2010 Glycemic changes after vitamin D supplementation in patients with type 1 diabetes mellitus and vitamin D deficiency. 2009 Genome-wide association study and a meta-analysis find that over 40 loci affect risk of type 1 diabetes. 1983 Specific high-affinity receptors for 1,25 dihydroxyvitamin D3 in human peripheral mononuclear cells: Presence in monocytes and induction in T lymphocytes following activation. 1995 Susceptibility to human type 1 diabetes at IDDM2 is determined by tandem repeat variation at the insulin gene mini satellite locus. 1994 A polymorphic locus near the insulin gene is associated with insulin-dependent diabetes mellitus. 2001 1alpha,25-Dihydroxyvitamin D3 has a direct effect on naive CD4+ T cells to enhance the development of Th2 cells.
1996 1,25-dihydroxyvitamin D3 reversibly blocks the progressions of relapsing encephalomyelitis, a model of multiple sclerosis.
1998 1,25-dihydroxyvitamin D3 prevents and ameliorates symptoms in two experimental models of human arthritis. 1998 1,25-dihydroxy-vitamin D3 restores sensitivity to cyclophosphamide-induced apoptosis in non-obese diabetic (NOD) mice and protects against diabetes. 1998 Prevention of autoimmune destruction of syngeneic islet grafts in spontaneously diabetic nonobese diabetic mice by a combination of a vitamin D3 analog and cyclosporine.
2000 Vitamin D receptor gene polymorphisms influence susceptibility to type 1 diabetes mellitus in the Taiwanese population. 1998 Prevention of type 1 diabetes in nonobese diabetic mice by late intervention with nonhyperclcemic analogs of 1,25-dihydroxyvitamin D3 in combination with a short induction course of cyclosporine A. 1997 The nonobese diabetic mouse as a model of autoimmune diabetes: Immune dysregulation gets the NOD. 1998 Inhibition of IL12 production by 1,25-dihydroxyvitamin D3: involvement of NF-?B down regulation by 1,25-dihydroxy vitamin D3. Vitamin K1 (phylloquinone) rich foods may reduce type2 diabetes as shown by latest study published in American Journal of Clinical Nutrition. Some foods rich in vitamin K include cooked broccoli, raw kale, raw spinach, raw leaf lettuce, raw Swiss chard, raw watercress and raw parsley. Enter your email address to subscribe to this blog and receive notifications of new posts by email.
Shop Suja Subscriptions and get 6, 18 or 48 bottles of deliciousness delivered right to your doorstep each month with FREE shipping! Vitamin D is one of the hardest nutrients to obtain through food alone, because relatively few foods contain high amounts of the nutrient.
Look for vitamin D3 (cholecalciferol) or D2 (ergocalciferol), as either will help you obtain optimal vitamin D status. It’s hard to determine exactly how much vitamin D is needed from food or supplements because sunshine provides the bulk our vitamin D from April-August. Symptoms of this problem include frequent urination, increased hunger and thirst, weight loss, fatigue, blurred vision and so on. Aloe vera juice can be diluted with water and consumed (half cup) before breakfast to deal with the problem. Practicing yoga on a regular basis can also provide relief from the problem of type 1 diabetes.
Intake of food items prepared with virgin coconut oil can help in alleviating the symptoms associated with the problem. Am from USA and am very happy to write about Dr Ariba for what he has don for me and my Mom. Summer sunshine makes most of us feel better, but there may be more to its benefits than just feeling good.
Sunlight comprises two types of solar radiation: UVA, which causes reddening and burning of the skin, and UVB.
Unfortunately, both UVA and UVB also increase the risk of skin cancer, including the most deadly type, melanoma, which is why you should always take a balanced approach to sunlight exposure. Only a few foods, such as fatty fish and mushrooms, contain vitamin D, so we get most of it from sunlight. This raises an important question about the actual source of vitamin D deficiency: could low vitamin D levels actually result from an unidentified underlying disease process (such as inflammation) leading to ill health? My colleagues and I previously found support for this theory when we discovered an association between low vitamin D levels and the development of type 2 diabetes.
But when we gave supplements of vitamin D to patients with low vitamin D levels who were already at risk of developing diabetes, there was no overall improvement in their sensitivity to insulin. This disconnect between low vitamin D levels increasing the risk of disease, and the failure of consuming more vitamin D (by increased sun exposure or supplementation) to reduce risk, could mean sunshine has unknown effects on health. Another important potential effect of sunlight is UV-induced suppression of the body’s immune system.
At first glance, this may seem to be a bad thing because it could increase the risk of infections and skin cancer. People who don’t get enough sunlight have altered cellular defence mechanisms that predispose them to excessive inflammation, which can result in autoimmune diseases. These diseases involve the body mistakenly attacking its own tissues, and include multiple sclerosis, lupus, type 1 diabetes and inflammatory bowel diseases, asthma and skin disorders such as psoriasis and atopic dermatitis. UVA has also been shown to lower blood pressure, increase blood flow and heart rate, all of which are beneficial to the heart and blood vessels. Future research will try to determine whether increasing vitamin D by UVB, or other sunlight-induced mechanisms such as altering the body’s immune defence mechanisms, are better for improving health outcomes, but at least a little sunshine definitely appears to be a good thing for health. Without myelin, the brain and spinal cord cannot communicate properly with the nerves in the rest of the body.Multiple sclerosis most commonly is first diagnosed in people between the ages of 20 and 40, but people can develop this disease at any age.
IntroductionThis chapter will review the role of vitamin D in the pathogenesis and treatment of type 1 diabetes mellitus.
Vitamin D supplement in early childhood and risk for type 1 (insulin-dependent) diabetes mellitus. Unlike other vitamins, our bodies have the ability to make our entire requirement from sunlight.
However, dark-skinned individuals, sunscreens, air pollution and other factors all negatively affect the body’s ability to produce vitamin D.
Further, it may result in nausea, fast heartbeat, unconsciousness, pain in the abdomen and so on.
Consumption of aloe vera juice (1 tablespoon) 2 to 3 times in a day can also help in the treatment. The juice extracted from fresh margosa leaves can be diluted with water and consumed (1 tablespoon) empty stomach every morning for a period of 2 to 3 months to treat the problem. Different yoga postures such as uttanpadasana, bhujangasana and paschimottasana can be practiced to get the desired results.
Intake of coconut water on a frequent basis can increase the production of the insulin hormone. You accept that you are following any advice at your own risk and will properly research or consult healthcare professional. We where both having diabetes Type 1 until that faithful day we found a post on the INTERNET of how a man was cure of that same diseases saying it cost him $1500 for the herbal cure I quickly collected the email of the Dr and emailed him immediately and behold he requested for out information which I did and the he told us how much it was going to cost and when we payed the fees and he sent us a parcel through a courier service and when we received it we drank it as prescribed and after some days everything was finally over now am so so have that am finally normal again. We use a Creative Commons Attribution NoDerivatives licence, so you can republish our articles for free, online or in print.
A growing body of evidence suggests sunlight itself – with adequate protection, of course – may actually be good for health. The latter increases the production of an inactive form or precursor of vitamin D by the skin, which is then activated by the liver and kidneys.
This means not enough sun exposure, or pigmentation of the skin (which diminishes the production of vitamin D precursors), often results in low vitamin D levels.
These include low bone density and broken bones due to osteoporosis, muscle weakness, diabetes, multiple sclerosis, cardiovascular disease, colon cancer and an overall increased risk of dying prematurely. In other words, could low vitamin D levels be the symptom rather than the cause of illness?
For every ten-unit decrease in blood vitamin D levels, we found a 10% increased risk of developing this form of diabetes over the following five years.
Nor was there a change in their blood glucose levels compared with those given inactive tablets.
These could include the impact of sunlight on daily biological rhythms, such as the one governing our sleep cycle (circadian rhythms), on reducing physical stresses on the body’s cells and by increasing heat production.
Solar radiation does this by altering the activity of the white cells involved in turning on the body’s defence mechanisms. But it can also have a protective role in reducing inflammation and therefore help against some inflammatory diseases. A little sunlight can reduce the numbers of the activated cells that lead to inflammation, and so the risk of getting these diseases. This is probably the result of UVA causing the release of nitric oxide from skin stores, which promotes widening of blood vessels. Guidelines try to minimise the risk of skin cancer while ensuring people can still harvest the health benefits of sunshine. The activation of the T-cell by various stimuli (antigens), is brought by major histocompatibility complex (MHC-HLA II).
At the level of the antigen-presenting cell (such as dendritic cells; DCs), 1?,25(OH)2D3 inhibits the surface expression of MHC class II-complexed antigen and of co-stimulatory molecules, in addition to production of the cytokine IL-12, thereby indirectly shifting the polarization of T cells from a Th1 towards a Th2 phenotype. While vitamin D does enhance calcium to maintain bone health, hundreds of published studies show that it may also help prevent autoimmune diseases like type 1 diabetes, multiple sclerosis and rheumatoid arthritis.
Some 90-95% of the vitamin D in the body comes from UVB rays that we convert in the skin to the nutrient.
It is caused by factors such as genetics, viral infection which affects the intestinal tract or hormonal disorder. An infusion can be created by soaking mango leaves in water before sleeping and consumed (after straining it) in the morning on a daily basis to control the problem. A natural drink can be prepared by boiling margosa leaves (half kilogram) and lemon (half kilogram) in water (1 liter) and consumed (1 cup) on a daily basis to obtain the desired results. Consumption of a mixture of Indian gooseberry and bitter gourd on a regular basis can help in dealing with various symptoms of the problem. But studies of supplementation with this vitamin have not always shown beneficial effects on treating these conditions. And seven minutes of sun exposure to the face, arms and hands at or before 11 am, or after 3 pm on most days in summer is adequate for getting enough sun for health benefits, especially when combined with exercise.
However, experts believe that the immune system plays a role in multiple sclerosis by attacking myelin, the fatty substance that coats and protects nerve fibers in the brain and spinal cord. Consult with your doctor or other health care provider before using any of these tips or treatments.
This figure shows also, inhibitors of T-cell activation: cytotoxic T lymphocyte antigen 4 (CTLA-4) and lymphoid tyrosine phosphatase (LYP).
In addition, 1?,25(OH)2D3 has immunomodulatory effects directly at the level of the T cell, by inhibiting the production of the Th1 cytokines IL-2 and IFN-? and stimulating the production of Th2 cytokines. We will summarize the results of in-vitro and animal studies and will conclude with a review of the relevant clinical trials.2.
They found that high dietary intake of phylloquinone is associated to reduce 50% chances of diabetes type2 in people at high risk of cardiovascular system diseases. And vitamin D is linked to enhanced muscular strength and athletic performance and may even play a role in weight management.
From November-March, fortified foods and supplements become increasingly necessary to obtain optimal amounts of vitamin D in your diet. Since you’re probably getting less than 600 IU per day right now, try incorporating more vitamin D-enriched foods into your diet to get at least 600 IU per day.
A powder prepared with the use of dried mango leaves can be consumed several times in a day to obtain quick relief.
Sources of vitamin A and vitamin D include cod liver oil, egg, milk, carrot, sweet potato and green leafy vegetables. However, your doctor may prescribe certain drugs to slow the progression of the disease and prevent and treat attacks.
ChamomileChamomile is another popular remedy for MS due to its antioxidant, anti-inflammatory and immune-boosting properties.Add 2 teaspoons of dried chamomileto a cup of hot water. DefinitionType 1 diabetes mellitus is an autoimmune disease in which the pancreas is unable to respond to secretagogue stimulation with appropriate insulin secretion. A recent University of California-Irvine and Mayo Clinic study found that serum vitamin D levels are highest in August and lowest in February. Both Th2 and Tregs can inhibit Th1 cells through the production of counteracting or inhibitory cytokines. Hyperglycemia develops when more than 70-90% of the insulin-producing beta cells are destroyed. From November through March, the lack of UVB rays in the Northern Hemisphere means we can’t produce vitamin D from sun exposure to our skin. Apple Cider VinegarApple cider vinegar is beneficial for your health when you are suffering from MS. Drink this relaxing tea twice daily.You can also try chamomile baths to reduce tension and relax your muscles. Together, these immunomodulatory effects of 1?,25(OH)2D3 can lead to the protection of target tissues, such as ? cells, in autoimmune diseases and transplantation. An autoimmune destructive process, which plays a central role in the development of type 1 diabetes mellitus, is facilitated by the subject’s own genetic susceptibility and by non-genetic factors. Its acetic acid content helps your body absorb more vitamins and minerals from the food you eat.
Vitamin D deficiency is a non-genetic factor that appears to be associated with an increased risk of developing type 1 diabetes mellitus. Moreover, it plays a substantial role in guarding against brain oxidative stress and neurological diseases.
The acute complications include life-threatening conditions like severe hypoglycemia or diabetic ketoacidosis (DKA).
Chronic diabetic complications can be divided into microvascular complications (retinopathy, neuropathy and nephropathy) and macrovascular complications (cardiovascular, cerebrovascular and peripheral vascular disease). It is rich in valuable nutrients and contains a high amount of vitamin C, a powerful anti-inflammatory and antioxidant agent. Severe microvascular and macrovascular complications can lead to renal failure (the most common cause of hemodialysis in the US), blindness or lower extremity amputations. In addition, it strengthens the immune system to enable it to function optimally.Eat 1 to 2 amla fruits daily.
EpidemiologyIn 2010, about 215,000 people younger than 20 years of age had diabetes (type 1 or type 2) in the United States.
AshwagandhaAnother popular Ayurvedic herb used to treat MS is ashwagandha, also known as withania somnifera or Indian ginseng. About 27% of those with diabetes (approximately 7 million Americans) do not know they have the disease.
Plus, it might decrease blood pressure and interfere with medications used to treat high blood pressure. Type 1 diabetes mellitus continues to be highly prevalent in many countries, with an overall annual increase estimated at 3% (International Diabetes Federation [IDF] 2010).
Natural historyThe natural history of type 1 diabetes is characterized by an autoimmune destruction of the beta cells in the islands of Langerhans in the pancreas. The autoimmune process has cellular and humoral components, leading to the destruction of the beta cells and a decreased insulin secretion.
As beta-cell mass declines, insulin secretion decreases until the available insulin no longer is adequate to maintain normal blood glucose levels.
After 70-90% of the beta cells are destroyed, hyperglycemia develops and diabetes may be diagnosed. In some patients years will go by before the onset of diabetes, while other patients may never develop beta cell insufficiency, perhaps due to the regaining of tolerance. Most patients with type 1 diabetes mellitus have one or more susceptible human leukocyte antigen (HLA) class II, and over 90% have beta cell autoantibodies present.
The appearance of circulating islet cell autoantibodies is the first detectable sign of this immune process.4.
However, extra-genetic components influence the penetrance of diabetes susceptibility genes. If data are obtained at a single point in time, the risk of type 1 diabetes mellitus between monozygotic twins can be as low as 30%, but if the monozygotic twins are followed long-term, the cumulative incidence of diabetes reaches 65% (Redondo et al., 2008).
In the same cohort of monozygotic twins, the rate of persistent autoantibody positivity, type 1 diabetes mellitus, or both, reached 78% (Redondo et al., 2008). To better understand the genetic susceptibility to diabetes, candidate gene studies were conducted in order to identify genes that are associated with autoimmune type 1 diabetes.Human leukocyte antigen (HLA) associations have been long recognized in many autoimmune diseases.
In type 1 diabetes mellitus, the HLA on chromosome 6p21 is well described and is considered to play an important role in more than 50% of the familial cases in Caucasians (Noble et al., 1996). HLA DR4-DQ8 or DR3-DQ2 haplotypes are detected in up to 90% of patients with type 1 diabetes mellitus (Devendra & Eisenbarth, 2003). First-degree relatives of the patients who carry the highest risk haplotype combination also have a higher risk of developing diabetes mellitus as compared to the relatives of diabetes patients who do not have this haplotype and who develop type 1 diabetes mellitus later in life (Gillespie et al., 2002).
Another HLA haplotype (DR15-DQ6) might have protective properties, and is found in a much larger percentage in the general population (20%) as compared to less than 1% in patients with type 1 diabetes mellitus (Eisenbarth & Gottlieb, 2004). Glutamic acid decarboxylase (GAD) antibodies are more frequent in patients with HLA DR3-DQ2, whereas insulin auto-antibodies (IAA) and protein tyrosine phosphatase-like protein antibodies (IA-2 antibodies) are more frequent in patients with HLA DR4-DQ8. The insulin gene contributes 10% to the genetic susceptibility in developing autoimmune diabetes (Bell et al., 1984). The risk of developing diabetes depends on the expression of the insulin protein in the thymus which can cause a defective central tolerance to the insulin molecule.
T cells are recognized to be a major part of the immune process in diabetes mellitus, and several genes involved in T cell regulation are associated with type 1 diabetes mellitus. Autoimmune processOne of the best animal models for type 1 diabetes mellitus is the nonobese diabetic mouse (NOD). NOD mouse develops type 1 diabetes mellitus spontaneously, over the course of a few months, allowing the investigators to study this process stage by stage.
Many reports describe in detail the genetics, the immune process, the influence of the environment and most importantly, the potential therapies to prevent, delay or reverse the destructive process that leads to type 1 diabetes mellitus in this model. Delovitch and Singh (Delovitch & Singh, 1997) reviewed the use of NOD mouse in the studies of type 1 diabetes mellitus. In NOD mice, the first step is the infiltration of the peri-islet regions of the pancreatic islets by dendritic cells (DC) and macrophages, followed by T cells (CD4+ and CD8+). It is followed by a slower, progressive T cell destruction of the beta cells (insulitis), by 4-6 months of age (Delovitch & Singh, 1997). Thus, the T cells and the dendritic cells are key players in the immune process leading to type 1 diabetes mellitus.The dendritic cells (DC) are antigen-presenting cells which originate from the bone marrow. After infiltrating the pancreas and undergoing antigenic maturation, DC secrete IL-12 and present the processed antigen (on their surface and in association with the major histocompatibility complex [MHC] class II) to other cells of the immune system (i.e. T cells) (see Fig 1).T cells are categorized mainly based on their immune actions, achieved via the different cytokines they secrete. T helper 2 cells (Th2) are important in humoral immunity (activate B cells and antibody production, down regulating Th 1 cells) and secrete type 2 cytokines: interleukins 4, 5, 6, 9 and 10 (Rabinovitch, 1998) (Fig. They have an inhibitory effect on the Th1 cells, which are destructive to the pancreatic beta cells. In the NOD mouse, it appears that the immunologic self-tolerance to pancreatic beta cells is lost. The disruption of the equilibrium between Th1 and Th2 cells in the thymus and in the periphery is believed to play a crucial role in the pathogenesis of autoimmune diabetes mellitus (Delovitch & Singh, 1997). Once Th1 cells are produced they will secrete interferon ? (IFN ?) and IL-2, leading to the activation of macrophages and cytotoxic T cells, which are destructive to the pancreatic beta cells (Adorini, 2001). The same Th1 cells will stimulate the IgG2a autoantibodies against the islet beta cells autoantigens (Delovitch & Singh, 1997). Autoimmune diabetes can be transferred from a diabetic NOD mouse to an unaffected mouse via T cells (Bendelac et al., 1987). NOD mice develop a spontaneous loss of T-cell tolerance to glutamic acid decarboxylase antibodies (GAD), leading to autoimmune diabetes (Kaufman et al., 1993). Exposure to glutamic acid decarboxylase (GAD65 and GAD67) led to an increased T cell proliferation as early as 4 weeks of life in NOD mice, coinciding with the onset of insulitis (Tisch 1993). Some of the other beta-cell antigens elicited an increased immune response after a few more weeks, but there were other beta-cell antigens that did not trigger an immune reaction (for example, amylin) (Tisch 1993). To further support the central role of GAD antigen in autoimmune diabetes, the beta-cell-specific suppression of GAD expression in antisense GAD transgenic NOD mice was demonstrated to prevent the production of diabetogenic T cells and the onset of diabetes (Yoon et al., 1999) In humans, the pancreas becomes infiltrated with mononuclear cells. Autoantibodies to insulin (IAA), glutamic acid decarboxylase (GAD) and insulinoma associated-2 antibody (IA-2) are demonstrated years before the clinical symptoms of diabetes. The presence of autoantibodies alone does not explain the development of diabetes, since it is recognized now that children born to type 1 diabetic mother with high antibody titers transferred through the umbilical cord do not develop diabetes more often than expected.
Environmental component The environment is implicated in the pathogenesis of type 1 diabetes mellitus by many studies. Environmental factors have an important role in initiating an immune process that ultimately leads to pancreatic beta cell destruction and clinically apparent diabetes mellitus.
Many environmental factors have been proposed, including viruses (rubella, mumps or coxsackievirus B4), toxic substances and cytotoxins. Before the eradication of rubella in most countries, congenital rubella was strongly associated with the development of type 1 diabetes mellitus (Menser et al., 1978). A recent meta analysis of observational studies has shown an association between type 1 diabetes and enterovirus infection (Yeung 2011). While some theories implicate viral infections in the pathogenesis of type 1 diabetes, a recent hypothesis argues that a decreased exposure to microbes may contribute to the current increase in autoimmune disease. This theory is known as “the hygiene hypothesis” (Gale, 2002).It is a known fact that the incidence of autoimmune diabetes follows a geographical pattern, with many studies reporting an association between type 1 diabetes and vitamin D status. A few large ecological studies describe a pattern of geographical variation, with an increased incidence of type 1 diabetes in the areas located north of the equator. Furthermore, seasons appear to also influence the incidence of type 1 diabetes, with the highest incidence during winter and the lowest during summer.
Typically, the treatment for type 1 diabetes mellitus involves insulin therapy, but in the last few years new therapies have been approved as well (for example, Symlin). For newly diagnosed patients with autoimmune diabetes, combination therapy has been suggested in an attempt to minimize beta cell destruction and prolong pancreatic function. The new therapeutic options include: immunotherapy, vaccines, drugs that influence T cell action, anti-inflammatory drugs (for example, one time use of anti-IL-1R drug), or long-term treatment with B cell components to induce regulatory T cells (oral or nasal insulin, insulin peptide therapy, GAD-Alum or the proinsulin DNA vaccines). Glucagon-like peptide 1-related drugs (GLP-1) could be also considered as a therapeutic option because they promote peritubular pancreatic cell growth (Von Herrath, 2010).5.
Vitamin DAlthough initially described as a “vitamin”, vitamin D is now recognized to be a hormone, synthesized in the human body and exerting its action on other organs via a nuclear receptor (vitamin D receptor, VDR).
Even though vitamin D can be obtained from the diet in small quantities, the main source of vitamin D is the skin.
Under the direct influence of ultra violet B light (UVB light), 7-dehydrocholesterol (DHC) (provitamin D3) is converted into pre-vitamin D3, which is then further converted into cholecalciferol (vitamin D3) via thermal isomerization. Interestingly, if pre-vitamin D3 continues to be exposed to UVB, it will be converted into biologically inactive metabolites (tachysterol and lumisterol), preventing a potential UVB- induced vitamin D intoxication (Holick, 1999) The other source of vitamin D is the diet, which contains cholecalciferol (vitamin D3), originating from animal sources, and ergocalciferol (vitamin D2), deriving from plants (Holick, 1999).Regardless of their source, once they enter into the circulation, forms of inactive vitamin D3 or D2 bind to the vitamin D-binding protein (DBP) and are transported to the liver. The inactive vitamin D is activated through a 2-step hydroxylation process via two hydroxylases that belong to the cytochrome P450- dependent steroid hydroxylases (CYP450). In the liver, vitamin D undergoes the first hydroxylation at C-25 via some of the CYP 450 vitamin D 25-hydroxylases, forming calcidiol (25-hydroxyvitamin D) (Prosser & Jones, 2004). The activity of 1?-hydroxylase in the immune cells is not under the regulation of parathyroid hormone and 1?-,25(OH)2D3, but rather under immune cytokine regulation. A defect in the up-regulation of 1?-hydroxylase after immune stimulation is described in NOD mouse (Overbergh et al., 2000). Extrarenal distribution of 1?-hydroxylase becomes important in understanding the extra-skeletal effects of vitamin D.VDR is part of the nuclear receptor super family of ligand-activated transcription factors, which also includes glucocorticoid, thyroid hormone and estrogen receptors. The gene for VDR is located on chromosome 12q12-14, and shows great polymorphism (Haussler et al., 1998). After 1,25 (OH)2D3 binds to VDR, it induces conformational changes that facilitate heterodimerization with the retinoid X receptor and the recruitment of nuclear receptor coactivator proteins, which then act on the chromatin.
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