein components of the corneocytes are involved in the development of various mild or severe skin diseases, including erythema, oedema, hyperplasia, “sunburn cell” formation, skin aging, contact dermatitis, atopic dermatitis, psoriasis, and skin cancers.1

The mechanism by which environmental insults exert a detrimental effect the skin barrier function is through the generation of oxidative stress, which overwhelms the skin’s defenses by quickly depleting the enzymatic (glutathione peroxidase, glutathione reductase, superoxide dismutase, catalase) and nonenzymatic (vitamin E, vitamin C, and glutathione) antioxidant capacity, thus leading to deleterious effects.1 The enzymes, including glutathione peroxidase, superoxide dismutase (SOD) and catalase (CAT) decrease the concentration of the most harmful oxidants, hence an inadequate antioxidant protection or excess ROS production generates oxidative stress and contributes to the development of cutaneous diseases and disorders.

Increased capacity for chemotaxis (the directional movement of cells in response to chemical stimuli), adhesion (the interaction of a cell with a neighbouring cell or with the underlying extracellular matrix, via specialized multi-protein adhesive structures) and increased ROS production in neutrophils, keratinocytes and fibroblasts of the skin matrix, have been reported in patients with psoriasis. Research results have shown that increased oxidative stress in these patients, as demonstrated by the high plasma malondialdehyde (MDA) levels and compromised levels of the antioxidant defense enzymes, have been observed even at the time of diagnosis itself. Other reports have suggested that, fibroblasts in the lesion-free skin of psoriasis patients have shown signs of increased oxidative damage even before the formation of the characteristic psoriatic plaque/lesions which may indicate the involvement of abnormal immune reactions leading to the onset of the disease.2

Sun UV rays, Ozone (O3 – the primary constituent of smog), cigarette smoke (CS) exposure, and pollutants, in addition to the natural process of aging, contribute to the generation of free radicals and reactive oxygen species (ROS) that interact with lipid-rich plasma membrane and initiate the so-called lipid peroxidation reaction cascade. The progressive depletion of antioxidant content in the stratum corneum leads to the cascade of effects which result in an active cellular response in the deepest layers of the skin. ROS is known to stimulate the release of pro-inflammatory mediators from a variety of skin cells. Skin inflammation, in turn, leads to skin infiltration by activated neutrophils and other phagocytic cells that generate further free radicals (both reactive oxygen and nitrogen species), thus establishing a vicious circle.1

 There is no doubt that the skin is continuously and simultaneously exposed to several oxidative stressors, and these can have additive, if not synergistic, effects. Whilst UV ray therapy has been proven to be an effective treatment for psoriasis and there is certainly anecdotal information that indicates sun exposure also improves psoriatic lesions, there has been little or no research on the effects of combined UV and O3 on the inducement and or exacerbation of psoriasis.  While environmental UV radiation penetrates into the epidermis (UV-B) or into the dermis (UV-A) and is known to induce the release of tissue-degrading enzymes, O3 oxidizes biological systems only at the surface. Therefore, because O3 and UV cooperatively damage subcutaneous (SC) components they exert an additive effect in cutaneous tissues. Research results have suggested that UV irradiation has been shown to compromise the skin barrier and simultaneous exposure to O3 may enhance this phenomenon by perturbing SC lipid constituents that are known to be critical determinants of the barrier function. It has been proposed that the by-products of O3-induced lipid oxidation penetrate the outer skin barrier and cause effects on constituents of the deeper epidermis that can lead to activation of transcription factors, such as Nuclear factor kappa B (NF-?B), which regulates a variety of proinflammatory cytokines. NF-?B is a protein transcription factor that orchestrates inflammation and other complex biological processes. It is a key regulatory element in a variety of immune and inflammatory pathways, in cellular proliferation and differentiation and in apoptosis. Therefore NF-?B is a crucial mediator involved in the pathogenesis of psoriasis.1,3,4,6

It has been theorized that responses to air pollutants may be age related, and several recent studies have shown that skin responses to pollutants are modulated by age. The free radical theory of aging is supported by finding that oxidative damage to biomolecules accumulates and increases with age. In aging skin, the process oxidative damage involves not only proteins, lipids and DNA but also is linked with alteration of the collagenous extracellular matrix in the dermis. The extensive research in the aging process of human skin found that levels of MMP-1 increased with age and contributed to fragmentation and disorganization of collagen fibers in the dermis. Researchers have also found that both a contact of fibroblasts with collagen fibers and collagen cross-links of collagen fibers are strongly reduced in aged skin (80% and 75%, respectively). Despite a large body of knowledge a detailed molecular mechanism of the skin aging is not fully recognized.1,5

Further research is required to determine exactly how air pollutants can induce and/or exacerbate psoriasis and other skin conditions. However one theory proposed for the most likely cause is thought to be due to skin injury caused by exposure to the chemical pollutant and the subsequent initiation of the Koebner effect.

See our blog “Koebner Phenomenon”, “Psoriasis and Chemical Exposure” and “Psoriasis and Smoking”


  • Valacchi et al.; Cancer Cutaneous responses to environmental stressors ; Annals Of The New York Academy Of Sciences;  Issue: Nutrition and Physical Activity in Aging, Obesity, and Cancer; Ann. N.Y. Acad. Sci. ISSN 0077-8923;
  • Ayala A. et al.; Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal; Oxidative Medicine and Cellular Longevity Volume 2014, Article ID 360438, 31 pages; file:///C:/Documents%20and%20Settings/marg/My%20Documents/Downloads/360438.pdf
  • Kadam P. et al.; Role of Oxidative Stress in Various Stages of Psoriasis; Ind J Clin Biochem (Oct-Dec 2010) 25(4):388–392; file:///C:/Documents%20and%20Settings/marg/My%20Documents/Downloads/12291_2010_Article_43.pdf
  • Goldminz AM. Et al.; NF-?B: an essential transcription factor in psoriasis.; J Dermatol Sci.2013 Feb;69(2):89-94. doi: 10.1016/j.jdermsci.2012.11.002. Epub 2012 Nov 14.
  • Kruk J., Duchnik E.; Oxidative Stress and Skin Diseases: Possible Role of Physical Activity; Asian Pacific Journal of Cancer Prevention, Vol 15, 2014
  • Burke KE,Wei H.; Synergistic damage by UVA radiation and pollutants.; Toxicol Ind Health May/June 2009 25: (4-5): 219-224