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Type 1 Diabetes Causes We know that in type 1 diabetes ultimately the insulin-producing cells of the pancreas are destroyed cheap sildalis line how to get erectile dysfunction pills, in most cases by the body’s own immune system order sildalis in india erectile dysfunction foods, but what triggers this destruction can vary from one person to another discount sildalis amex erectile dysfunction drugs dosage. Genetic factors may predispose the insulin-producing cells to damage through either impaired defense mechanisms, immune system oversensitivity, or some defect in tissue regeneration capacity. The entire set of genetic factors linked to type 1 has been termed “susceptibility genes,” as they modify the risk of diabetes but are neither necessary nor sufﬁcient for disease to develop. These results and others indicate that environmental and dietary factors are more important than a true genetic predisposition in most cases. Such a rise simply cannot be explained by an increased number of people genetically predisposed to type 1. Changes to the human genetic code across large populations take much more than one generation to occur. Environmental and Dietary Risk Factors Accumulating data indicate that abnormalities of the gut’s immune system may play a fundamental role in the immune attack on beta cells and the subsequent development of type 1. What appears to happen in the development of some cases of type 1 is the development by the gastrointestinal immune system of antibodies that ultimately attack the beta cells. It is interesting to consider that poor protein digestion may contribute to type 1. Poorly digested dietary proteins can cross-react with proteins on or within the beta cells of the pancreas. In humans, two dietary proteins that may be incriminated are those found in milk (which contains bovine serum albumin and bovine insulin) and wheat (which contains gluten). For example, dietary bovine insulin differs from human insulin by only three amino acids. If a person develops antibodies to bovine insulin, there is a good chance that these antibodies will also attack the person’s own insulin. In addition to causing antibody-mediated destruction of the beta cells, bovine insulin is able to activate T cells in those predisposed to diabetes in a manner that can lead to beta cell destruction by direct attack by T killer cells. Strong evidence implicates dietary factors such as cow’s milk and gluten as important triggers of the autoimmune process that lead to type 1. In contrast, breastfeeding has been identiﬁed as an important factor in establishing proper intestinal immune function and reducing the risk of type 1. It is well known that breastfeeding confers a reduction in the risk of food allergies, as well as better protection against both bacterial and viral intestinal infections. In case-controlled studies, patients with type 1 were more likely to have been breastfed for less than three months and to have been exposed to cow’s milk or solid foods before four months of age. A critical review and analysis of all relevant citations in the medical literature indicated that early cow’s milk exposure may increase the risk about 1. There is also considerable evidence that sensitivity to gluten—the major protein component of wheat, rye, and barley—may also play a role. Celiac disease, like type 1 diabetes, is associated with intestinal immune function abnormalities. And, as with diabetes, breastfeeding appears to have a preventive effect, while the early introduction of cow’s milk is believed to be a major causative factor. Not surprisingly, the highest levels of antibodies to cow’s milk proteins are found in people with celiac disease. All of these viruses replicate in the gut and cause stimulation of the intestinal immune system; this may activate the insulin-speciﬁc immune cells to seek out and destroy beta cells. These viruses and others are also capable of infecting pancreatic beta cells, causing the leukocytes to attack and destroy the beta cells in an attempt to kill the virus. Another possibility is that gastrointestinal virus infections may increase intestinal permeability, leading to absorption of the intact protein; this then enhances the antibody response to dietary bovine insulin. The severe “leaky gut” or increased small-intestine permeability that occurs during and for some time following rotavirus infections (one of the most common causes of acute diarrheal illness in children) exposes the gut-associated immune cells to large quantities of intact proteins. Vitamin D Deficiency Emerging evidence indicates that vitamin D supplementation from cod liver oil and other sources during early childhood can prevent type 1 diabetes. One study found that the use of vitamin D from cod liver oil during pregnancy signiﬁcantly reduced the frequency of type 1 in their children. Because vitamin D can be produced in the body by the action of sunlight on the skin, lack of sun exposure during childhood may also play a role and partially explain the higher type 1 rates in northern countries. In recent observational studies, vitamin D has been shown to prevent the development of autoimmune conditions, including attacks on beta cells; the degree of protection is dose dependent. The mechanisms responsible for this effect may be related to improved cell membrane function, leading to enhanced antioxidant status and suppression of the formation of inflammatory compounds known as cytokines. Nitrates are produced by agricultural runoff from fertilizers; they are also used in cured or smoked meats such as ham, hot dogs, bacon, and jerky to keep the food from spoiling. Infants and young children are believed to be particularly vulnerable to the harmful effects of nitrate exposure. One of the most alarming features of type 1 is that it is becoming much more prevalent, with a current growth rate of 3% per year worldwide. Increased nitrate exposure may be a key factor; nitrate levels in ground and surface waters of agricultural regions have increased over the past 40 years. Nitrate contamination occurs in geographic patterns related to the amount of nitrogen contributed by fertilizers, manure, and airborne sources such as automobile and industrial emissions. Nitrate exposure may explain why some geographic pockets have a substantially higher rate of type 1. Parents would do well to break the habit of feeding children hot dogs, cold cuts, and ham. Health food stores now carry nitrate-free alternatives to these rather toxic food choices. Also, investing in a high-quality water purifier is good insurance against ingesting nitrate-contaminated drinking water. Early Treatment and Possible Reversal of Type 1 Diabetes Early intervention in type 1 designed to affect the autoimmune or oxidative process theoretically may be capable of lengthening the “honeymoon” phase (the time before insulin becomes absolutely necessary) or even completely reversing the damage. Two substances that may have some beneﬁt in this regard are niacinamide and epicatechin. Niacinamide The niacinamide form of vitamin B3 has been shown to prevent some of the immune-mediated destruction of pancreatic beta cells and may actually help to reverse the damage. In a study of newly diagnosed type 1 diabetics, seven patients were given 3 g niacinamide per day and nine were given a placebo. After six months, ﬁve patients in the niacinamide group and two in the placebo group were still not taking insulin and had normal blood glucose and hemoglobin A1C. At 12 months, three patients in the niacinamide group but none in the placebo group were in clinical remission. As of 2004, there had been 12 studies of niacinamide treatment in patients with recent-onset type 1, or type 1 of less than ﬁve years’ duration, and who still had some functional beta cells. Of 10 double- blind, placebo-controlled studies, 5 showed a positive effect compared with a placebo in terms of prolonging the period in which insulin was not yet required, lower insulin requirements when the hormone was required, improved metabolic control, and increased beta cell function as determined by secretion of a substance known as C-peptide. In the 5 studies that showed a positive result, patients had a higher baseline fasting C-peptide level, and patients were generally older than in the negative studies. The ﬁrst of these studies, the Deutsche Nicotinamide Intervention Study, did not show much of an effect with 1. It is possible that such a formulation did not allow for sufﬁcient peak levels of niacinamide to block autoimmune mechanisms.
Tamoxifen and gallstone formation in postmenopausal breast cancer patients: retrospective cohort study 120mg sildalis for sale erectile dysfunction fatigue. Aging per se is an independent risk factor for cholesterol gallstone formation in gallstone susceptible mice purchase sildalis with visa erectile dysfunction medication does not work. Lack of correlation between serum lipoproteins and biliary cholesterol saturation in patients with gallstones discount generic sildalis uk erectile dysfunction protocol + 60 days. Relationship between main bile components, serum cholesterol and serum triglycerides. Inﬂuence of legume intake on biliary lipids and cholesterol saturation in young Chilean men. Gallstone formation in hamsters: effect of varying animal and vegetable protein levels. A buckwheat protein product suppresses gallstone formation and plasma cholesterol more strongly than soy protein isolate in hamsters. Stronger suppression of plasma cholesterol and enhancement of the fecal excretion of steroids by a buckwheat protein product than by a soy protein isolate in rats fed on a cholesterol-free diet. A buckwheat protein product suppresses 1,2-dimethylhydrazine-induced colon carcinogenesis in rats by reducing cell proliferation. Diet and gall stones: effects of reﬁned and unreﬁned carbohydrate diets on bile cholesterol saturation and bile acid metabolism. Glycemic load, glycemic index, and carbohydrate intake in relation to risk of cholecystectomy in women. Dietary risk factors for clinically diagnosed gallstones in middle-aged men: a 25-year follow-up study (the Zutphen Study). Cholelithiasis and dietary risk factors: an epidemiologic investigation in Vidauban, southeast France. International Journal of Obesity and Related Metabolic Disorders 1995; 19: 593–595. Coffee stimulation of cholecystokinin release and gallbladder contraction in humans. Coffee intake is associated with lower risk of symptomatic gallstone disease in women. Phosphatidylcholine-enriched diet prevents gallstone formation in mice susceptible to cholelithiasis. Olive-oil-enriched diet: effect on serum lipoprotein levels and biliary cholesterol saturation. Dietary ﬁsh oil effects on biliary lipid secretion and cholesterol gallstone formation in the African green monkey. Dietary fish oil inhibits cholesterol monohydrate crystal nucleation and gallstone formation in the prairie dog. Fish oil increases bile acid synthesis in male patients with hypertriglyceridemia. Fish oil (n-3) polyunsaturated fatty acids beneﬁcially affect biliary cholesterol nucleation time in obese women losing weight. Medicinal treatments of cholesterol gallstones: old, current and new perspectives. Adjunct to bile-acid treatment for gall-stone dissolution: low-dose chenodeoxycholic acid combined with a terpene preparation. Pilot study of combination treatment for gall stones with medium dose chenodeoxycholic acid and a terpene preparation. Changes in the content and composition of collagen in the glaucomatous eye—basis for a new hypothesis for the genesis of chronic open-angle glaucoma. Regional differences in the structure of the lamina cribrosa and their relation to glaucomatous optic nerve damage. Further contributions on the value of osmotic substances as means to reduce intra-ocular pressure. Clinical evaluation of glycerin-sodium ascorbate solution in lowering intraocular pressure. Effects of Mirtogenol on ocular blood ﬂow and intraocular hypertension in asymptomatic subjects. Effect of Ginkgo biloba extract on preexisting visual ﬁeld damage in normal tension glaucoma. The effect of oral magnesium therapy on visual field and ocular blood flow in normotensive glaucoma. The effects of mild, moderate, and severe exercise on intraocular pressure in glaucoma patients. Effect of bicycle ergometer test on intraocular pressure in elderly athletes and controls. Gout and the risk of type 2 diabetes among men with a high cardiovascular risk proﬁle. Beneﬁcial effects of weight loss associated with moderate calorie/carbohydrate restriction, and increased proportional intake of protein and unsaturated fat on serum urate and lipoprotein levels in gout: a pilot study. Inhibitory action of quercetin on xanthine oxidase and xanthine dehydrogenase activity. School of Medicine, The University of Queensland, Brisbane, Queensland, Australia, 1991–1992. Department of Orthopaedics, Kovai Medical Center and Hospitals, Coimbatore, India, 1995. Glutathione, glutathione S-transferase and reactive oxygen species of human scalp sebaceous glands in male pattern baldness. Effect of oral intake of choline-stabilized orthosilicic acid on hair tensile strength and morphology in women with fine hair. Speciﬁc immunotherapy for allergic rhinitis to grass and tree pollens in daily medical practice—symptom load with sublingual immunotherapy compared to subcutaneous immunotherapy. Daily quercetin supplementation dose-dependently increases plasma quercetin concentrations in healthy humans. The variable plasma quercetin response to 12-week quercetin supplementation in humans. Effect of enzymatically modiﬁed isoquercitrin, a ﬂavonoid, on symptoms of Japanese cedar pollinosis: a randomized double-blind placebo-controlled trial. Preventative effect of a ﬂavonoid, enzymatically modiﬁed isoquercitrin on ocular symptoms of Japanese cedar pollinosis. Clinical effects of apple polyphenols on persistent allergic rhinitis: a randomized double-blind placebo-controlled parallel arm study. Journal of Investigative Allergology and Clinical Immunology 2006; 16(5): 283–289. The effectiveness of physiotherapy and manipulation in patients with tension- type headache: a systematic review.
They should also watch their consumption of foods with moderate levels of purine order sildalis online now erectile dysfunction hypogonadism, including dried legumes discount 120 mg sildalis mastercard impotence at 52, spinach order 120mg sildalis visa erectile dysfunction medicine pakistan, asparagus, other types of fish, poultry, and mushrooms. Low-Oxalate Diet Dietary oxalate may be responsible for as much as 80% of the urine oxalate in some people with recurrent kidney stones, indicating that restricting dietary oxalate intake may have a protective action. A low-oxalate diet is usually deﬁned as one containing less than 50 mg oxalate per day, so foods that have high or moderate levels of oxalate should be avoided. Oxalate Content of Selected Foods Very high oxalate, >50 mg per serving • Vegetables Beets (greens or root) Okra Spinach Swiss chard • Fruits Figs, dried Rhubarb • Grains Buckwheat • Nuts and seeds Almonds Peanuts Peanut butter Sesame seeds High oxalate, >10 mg per serving • Vegetables Celery Collards Dandelion greens Eggplant Escarole Green beans Kale Leeks Parsley Parsnips Peppers, green Potatoes Pumpkin Squash, yellow summer Sweet potatoes Tomato sauce, canned Turnip greens Watercress • Fruits Concord grapes Kiwi Lemon peel Lime peel Orange peel • Grains Bread, whole wheat Oatmeal Popcorn Spelt Wheat bran Wheat germ Whole wheat flour • Legumes Garbanzo beans Lentils Soybeans and all soy products • Nuts and seeds Brazil nuts Hazelnuts Pecans Sunflower seeds • Miscellaneous Beer Chocolate Cocoa Soy sauce (1 tbsp) Tea, black or green Moderate oxalate, 6 to 10 mg per serving • Vegetables Asparagus Artichokes Broccoli Brussels sprouts Carrots Cucumber Garlic Lettuce Mushrooms Mustard greens Onions Pumpkin Radishes Snow peas Tomato, fresh Tomato sauce, canned (1/4 cup) • Fruits Apples Apricots Blackberries Blueberries Cherries, sour Cranberries, dried Currants, black Oranges Peaches Pears Pineapple Plums Prunes Red raspberries Tangerines • Grains Bagel (1 medium) Barley, cooked Bread, white (2 slices) Corn Corn tortilla (1 medium) Cornbread Cornmeal, yellow (1 cup dry) Cornstarch (1/4 cup) Pasta Rice, brown Spaghetti White flour • Legumes Lima beans Split peas • Nuts and seeds Cashews Flaxseed Walnuts • Herbs Basil, fresh (1 tbsp) Dill (1 tbsp) Ginger, raw, sliced (1 tsp) Malt powder (1 tbsp) Nutmeg (1 tbsp) Pepper (1 tsp) • Miscellaneous Coffee Red wine Sardines Tea, rose hip Low oxalate, 2 to 5 mg per serving • Vegetables Acorn squash Arugula Ketchup (1 tbsp) Onions Peppers, red Zucchini • Fruits Avocado Cantaloupe Cherries, sweet Cranberries Grapes Lemons Limes Raisins • Grains Rice, white Rice, wild Rye bread • Legumes Peas, green • Nuts and seeds Coconut • Herbs Cinnamon, ground (11/2 tsp) Ginger, powdered (1 tbsp) Mustard, Dijon (1/4 cup) Thyme, dried (1 tsp) • Miscellaneous Beef Chicken Corned beef Eggs Fish (haddock, plaice, and flounder) Ham Lamb Pork Turkey Venison Nutritional Supplements Vitamin C Vitamin C is often cited in the medical literature as a potential factor in the development of calcium oxalate kidney stones. However, numerous studies have now clearly demonstrated that high doses of vitamin C do not cause kidney stones. Studies have shown that vitamin C ingestion of up to 10 g per day does not have any effect on urinary oxalate levels. One trial showed that 120 mg inositol hexaphosphate signiﬁcantly reduced the formation of calcium oxalate crystals in the urine of people with a history of kidney stone formation, in only 15 days. Since dietary management is effective, relatively inexpensive, and free of side effects, it is the treatment of choice. The speciﬁc treatment is determined by the type of stone and may include reducing urinary calcium, reducing purine intake, avoiding high-oxalate foods, increasing foods high in magnesium-, and increasing foods rich in vitamin K. Note: In acute cases, surgical removal or breaking up the stone with sound waves (lithotripsy) may be necessary. For Calcium Stones Diet Follow the general recommendations given in the chapter “A Health-Promoting Diet. Increase consumption of magnesium-rich foods (barley, bran, corn, buckwheat, rye, soy, oats, brown rice, avocados, bananas, cashews, coconut, peanuts, sesame seeds, lima beans, potatoes). For Cystine Stones • Avoid methionine-rich foods (soy, wheat, dairy products, ﬁsh, meat, lima beans, garbanzo beans, mushrooms, and all nuts and seeds except coconut, hazelnuts, and sunflower seeds) • Alkalinize the urine by eating an alkaline-rich diet and taking magnesium citrate (250 mg elemental magnesium three times daily): optimal pH is 7. Degeneration of the macula is the leading cause of severe visual loss in the United States and Europe in people 55 or older, and is second to cataracts as the leading cause of decreased vision in people over 65. It is estimated that more than 150,000 Americans are legally blind from age-related macular degeneration, with 20,000 new cases occurring each year. However, decreased blood and oxygen supply to the retina is the key factor leading to macular degeneration. The patient may note that straight objects appear distorted or bent, that there is a dark spot near or around the center of the visual ﬁeld, and that, while he or she is reading, parts of words are missing. This extrusion, which can be seen with the aid of an ophthalmoscope, is referred to as drusen. The disease progresses slowly, and only central vision is lost; peripheral vision remains intact. Because the disease can rapidly progress to a point at which laser surgery cannot be used, treatment should be performed as soon as possible. These drugs can shrink the abnormal blood vessels and improve vision when injected directly into the vitreous humor of the eye. Examples of these agents include ranibizumab (Lucentis), bevacizumab (Avastin), and pegaptanib (Macugen). While a number of genetic markers have been identiﬁed, a family history may be the easiest screening method. The lifetime risk of developing late-stage macular degeneration is 50% for people who have a relative with macular degeneration, vs. Presumably this protection is the result of greater intake of antioxidant vitamins and minerals. The macula, especially its central portion, the fovea, owes its yellow color to its high concentration of lutein and zeaxanthin. These yellow carotenoids function in preventing oxidative damage to the area of the retina responsible for ﬁne vision and have a central role in protecting against the development of macular degeneration. It is important to note that beer consumption increases drusen accumulation and the risk of exudative macular disease and therefore should be avoided. Fifteen of the treated patients showed improvement in their vision by one line or more on a vision acuity chart, compared with only 6 of the control group. In addition, only 3 of the 38 in the treatment group lost one line or more of vision, compared with 13 in the control group. In a randomized, double-blind, placebo-controlled trial, 5,442 female health care professionals 40 years or older with preexisting cardiovascular disease or three or more cardiovascular disease risk factors randomly received a combination of folic acid (2. Patients receiving lutein (10 mg) alone or in combination with other vitamins and minerals in a broad-spectrum supplementation formula showed improvements in visual function. Flavonoid-Rich Extracts Flavonoid-rich extracts of bilberry (Vaccinium myrtillus), ginkgo biloba, grape seed, or pine bark (e. In addition to exerting excellent antioxidant activity, all of these extracts have been shown to have positive effects on retinal blood ﬂow and function. The anthocyanosides of bilberry have a very strong afﬁnity for the retinal pigmented epithelium, reinforcing the collagen structures of the retina and preventing free radical damage. However, ginkgo biloba extract (24% ginkgo ﬂavonglycoside content) is perhaps a better choice if a person is also showing signs of decreased blood flow to the brain. Because free radical damage and lack of blood and oxygen supply to the macula appear to be the primary causes of macular degeneration, consumption of antioxidant supplements and promotion of retinal blood flow are the keys to effective treatment. Six to 12 months without a menstrual period is the commonly accepted rule for diagnosing menopause. The time prior to menopause is referred to as perimenopause, and the time after menopause is referred to as postmenopause. During perimenopause, many women ovulate irregularly, owing to either decreased secretion of estrogen or resistance of the remaining follicles to ovulatory stimulus. Many conventional doctors still see menopause as a disease rather than a normal physiological process. This view is in stark contrast to the perspective of many cultures, where menopause is viewed as a natural part of the life process and a positive event in a woman’s life. In fact, in many parts of the world, most women do not experience the symptoms Americans tend to associate with menopause. This observation raises some interesting questions about menopause as a sociocultural event. However, there are certainly important dietary and environmental factors to consider as well. The goal of this chapter is to answer that question and provide a natural approach to menopause and the postmenopausal period. Causes Menopause is thought to occur when there are no longer any viable eggs left in the ovaries. This number drops to around 300,000 or 400,000 at puberty, but only about 400 of these ova will actually mature during the reproductive years. With age, the absence of active follicles (the cellular housing of the egg) results in reduced production of estrogen and progesterone.