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Therefore buy extra super viagra 200 mg free shipping, the notion of replenishing these agents through dietary intake in order to reduce joint symptoms has been proposed extra super viagra 200mg free shipping. Orally administered glucosamine is detectable at low levels in the sera of human subjects order 200 mg extra super viagra with amex, but there has been no direct demonstration that glucosamine is incorporated into cartilage (63) buy extra super viagra 200mg with visa. In the subjects who took 1,500 mg of glucosamine sulfate mixed with water, the serum glucosamine levels reached a maximum of 4. Based on the low serum levels achieved, the investigators concluded that it was unlikely that glucosamine contributed to proteoglycan synthesis in vivo. In addition to simply serving as building blocks of cartilage, glucosamine and chondrointin might affect the metabolism of cartilage constituents. It was shown in in vitro studies that glucosamine could stimulate proteoglycan synthesis by human chondrocytes and become incorporated into glycosaminoglycans (62,64). In animal studies, glucosamine reduced cellular production of inflammatory mediators and inflammation (65). Although the majority of earlier trials seem to suggest modest benefit in terms of pain relief as well as objective improvements, more recent meta- analyses of the studies indicated that the benefits might not be as great. One of the most widely cited clinical trials that showed benefits of glucosamine was carried out in Europe. At the end of the trial, the subjects who were treated with glucosamine had an average of 11. Overall, when compared with placebo, glucosamine showed a 28% improvement in pain and 21% improvement in function using the Lequesne Index. When the analysis was restricted to eight studies with the highest quality utilizing adequate allocation concealment, there was no improvement in pain or function (68). One study involved 120 subjects who took daily chondroitin in the form of 800 mg bovine chondroitin sulfate mixed in water or placebo for Months 0 to 3 and 6 to 9. The treatment group also had less radiographic changes than the placebo group (69). In subgroup analysis of subjects with moderate to severe pain, the combi- nation of glucosamine and chondroitin, but neither alone, was better than placebo at relieving symptoms. This apparent benefit, however, must be interpreted with caution because the positive control group of patients treated with celecoxib did not show improvement. There was a very high placebo-response rate of 60% and most of the patients had a mild degree of pain. Both of these effects may make it more difficult to detect differences between treatment arms. Other concerns raised included limitations induce the high attrition rate of 20% and the lack of sophisticated methodological analysis. Finally, the prepa- ration of glucosamine used in the study was glucosamine hydrochloride rather than glucosamine sulfate. Glucosamine sulfate is the form that is widely available in the United States and has been the preparation used in other studies reporting efficacy (11,71). The significance of using glucosamine hydrochloride preparation, rather than glucosamine sulfate, in this trial remains uncertain. Furthermore, the dosages are standardized based on rigorous efficacy and safety trials, and the 102 Part I / Introduction to Rheumatic Diseases and Related Topics manufacturers are required to collect and report their post-marketing experiences. Supplement preparations may or may not contain the correct dosages or even the advertised ingredients. Many of the herbal and dietary supplements have not undergone trials showing proof of efficacy or safety. Nonetheless, clinical trials have been carried out on several plant-based supplements. Ground up willow bark has been used as an analgesic and antipyretic remedy since ancient times dating to Egyptian, Greek, and Roman civilizations. Aspirin (acetylsalicylic acid) is a refined product of the willow bark extract salicin. In a 4-week randomized double-blind study, 210 patients with low back pain received low-dose (393 mg) or high-dose (786 mg) dry willow bark extract or placebo daily. The principle outcome measure was the number of patients who were pain-free and did not use a rescue analgesic for at least 5 days by the end of the study. After 6 months, both the high- and low-dose treatment groups (39 and 21%, respectively) were significantly less likely to have used the rescue analgesic than the placebo group (6%) (75). In this study, 78 patients were randomized to receive two tablets of willow bark (240 mg salicin per day) or placebo for 2 weeks after a washout period of 4 to 6 days with placebo. The efficacy of this agent needs further confirmation especially in trials longer than 4 weeks. The tubers of this perennial plant are used in African folk medicine for relief of pain caused by rheumatism. Significantly higher numbers of patients were pain-free in the treated groups compared with the placebo group (45). Ginger has a long history of medicinal use in the Chinese and Ayurvedic traditions. Rhizomes of several ginger species, in both oral and topical forms, are used to treat a variety of inflammatory and arthritic conditions. Extracts of ginger have been reported to decrease joint pain and swelling in patients with arthritis. Anti-inflammatory effects have been shown in in vitro and animal model experiments (77). The study was a double- blind, placebo-controlled clinical trial that spanned 6 weeks of treatment with ginger extract or placebo. The treatment group had greater improvement in primary outcome of reduction in knee pain on standing (63 vs 50%; p = 0. Patients who received the ginger extract had more gastrointestinal complaints (59 vs 21%), but the symptoms were mild. Based on these measurements the efficacy was ibuprofen ginger extract placebo. However, statistically significant effect of ginger extract was seen only by explorative statistical methods in the first period of treatment before crossover (79). Its long history of use dates back to 16th- century China, when its roots, leaves, and flowers were used for medicinal purposes. The modern-day medicinal form of the herb is derived from the root, not the flower or the vine (45). The therapeutic and adverse effects are likely due to diterpenoid compounds with epoxide structures. These compounds have been shown to have immunosuppressive and anti-inflammatory effects in in vitro and in vivo studies. Patients were randomized to placebo, low-dose (180 mg per day), or high-dose (360 mg per day) of Tripterygium extract. Beneficial effect was also seen in the low-dose group when compared with the placebo group (80). The number of patients who withdrew because of side effects was similar in both groups. Considerable toxicity has been associated with the use of Thunder God Vine in anecdotal reports. This herb has been used as an antipyretic and anti- inflammatory folk remedy for centuries. Its use dates back to ancient Greek civilization when it was prescribed to treat inflammations and hot swellings (45). The leaves can be chewed fresh or dried and made into tablets, which are available in the United States and Europe. It inhibits, in a dose-dependent fashion, the production of prostaglandins and leukotrienes by human polymorphonuclear leukocytes. Both crude feverfew extracts and purified parthenolide can inhibit adhesion molecule expression on rheumatoid synovial fibroblasts. Feverfew has an additional molecular mechanism of inhibiting the release of nuclear factor- B, an important transcription factor in the expression of multiple genes involved in the inflammatory process (45). Feverfew may increase bleeding time, thus, it should be avoided in patients with coagulopathy or on warfarin.

During the last two decades cheap extra super viagra 200 mg with mastercard, several new immunosuppressive agents have been tested in patients with myositis with inconsistent results cheap extra super viagra online amex, as is discussed further order 200 mg extra super viagra free shipping, and improved therapy is still required (812) purchase extra super viagra 200mg overnight delivery. Although muscle symptoms predominate, other organ systems are frequently affected. The type of skin rash varies and could affect all parts of the body, although the most characteristic rash is localized to the eyelids, characterized by a red or purple rash with edema, called heliotropic exanthema. Another typical skin rash for dermatomyositis is seen on the dorsal side of the finger joints or hand and is characterized by small red to purple slightly elevated papules (Gottrons papules). Chronic nonin- fectious inflammation causing symptoms like cough or breathlessness is common and could vary from mild to severe. Involvement of the respiratory muscles of the chest may also cause breathlessness and impairment of physical activities. Although the heart is a muscle, clinical manifestations of heart involvement are less common, but may occur and give rise to symptoms such as arrhythmia or congestive heart failure. Muscle Tissue Features A typical finding in polymyositis and dermatomyositis is inflammation in muscles and muscle fiber damage. The inflammation is characterized by the presence of inflam- matory cells such as lymphocytes and macrophages. This can be seen in muscle biopsies, which are helpful both for diagnosis and to exclude other muscle disorders. In the muscle tissue of patients with myositis, several inflammatory and immune- mediating molecules are produced. These are likely to be important for the clinical symptoms and for the muscle fiber damage and loss of muscle strength. These molecules are of interest as targets for new therapies that are more specific than gluco- corticoids and other immunosuppressants that are used today. A better under- standing of the key molecules that cause the disease could lead to the development of new and better therapies for patients with polymyositis or dermatomyositis. Molecules Present in Muscle Tissue in Inflammatory Conditions Cytokines are important signaling molecules in inflammatory responses and immune regulation. These cytokines are secreted by cells in the immune system and by endothelial cells in the lining of blood vessels. Endothelial cells control the passage of compounds and white blood cells into and out of the bloodstream (19). Hypoxia could also be a consequence of loss of microvessels, capillaries, in muscle tissue that is a typical finding in dermatomyositis. Interestingly, a loss of capillaries seems to be an early event in dermatomyositis. More recently, we have also observed a reduced number of capillaries in muscle tissue in patients with polymyositis (unpublished data). As oxygen supply is crucial for aerobic muscle metabolism, hypoxia can have several negative consequences that affect the working capacity of muscles and could also affect the nutritional status of patients with chronic muscle inflammation. Pharmacological Treatment As presented earlier, glucocorticoids have become the cornerstone of treatment since 1950 when they were first introduced. Although treatment with glucocorticoids made a dramatic improvement in patient survival, it soon became apparent that some patients with myositis do not respond at all and very few patients recover their former muscle performance. Furthermore, as also discussed previously, a disadvantage of high-dose glucocorticoid treatment is the substantial risk of side effects. For these reasons, combination therapies with other immunosuppressive agents have been developed. Today, glucocorticoids are still recommended as baseline treatment (starting doses of 0. Other therapies that are used in severe cases are cyclophosphamide, cyclosporine A, mycophenylate mofetile, tacrolimus or infusions with high doses of intravenous immunoglobulin. Only a few of these drugs have been tested in controlled trials of adequate size and duration to show beneficial effects. They are mostly used based on observed beneficial effects in occasional individuals or reported case series. Glucocorticoids can have profound negative effects on metabolism, making the immunosuppressive treatment of myositis an important issue with regard to nutritional status in patients with polymyositis and dermatomyositis. Prognosis Currently, there is only limited information available on the survival rate of patients with polymyositis and dermatomyositis. The few studies are mainly based on cohorts from one hospital; they are not population based and they include only a small number of patients. With this limitation in mind, the 5-year survival was estimated to be 95% and 10-year survival to be 85 or 89% in two recent papers (28,29). This may be a catabolic effect caused by the systemic chronic inflammation, or it may be a side effect of long-term glucocorticoid treatment, which is a well-known muscle catabolic agent. In patients with myositis, muscle wasting may also be caused by muscle atrophy and damage as a consequence of muscle inflammation, or to nutritional deficits depending on difficulties with swallowing. Because of the inflammatory process and to glucocorticoid treatment, muscle mass may be replaced by fat and muscle wasting may not always be signaled by weight loss. A more appropriate way to follow nutritional status is by assessment of body composition. This can be done by a dual energy X-ray absorptiometry scan, typically used for bone densitometry. Little detailed information on nutritional status is available in the literature that is specific for polymyositis and dermatomyositis. Here, we summarize available infor- mation that we find relevant for patients with myositis after a literature survey. The oxygen is provided to muscle by blood vessels including the small capillaries. By using the macronutrients carbohydrates (glycogen), proteins (amino acids) and fat (fatty acids and glycerol)energy is produced in the mitochondria in muscle cells, and the muscle will be able to contract (30). Glucocorticoids A special problem in patients with myositis that may affect nutritional status is their need for long-term (often over months to years), high-dose, glucocorticoids. Glucocorticoids are used to suppress muscle inflammation by acting on most cell types. The effects on T lymphocytes and macrophages are both direct and indirect, by influencing the mediators released by these cells (31,32). Via this mechanism, blocked gene expression of proinflammatory cytokines will occur and therefore the amount of these inflammatory molecules will decrease. As mentioned previously, it was noticed early that treatment with glucocorticoids had negative effects on muscles and may induce muscle atrophy and also a catabolic state. Glucocorticoids act in several ways to retard growth and promote muscle protein breakdown (35). Some strategies that could possibly be undertaken to counteract these negative effects of glucocorticoids are discussed later. Role of Exercise The catabolic effect of glucocorticoids on muscle tissue is likely to contribute to muscle wasting in patients with myositis who are also affected by catabolism from the muscle inflammation and from physical inactivity as well. In patients who have undergone renal transplant, the negative effect of low or moderate doses (1012 mg per day) of glucocorticoids on muscles was reversed by physical exercise. There are numerous benefits of exercise in terms of nutritional status in healthy individuals. Although many of these effects have not been evaluated specifically in patients with myositis, they could be assumed to be attributable to these patients. In healthy individuals, the muscle protein metabolism after exercise is negative and food intake is needed in order to gain muscle mass. Because patients with myositis already experience a catabolic state owing to glucocorticoid treatment, the post-exercise meal could be even more important to prevent further muscle protein breakdown. This is best achieved by digesting a combination of carbohydrates and protein after the exercise bout (52). It seems as if early post-exercise ingestion of a nutrient supplement, as opposed to ingestion 2 hours after training, enhances the anabolic effect of whole-body protein (53,54). The fact that patients with myositis are in a catabolic state caused by inflammation and steroid use, this approach, otherwise mostly used by athletes, might be of use in these patients.

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It also includes a definition of the terms: bioavailability including bioaccessibility and bioactivity buy on line extra super viagra. Likewise buy extra super viagra 200mg fast delivery, the main advan tages and disadvantages of these in vitro methods versus in vivo approaches 200 mg extra super viagra amex, the improve ment of these models with the inclusion of cell lines buy 200 mg extra super viagra fast delivery, and a short comment on the main effects that digestion and/or fermentation have on bioactive compounds are included. On the other hand, a short description is provided of the studies involving the use of human simulated gastrointestinal digestion and/or colonic fermentation procedures, and of the sub sequent bioactivity-guided assays with cell line models. Simulated gastrointestinal digestion assays Bioavailability is a key concept for nutritional effectiveness, irrespective of the type of food considered (functional or otherwise). Only certain amounts of all nutrients or bioactive com pounds are available for use in physiological functions or for storage. From the nutritional point of view, bioavailability is defined as the proportion of a nutrient or bioactive compound can be used for normal physiological functions [16]. This term in turn includes two additional terms: bioacces sibility and bioactivity. Bioaccessibility has been defined as the fraction of a compound that is released from its food matrix in the gastrointestinal tract and thus becomes available for intes tinal absorption. Bioaccessibility includes the sequence of events that take place during food digestion for transformation into potentially bioaccessible material, absorption/assimilation through epithelial tissue and pre-systemic metabolism. Bioactivity in turn includes events linked to how the bioactive compound is transported and reaches the target tissue, how it in teracts with biomolecules, the metabolism or biotransformation it may undergo, and the gen eration of biomarkers and the physiologic responses it causes [12]. Depending on the in vitro method used, evaluation is made of bioaccessibility and/or bioactivity. In vitro methods have been developed to simulate the physiological conditions and the se quence of events that occur during digestion in the human gastrointestinal tract. In a first step, simulated gastrointestinal digestion (gastric and intestinal stages, and in some cases a salivary stage) is applied to homogenized foods or isolated bioactive compounds in a closed 134 Oxidative Stress and Chronic Degenerative Diseases - A Role for Antioxidants system, with determination of the soluble component fraction obtained by centrifugation or dialysis of soluble components across a semipermeable membrane (bioaccessible fraction). Simulated gastrointestinal digestion can be performed with static models where the prod ucts of digestion remain largely immobile and do not mimic physical processes such as shear, mixing, hydration. Dynamic models can also be used, with gradual modifications in pH and enzymes, and removal of the dialyzed components thereby better simulating the actual in vivo situation. All these systems evaluate the aforementioned term bioaccessibili ty, and can be used to establish trends in relative bioaccessibility. The principal requirement for successfully conducting experimental studies of this kind is to achieve conditions which are similar to the in vivo conditions. Interactions with other food components must also be taken into account, since they can influence the efficiency of digestion [12, 17]. A recent overview of the different in vitro digestion models, sample conditions and enzymes used has been published by Hur et al. En lipophilic compounds such as carotenoids and phytosterols, it is necessary to form mixed micelles in the duodenal stage through the action of bile salts, phospholipases and colipase. This allows the compounds to form part of the micelles, where they remain until uptake by the enterocytes [18]. In the case of lycopene, during digestion isomerization of trans-lycopene may occur with the disadvantage that trans-isomers are less soluble in bile acid micelles [19]. Salivary and gastric digestion exert no substantial effect on major phenolic compounds. However, polyphenols are highly sensi tivity to the mild alkaline conditions in pancreatic digestion, and a good proportion of these compounds can be transformed into other unknown and/or undetected forms [20]. Bioactive compounds such as dietary fiber, carotenoids, polyphenols and phytosterols un dergo very limited absorption, and may experience important modifications as a result of actions on the part of the intestinal microbiota. Small intestine in vitro models are devoid of intestinal microbes, and are designed to only replicate digestion and absorption processes; as a result, they are unable to provide information on intestinal fermentation processes. The incorporation of colonic/large intestine fermentation offers a better approximation to the in vivo situation, and allows us to study the effect/interaction between these compounds and the intestinal microbiota. In vitro colonic fermentation models are characterized by the inoculation of single or mul tiple chemostats with fecal microbiota (of rat or human origin) and operated under phys iological temperature, pH and anaerobic conditions. There are two types of colonic fermentation models: batch culture and continuous cultures. Batch culture describes the growth of pure or mixed bacterial suspensions in a carefully selected medium with out the further addition of nutrients in closed systems using sealed bottles or reactors containing suspensions of fecal material under anaerobic conditions. The advantages of batch fermentation are that the technique is inexpensive, easy to set up, and allows large number of substrates of fecal samples to be tested. However, these models have their weakness in microbiological control and the need to be of short duration in or der to avoid the selection of non-representative microbial populations. Several of the pub lications in this field are based on a European interlaboratory study for estimation of the fermentability of dietary fiber in vitro [23]. Continuous cultures allow us to control the rate and composition of nutrient feed, bacterial metabolism and the environmental conditions. These models simulate proximal (single-state models) or proximal, transverse and distal colonic regions (multistage models). Continuous cultures are used for performing long-term studies, and substrate replenishment and toxic product removal are facilitated - thereby mimicking the conditions found in vivo. The most variable factor in these models is the technique used for fecal inoculation. The use of liquid fecal suspension as inoculum, where the bacterial populations are in the free-cell state, pro duces rapid washout of less competitive bacteria; as a result, the operation time is less than four weeks. The formation of fecal beads from the immobilization of fecal microbiota in a porous polysaccharide matrix allows release of the microbiota into the culture medium, with better reproduction of the in vivo flora and longer fermentation times [21, 22]. Artificial continuous models including host functions/human digestive functions have been developed. Models of this kind control peristaltic movement, pH and gastrointestinal secre tions. They incorporate some host functions; however, they do not reproduce immune modulating and neuroendocrine responses. A re maining challenge is the difficulty of establishing a representative human gut microbiota in vi tro. Combined systems that include the fractions obtained from simulated human digestion (gastrointestinal and/or colonic fermentation) and the incorporation of cell culture-based models allow us to evaluate bioaccessibility (estimate the amount of bioactive compounds assimilated from the bioaccessible fraction by cell culture) and to conduct bioactivity stud ies. The Caco-2 cell model is the most widely used and validated intestinal epithelium or hu man colon carcinoma cell model. Although colonic in origin, Caco-2 cells undergo spontaneous differentiation in cell culture to form a monolayer of well-polarized cells at confluence, showing many of the functional and morphological properties of mature human enterocytes (with the formation of microvilli on the brush border membrane, tight intercel lular junctions and the excretion of brush border-associated enzymes) [26]. However it must be mentioned that this cell line differs in some aspects from in vivo conditions. Likewise, the model lacks regula tory control by neuroendocrine cells and through the blood [27]. The combination of in vitro human intesti nal cell models with in vitro digestion models in turn creates an advanced in vitro model sys tem where samples obtained from host responses lacking in in vitro digestion models can be directly applied to monolayer cell models for host function studies [21]. Bioactivity of digested/fermented foods or related target bioactive compounds in cell lines The chemopreventive properties of bioactive compounds have been investigated in cultured cells exposed to individual compounds. However, gut epithelial cells are more likely to be exposed to complex food matrixes containing mixtures of bioactive and antioxidant in vivo compounds [6]. In addition, food matrixes undergo a digestion process that may affect the structure and properties of the bioactive compounds. Therefore, the in vitro protective ef fects of antioxidant bioactive compounds do not necessarily reflect in vivo chemoprotection, which is more likely due to the combined effects of all the bioactive components present in the food [28]. In addition, other mechanisms of chemoprevention could involve protection against genotoxic compounds or reactive oxygen species [31]. It recently has been stated that the measurement of cellular bioactivity of food samples cou pled to in vitro digestion can provide information close to the real-life physiological situation [32]. In this sense, we surveyed more than 30 studies conducted in the past 10 years, involv ing human simulated gastrointestinal digestion and/or colonic fermentation procedures and subsequent bioactivity-guided assays with cell line models. The chemopreventive effect of digested foods or bioactive constituents in cell lines is sum marized in Table 1. From the 22 studies surveyed, and according to the digestion meth od used, it can be seen that most of them involve solubility (n = 17) versus dialysis (n = 5).

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Vitamin B2 purchase cheap extra super viagra on line, 40 capsules (12 gm) stirred into honey or maple syrup (sterilized) and taken in a single dose cheap extra super viagra 200mg fast delivery. Vitamin D3 (cholecalciferol) 25 purchase extra super viagra canada,000 units daily trusted extra super viagra 200mg, to soften tumors by removing their calcium deposits. Take 40 500 mg capsules of glutathione (only 20 capsules on days 15-21) stirred into a beverage. Breakfast Take 10 drops phytic acid in cup water, then take 20 drops oregano oil, then take 2 gm vitamin C. Midmorning Take 40 300 mg capsules of vitamin B2, stirred into honey or sterilized maple syrup (only 20 capsules on days 15-21). Prepare the kidney (1 cups) and liver (2 cups) herb con- coctions to sip throughout the day. Day 9 Clear the toxins that emerged from your tumors yesterday using a low dose of glutathione and vitamin B2. Coenzyme Q10 remains at a high dose to continue catching dyes and other toxins being released from tumors. Take 10 500 mg capsules of glutathione stirred into honey (20 capsules on days 15-21). If you had less than one gallon, drink more liquids today and continue collecting. If you had more than one gallon, con- tinue to drink as much liquids and you can stop collecting urine. Continue to alternate high dose and low dose vitamin B2 and glutathione treatments. This is a compromise between high and low doses in order to accomplish some of each. If you were using the Topical Tumor Shrinkers, and you took last week off (because of hypervitaminosis A) you may be ready to resume (including oral vitamin A). If you have 4 or 5 large tumors, chances are they will open one at a time; this is an advantage. This will not happen unless even small leftover bits of dyes, asbestos, inorganic germanium and lanthanides have left the body. You should also assume you are reinfect- ing with parasites from raw unsterilized food. Find a dentist using digital X-rays to be sure there is no leftover plastic or a tattoo. If your mouth has the odor of decay, water pick for a whole day, one half hour on and one half hour off. Stop using any herb or spice or supplement from a can or bottle unless it is treated with vitamin B2 and hydrochloric acid. Of course, you have been reinfecting from your own draining tumors, too, which is unavoidable. Continue the high-dose, low-dose alternating regimen for vitamin B2 and glutathione during the third week if the scan still shows the original tumors. Continued Care If symptoms have subsided and the scan and blood test show improvement, continue the supplements at a reduced level of your own choosing. Gaining weight is the single mysterious event your body can accomplish if it is well. Your liver is not yet able to make and store sugar or change stored sugar to blood sugar. Adding dairy foods (Kosher only, properly steril- ized), will help you reach this. Digestive enzymes (see Sources) can help greatly in relieving an over-full feeling, especially when sup- plements take up so much room. You might also wish to remain discreetly silent about it in order not to offend him/her. There is an element of mystique created around test results in order to keep them off-limits to patients and hold them hostage. Not only can you learn to interpret blood test results, you can learn not to panic or take up doctors time needlessly. Sharpen this new talent on all the blood test results given for the case histo- ries, and then apply it to yourself. Remember, though, not to add your state of psychological distress over reading your own blood test to your doctors burden. Find solace in the fact that you are going to learn to solve most problems yourself, right now! Your blood test results are easy to understand, although the form looks complicated. The normal results will be given as a range because healthy people can be expected to vary to some extent. Your first step is to fit your result into the normal range given on your printout to see whether it is above, below, or in the middle of it. The Perfect Blood Test Photocopy the next page and use it as a bookmark and refer- ence while reading this chapter and the case histories (True Sto- ries) that follow. To understand the meaning of a result using a different range, you should know how the range was decided. One of the very large testing labs analyses the blood sugar results for, say, the last 10,000 patients it has tested. It is as- sumed that they represent the healthy population (which is, of course, not true, since illness brought them to the lab for testing to begin with). Then ninety-five percent of all these patients results are clustered around this average to make a normal curve. If, in reality, only 80% are healthy, very many people are not being attended and conse- quently not being alerted to the need for improvement because they are assigned to the normal group. A concept of sick or not sick depending on whether you fit into the values seen for 95% of the patient population is misleading. Dont let a physicians reassurance that everything is normal fool you into thinking you are normal (meaning healthy). Your standard should be higher than statistically normal, your standard should be healthy. I determined them by ob- serving at least two thousand patients closely, most with a series of tests that spanned a period from the time they arrived with 111 Berkow, R. It is based on judgment, not statistics, and it wouldnt surprise me if others disagree with me. However the body stays surprisingly constant when it is healthy, making the task of identifying healthy values fairly easy. Sometimes your laboratory will have a wildly different range for a particular test than the ranges I have listed, even though the units are identical! You should scale your re- sult, then, before comparing it to the ranges in my chart. For ex- ample if your labs range goes from 240 to 380 but our labs range goes from 120 to 200, you can assume that your labs procedures roughly double the results. Therefore you must di- vide your result in half before comparing it to our labs range. The liver should always be able to make blood sugar for you, even if you have not eaten recently. If yours is below eighty, the liver is not able to keep your level up, either because its stores are empty, or for other reasons. Cancer patients have a special disability in that part of their liver metabolism that makes and stores blood sugar. At the same time, cancer patients use up more blood sugar than normal, healthy persons, so the blood sugar drops as cancer advances. If your blood sugar is already below seventy, you must eat throughout the day to re-nourish your body. You must work hard to eat enough high calorie, nu- tritious food to keep this figure from dropping.