One of the more difficult things for a parent to endure is seeing a child suffer from a chronic condition. It’s especially hard if the condition affects the skin, which often attracts unwanted attention and can cause psychological distress as well. Eczema is one of the most common skin disorders in young children and some adults. It may affect as many as 20% of children in the USA. Eczema is defined by an irritation and swelling of the skin that frequently involves extreme dryness and itchiness. There are conventional treatments available for eczema, but they carry the risk of serious side effects. One reason is the need for long term term treatment, as eczema is incurable. In addition, the condition frequently covers large areas of skin, thereby necessitating large amounts of medication. The April 2009 issue of the Journal of Alternative and Complementary Medicine provides a viable and safe alternative to the potentially dangerous drugs that are in use today. A trial was set up to investigate the efficacy of a Vitamin B12 cream in the treatment of children with atopic dermatitis (eczema).
Twenty-one patients with ages ranging from 6 months to 18 years enrolled in this 4 week trial. Each volunteer applied either a Vitamin B12 cream or a placebo cream to symptomatic areas on opposite sides of their bodies. For instance, the B12 cream was only applied to the right side and the placebo was exclusively used to treat the left side. This allowed for a comparison model for the two treatments. At the end of weeks 2 and 4, an investigator performed skin checks using a “standardized scoring system”. The findings were expressed in this manner, “Skin treated with topical vitamin B(12) improved significantly more than placebo treated skin at 2 and 4 weeks. Topical vitamin B(12) should be considered as a treatment option in children with eczema.” In May of 2004 another study was presented in the British Journal of Dermatology. It was a larger experiment that focused on adults with eczema. In it, 49 participants applied a Vitamin B12 cream or a placebo cream to opposite sides of their bodies.
They did so for a total of 8 weeks. Those applying the B12 cream noted a 55% improvement in their eczema symptoms. When the volunteers were asked to describe the effects of both creams, in most cases they evaluated the B12 cream as being “good” and “very good”. The placebo cream was generally described as being of “moderate” use or providing “poor” results. Based on symptom regression and patient feedback, the researchers concluded that, “These results document a significant superiority of vitamin B(12) cream in comparison with placebo with regard to the reduction of the extent and severity of atopic dermatitis. Furthermore, the treatment was very well tolerated and involved only very low safety risks for the patients.” It appears that other severe and chronic skin maladies are receptive to topical B12 treatment as well. In 2001, a study was described in the journal Dermatology. This time the focus of the scientific inquiry was the management of chronic plaque psoriasis with an avocado oil and B12 cream.
Instead of a placebo, a Vitamin D based medication was compared to the B12 cream. Vitamin D analogs have been traditionally used with some success in managing the symptoms of psoriasis. Exposure to natural sunlight, which the skin uses to produce Vitamin D, is also known to benefit some psoriasis sufferers. Over the course of 12 weeks, 13 female and male volunteers were provided both treatments. Once again, the investigators utilized a “right/left side comparison technique” to determine the respective effects of each type of treatment. The Vitamin D based medication brought about quicker results, but they tended to fade after 8 weeks. The avocado oil/B12 cream’s positive effects remained constant throughout the 12 week period, and both the patients and the investigators found that it was better tolerated. Because of the more consistent therapeutic effect and greater tolerability, the B12 topical was considered better suited for the “long-term treatment of psoriasis.”
It’s great to know that there are safe and natural topical treatments that can help reduce the symptoms of eczema and psoriasis. But it’s important to remember that what you put into your body can also have a profound effect on the condition of your skin. In particular, food allergies and sensitivities, an imbalance of the good and bad bacteria in the digestive system and a lack of healthy fats in your diet can all contribute to the worsening of skin conditions such as eczema. If we only approach skin disorders from the outside in, we’re missing a big part of the picture. Please check out the “Comments & Updates” section of this blog – at the bottom of the page. You can find the latest research about this topic there!Psoriasis is a chronic inflammatory skin condition with an increased risk of cardiovascular disease. This risk has been attributed to an association with many independent risk factors including obesity, hypertension, smoking, and dyslipidemia. Psoriasis patients also have lower levels of folate and conversely higher levels of homocysteine, which in itself is a risk factor for cardiovascular disease.
It has been postulated that low folate levels in this group may be a direct cause of hyperhomocysteinemia and therefore a treatable risk factor by folate supplementation. This paper looks at the literature published to date on the relationship between psoriasis, homocysteine, and folate levels.Psoriasis is a chronic recurrent inflammatory skin condition. Its prevalence varies among ethnic groups, but it affects approximately 1–3% [1] of the population in industrialised countries. Its clinical course can vary greatly in terms of morphology, distribution, and severity of the disease. In its commonest subtype it is characterised by the formation of discrete, pink, scaly plaques occurring at various sites on the body. It affects men and women equally and is seen in all races [2]. Although it can present at any age, it occurs most frequently between the ages of 15 and 20 and again between 50 and 60 years of age.Psoriasis has very significant psychosocial morbidity which appears independent of objective disease severity [3, 4].
It is also associated with an increased risk of cardiovascular disease and mortality [5–8]. Indeed patients with psoriasis have almost twice the risk of cardiovascular disease when compared with normal controls [9, 10]. The exact reason for this increased risk is unknown. A number of studies have shown significantly increased rates of hypertension, dyslipidemia, diabetes mellitus, smoking, and excessive alcohol consumption in patients with psoriasis [11]. Neimann et al. found that patients with severe psoriasis had an increased risk of diabetes (odds ratio (OR), 1.62; 95% confidence interval (CI), 1.3–2.01), obesity (OR, 1.79; 95% CI, 1.55–2.05), and smoking (OR, 1.31; 95% CI, 1.17–1.47) compared with controls [12]. Prodanovich et al. also found a higher prevalence of these risk factors in patients with psoriasis. However, even after controlling for these variables, they found a higher prevalence of ischemic heart disease (OR 1.78; 95% CI, 1.51–2.11), cerebrovascular disease (OR, 1.70; 95% CI, 1.33–2.17), and peripheral vascular disease (OR, 1.98; 95% CI, 1.32–2.82) when compared with controls.
Indeed they also found psoriasis to be an independent risk factor for mortality (OR, 1.86; 95% CI, 1.56–2.21) as a result of the association with atherosclerosis [13]. These risk factors in combination with the chronic inflammatory process are thought to be significant components in the development of vascular disease [9, 14]. Links with alterations in levels of folate and homocysteine in patients with psoriasis have also been implicated in contributing to the propagation of atherosclerosis and atherothrombotic events [9, 15, 16]. Recent case control studies have demonstrated that patients with psoriasis have lower levels of folate in comparison to normal controls [9, 15, 17, 18]. The exact aetiology of this association remains unclear. Postulated mechanisms include alterations in gut absorption of folate due to microscopic inflammatory changes seen in the bowel mucosa of patients with active psoriasis and psoriatic arthritis [15]. A more likely explanation however probably relates to the accelerated keratinocyte turnover seen in patients with psoriasis.
This action results in excessive consumption of folate used to methylate DNA in these actively dividing cells thus lowering folate levels [9].Conversely homocysteine levels are elevated in psoriasis patients [9, 15, 17]. In one case-controlled study this was found to directly correlate with disease severity and to be inversely related to plasma folate levels [15]. Plasma homocysteine is an independent risk factor for cardiovascular disease [19, 20], peripheral vascular disease, cerebrovascular disease and possibly Alzheimer’s diseases. The magnitude of this risk is equivalent to the risk of smoking or dyslipidemia [9]. Hyperhomocysteinemia (>15 umol/L) is thought to favour atherosclerosis and vascular thrombosis by a number of mechanisms. These include damaging endothelial cells, promoting clot formation, decreasing flexibility of blood vessels leading to aortic stiffness, and reducing blood flow velocity [20]. The endothelial dysfunction is thought to result from the accumulation of asymmetrical dimethylarginine (ADMA) which is a natural inhibitor of nitric oxide synthase.
As a result there is a reduction in the production of the vasodilator nitric oxide which protects the vessel wall against the pathogenesis of atherosclerosis and thrombosis (Figure 1).Figure 1: Proposed mechanism of homocysteine-induced endothelial dysfunction and atherogenesis [21].It has been suggested that hyperhomocysteinemia in addition to other factors may be caused by reduced levels of folate in these patients [9, 15]. Coenzymes methylene tetra-hydrofolate, methylcobalamin, and pyridoxal phosphate are essential for three of the enzymes involved in the metabolism of homocysteine and are dependent on folate, vitamin B12 and B6, respectively. Hence in patients with severe psoriasis who have large areas of rapid skin turnover and increased keratinocyte activity, there is excessive consumption of folate. This in turn results in reduced breakdown and elevated serum levels of homocysteine with all of its adverse effects. It appears from this paper that patients with psoriasis have lower levels of folate and higher levels of homocysteine than normal controls.
As psoriasis is associated with an increased risk of cardiovascular morbidity and mortality and homocysteine is an independent risk factor for cardiovascular disease, it may seem intuitive that managing this risk factor would have beneficial effects in terms of cardiovascular mortality and morbidity. The possible benefit of folate supplementation seems logical [22]. Folate has long been used in combination with methotrexate in the management of psoriasis, psoriatic arthritis, and rheumatoid arthritis. Here it is effective in reducing gastrointestinal side effects and liver function test abnormalities [23]. In a retrospective cohort study looking at over seven thousand patients with psoriasis, methotrexate was found to reduce the incidence of vascular disease and this reduction was further enhanced when folic acid was added (Figure 2) [24].Figure 2: Proposed action of combination therapy, in addition to risk factors such as age, sex, hypertension, and dyslipidemia, homocysteine and inflammation lead to increased incidence of vascular disease.
Consequently reducing inflammation with methotrexate and hyperhomocysteinemia by folic acid may lead to a decreased incidence of vascular disease for patients with psoriasis [24].However, homocysteine levels can be elevated for other reasons including obesity, hypertension, smoking, and excessive alcohol consumption all of which have significant prevalence in the psoriatic patient population [11]. Armitage et al. in a double-blinded randomised control trial assessed the beneficial effects of lowering homocysteine levels in over 12,000 post-MI patients. They failed to demonstrate any benefit in vascular outcomes from long-term reductions in homocysteine with folate and vitamin B12 supplementation [25]. It is possible that hyperhomocysteinemia in psoriasis is independent of folate deficiency and instead is linked with other risk factors such as hypertension and obesity [9]. “The psoriatic march”, a concept of how severe psoriasis may drive cardiovascular morbidity, suggests a process of genetic susceptibility triggered by environmental factors and immune responses.