Multiple Sclerosis (MS)

Multiple sclerosis (MS) is an autoimmune disease in which the myelin sheath surrounding both peripheral and central nerve axons is targeted and broken down. Without adequate myelin sheaths, neurons fire abnormally, and paralysis or death may result (Steinman, 1996).

In this disease, the womens are affected more often than men and age at onset of the clinical symptoms is typically between 20 and 40 years (VanAmerongen et al., 2004). Besides

that, first degree relatives of MS patients are 20–40 times more likely to acquire the disease than others, and the monozygotic twin of a patient is at greater risk (an additional 10 fold risk) (Ebers and Sadovnick, 1994).

The MS is characterized by a chronic course of relapses followed by periods of stability (Cantorna et al., 1996). Being that diagnostic criteria for MS include clinical and paraclinical laboratory assessments (Polman et al., 2010).

The risk of developing MS, a relatively common cause of disability among young adults, is determined by a combination of genetic and environmental factors. The latter include Epstein-Barr virus (EBV) infection, cigarette smoking, dysfunction of the immune system (autoimmunity), genetic susceptibility and inadequate serum concentrations of VD (Ascherio and Munger, 2007; Ebers and Sadovnick, 1994). Although EBV is nearly ubiquitous, there are no eff ective vaccines or treatments for EBV infection, leaving smoking cessation and VD supplementation as the only available interventions that might result in a reduction in the global burden of MS (Ascheri et al., 2010).

The neuroimmunomodulatory effects of VD3 in the CNS suggest the effect of this hormone in resolving MS (Brachet, et al. 2000), besides that, the serum VD concentrations have been associated with a high incidence of MS (Torkildsen et al, 2008).

In this sense, studies indicated that the over 70% of MS cases in the USA and Europe could be prevented by increasing of serum VD3 concentrations in adolescents and young adults (Holick, 2008B; Prentice, 2008).

The prevalence of MS worldwide increases as one moves further north or south away from the equator (Hayes et al., 1997). The prevalence rate for MS is nearly zero for people living at the equator, and increases to over 50 cases per 1,000,000 individuals in the north or south of the equator (Hayes, 2000). One hypothesis is that sunlight exposure and the resulting increase in VD may exert a protective effect (Goldberg, 1974). Yet, studies indicate lower winter calcium and phosphate levels, which may indicate a relative VD3 deficiency in MS (Soilu-Hanninen et al., 2008).

The VD3 has long been known as a preventive factor for the models of animal of the human autoimmune demyelinating CNS disease MS (Lemire et al., 1991). Besides that, the VD3 deficiency in animals can aggravate of symptoms in MS, while its supplementation can prevent or block its progression with a dose dependent effect in animals (Cantorna et al., 1996; Spach and Hayes, 2005).

In this context, it has been shown that VD3 have strong immunoregulatory effects and its supplementation prevents a model of MS in animals, through delays blocking the progression of model. Furthermore, the VD ordeal aggravates the clinical signs on the model (Cantorna et al., 1996; Garcion et al., 2002). Likewise, low VD levels may aggravate its severity (VanAmerongen et al., 2004).

3.3. Schizophrenia (SZ)

Schizophrenia (SZ) is a debilitating mental illness (psychiatric disorders) that affects 1% of the population. Your symptoms occur usually in young adulthood and persist for the entire lifetime, being almost totally disabling. This disease is multifactorial in origin, with both genetic and environmental contributions likely playing an important role in the manifestation of symptoms (Sawa and Snyder, 2002).

Your diagnosis is based on the simultaneous presentation of two types of symptoms that reflect a psychotic disturbance: “positive” symptoms that include delusions, hallucinations, and bizarre thoughts, and negative symptoms that include social withdrawal with affective flattening, poor motivation, and apathy. Patients with affective disorders such as bipolar disorder may exhibit a subset of the psychotic symptoms associated with SZ, such as hallucinations, but these disorders generally have a distinct constellation of symptoms and familial incidence (Andreasen et al., 1996).

Studies pharmacological point to a central role for several neurotransmitters, including dopamine, glutamate, and serotonin, that may interface with neurodevelopmental defects reflecting disease related genetic aberrations (Sawa and Snyder, 2002).

The diagnosis of SZ is based on the simultaneous presentation of two types of symptoms that reflect a psychotic disturbance: “positive” symptoms that include delusions, hallucinations, and bizarre thoughts, and negative symptoms that include social withdrawal with affective flattening, poor motivation, and apathy (Andreasen, 1996).

Studies postulates that etiologic and pathogenic factors of SZ occur in gestation interrupting thus, the course of normal neural development, resulting in pathologic alterations of specific neurons, and the circuits they form, ultimately resulting in malfunction (Lewis, 1997; McGrath et al., 2010). These neurodevelopmental aberrations present after a period of one to three decades. The events that trigger the formal onset of the illness are not known but are thought to include normal (Lieberman, 1999).

VD3 deficiency has been linked to an increased incidence of SZ and depression (McGrath et al., 2002). Maintaining VD3 sufficiency in utero and during early life, to satisfy the VDRs transcriptional activity in the brain, may be important for brain development as well as for maintenance of mental function later in life (Eyles et al., 2005).

The marked seasonal variations in the serum level of VD3, may be linked to the seasonality of SZ births (McGrath et al., 2004A), since many studies report that the rate of people born with SZ is higher in the winter and spring months (Pile, 1951; Torrey et al., 1997). In addition, migrants of dark-skinned, also have of an increased risk of development of SZ (McGrath, 1999). This within year fluctuation may too correlated with latitude, with greater variation in sites further away from the equator (Davies et al., 2003).

Studies have also demonstrated that, city-born individuals have an increased risk of developing SZ (Jablensky, 1999; Marcelis et al., 1998), since the risk of VD3 deficiency is higher in the cityies, which to reflect reduced sun exposure (as a consequence of pollution and the built-up environment), and reduced outdoor activity in city-dwellers (Holick, 1995). In this context, for McGrath et al. (2010A) the urban birth risk factor for SZ may be too the result of increased prevalence of low maternal VD3 in the city compared to rural settings.