6 Signs of Childhood Diabetes

Diabetes is an increasingly prevalent chronic disease among children. However, recognizing the symptoms of diabetes is a challenge for most parents.  Childhood

Signs of Childhood Diabetesdiabetes might not be recognized until the child is very ill primarily because the changes are usually subtle and the onset is quite slow. Although discovering that your child is suffering from diabetes can be distressing for any parent, it is better to find out early enough than to miss the signs of diabetes completely.

What are the signs of diabetes in children?

  1. Unquenchable Thirst

Children with undiagnosed diabetes are constantly thirsty.Signs of diabetes in children This is mainly because as blood glucose builds up in the bloodstream, more fluid is pulled from the body tissues. Moreover, these children may crave cold drinks and sweets. In case the water in the blood is not sufficient, the body extracts water from surrounding tissues. Therefore, the body becomes dehydrated and the thirst mechanism kicks in.

  1. Frequent Urination

The urge to urinate a lot is one of the most common early signs of childhood diabetes. In this case your child goes to the restroom more often than normal or starts wetting the bed all of a sudden even though they were toilet trained before. Since the child is drinking more, they will also visit the restroom more. However, there can be other reasons for frequent urination such as the inability of the child to empty the bladder completely, urinary tract infection or Daytime Urinary Frequency Syndrome which is formally known as Pollakiuria.

  1. Rapid Loss in Weight

This is an extreme symptom of diabetes in children mainly because children rarely lose weight. In this case, the child still loses weight even when they continuously consume plenty of food. Weight loss is usually caused by inadequate supply of energy in the body. Therefore, the body extracts energy from reserved fat stores. Besides making the immune system weaker, excessive weight loss in children might also result in weakness and tired feelings. Drastic weight loss in children is a very dangerous sign whether diabetes is involved or not and the child should be taken to the doctor immediately.

  1. Yeast Infection

Excessive weight loss makes the immune system weaker and prone to plenty of infections. The child might develop rashes on the skin due to yeast infection. Therefore, it is vital to give your child plenty of water to drink and feed him/her a healthy diet.

  1. Extreme Hungersymptoms of diabetes in children

A child suffering from diabetes might eat constantly without gaining weight. This can be attributed to inability of the body to utilize food and in effect the food simply flows through the child’s digestive system.

  1. Blurred Vision

The decreased level of fluid in the blood and body tissues including the eye lenses might create vision difficulties. This might cause various eyesight problems including blurred vision. Unfortunately, the child might be unable to detect or even complain about problems with their eyesight.

Untreated diabetes might have serious consequences for the child. Some of the short term risks include hypoglycemia (low blood sugar), hyperglycemia (high blood sugar), and increased ketones in urine (ketoneacidosis). Some of the lifelong or long term risks include; nerve and vascular damage, amputations, blindness, and increased risk of stroke and heart attack. Besides identifying the signs of diabetes in children, it is also the parents’ responsibility to ensure that the child gets proper diagnosis and also takes medication as instructed by the doctor.

Other Signs of Childhood Diabetes

diabetes in children
Signs of Diabetes in Children

Breath that smells sweet and like fruit is one of the warning signs of childhood diabetes. This symptom can also be sneaky in that it may be explained absent from the fruity flavored toothpastes that youngsters use as of late or from the nutritious fruit snacks that they’re fed. The sweet scent of their breath is really a consequence of diabetic ketoacidosis, that is the body’s attempt to get rid of acetone through the respiratory system. Sweet smelling breath is often a signal that poisonous ketones (acid by-products of fats being broken down for power) are constructing up inside the entire body. This symptom out of many signs of childhood diabetes is really a indicator that they urgently demand diabetes medication.

Get Childhood Diabetes under Control!

Good eating habits and regular exercise, even for your children (and for yourselves as role models) goes a very long way to stabilising Childhood Diabetes.

What are signs of Diabetes in Children

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Is diabetes heredity?

is diabetes hereditary
is diabetes hereditary

Is diabetes hereditary is a question that a growing number of people are asking. This is especially true now that diabetes rates are increasing each and every day, and as of now juvenile diabetes is fast becoming the single biggest chronic health problem faced by the modern population of young people. The answer to is diabetes hereditary isn’t always apparent and studies have been going on for years to answer the question and yet a clear answer is not forthcoming as doctors, scientists, and analysts struggle to find the single greatest causative factor for the disease in the hopes that once the cause is found a cure will soon follow. Diabetes may well be genetically induced and if so then the defective gene may be some day isolated so that prenatal diagnosis can be made and perhaps a cure found through gene therapy and or in-vitro treatments. Though as of this writing such types of therapy belong in the realms of science fiction rather than in the realm of what is medically possible with the limited amount of knowledge and technology available today.

For many people the question is diabetes hereditary is one that is asked when they or a family member has the disease and they want to know the chances of passing it on to their children, either before having children or in order to be more vigilant for symptoms in the children they already have. Diabetes can be a heredity thing and the best thing that you can do in order to prevent yourself from getting diabetes and making sure that you take care of yourself as well as your health is to make sure that you get plenty of diet and exercise. By eating right and making sure that you take care of yourselves you can rest assured that in the long run you can possibly prevent yourself from getting an illness such as diabetes and also make sure that you can live a longer, healthier life.

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Is Type 1 Diabetes Hereditary?

 

is type 1 diabetes hereditary
is type 1 diabetes hereditary

Is Type 1 diabetes hereditary is a question that a growing number of people are asking.

This is especially true now that diabetes rates are increasing each and every day, and as of now juvenile diabetes is fast becoming the single biggest chronic health problem faced by the modern population of young people. The answer to is type 1 diabetes hereditary isn’t always apparent and studies have been going on for years to answer the question and yet a clear answer is not forthcoming as doctors, scientists, and analysts struggle to find the single greatest causative factor for the disease in the hopes that once the cause is found a cure will soon follow. Diabetes may well be genetically induced and if so then the defective gene may be some day isolated so that prenatal diagnosis can be made and perhaps a cure found through gene therapy and or in-vitro treatments. Though as of this writing such types of therapy belong in the realms of science fiction rather than in the realm of what is medically possible with the limited amount of knowledge and technology available today.

For many people the question is type 1 diabetes hereditary is one that is asked when they or a family member has the disease and they want to know the chances of passing it on to their children, either before having children or in order to be more vigilant for symptoms in the children they already have. It does seem that there is an increased risk of developing type 1 diabetes if a parent, especially the father has the disease, and an even greater chance if a sibling has it. When a person asks themselves is type 1 diabetes hereditary they should remember that even though there may be an increased risk of the disease in those with close family who have the disease there is absolutely no guarantee that they or their offspring will ever develop diabetes.

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Diabetes Mellitus and Tuberculosis: The Science of Denial by Dr. Lawrence Broxmeyer

Diabetes Mellitus and Tuberculosis

Summary The thought that tuberculosis and its family of mycobacteria could cause diabetes seems farfetched, but is not.

If this weren’t true, then why would the Massachusetts General Hospital recently announce human trials with dilute cow tuberculosis (BCG) to attempt cure of type 1 juvenile diabetes, a disease historically thought by some to be caused by human tuberculosis. In nature, strains of tuberculosis, animal or human, have long been known to compete, change and destroy one another. And they do this through attack with their viral mycobacteriophage armament, which live inside all strains of tuberculosis. So injecting BCG into diabetic patients has nothing to do with “bolstering their immunity”, a favored explanation among trial investigators. It has to do rather with hand-to-hand viral phage (mycobacteriophage) combat between the dilute cow tuberculosis being injected and a prime suspect for the cause of the disease itself, human tuberculosis.

The peculiar relationship and frequent association of diabetes mellitus and tuberculosis has been observed for more than 2000 years, yet the reason for this is, to this day, not known. Before the discovery of insulin, a diagnosis of diabetes was a death sentence within 5 years, and the usual cause of that death was tuberculosis.

In the 5th century, tuberculosis was already being portrayed as a ‘‘complication” of diabetes, a view little changed to this day, parroting Root’s original 1934 description of ‘‘a one-sided relationship”: tuberculosis still seen as a common complication of diabetes, while diabetes is thought to be no more common among TB patients than in the population at large. To Nichol’s, this was ‘‘not logically tenable” and in his study of 178 otherwise healthy, non-diabetic military men with tuberculosis at Fitzsimmons Army Hospital, one-third had abnormal glucose screening tests. But despite his findings and those of Reaud in New York as well as others, this was not being recognized elsewhere, and Nichols wanted to know why. His conclusion: that the incidence of diabetes among tuberculosis patients was considerably underestimated and that in tuberculosis patients, diabetes develops quite commonly. Diabetes was easy to detect. Tuberculosis and the mycobacteria were not.

The evidence for a tubercular cause of diabetes is mounting. Schwartz and Haas both linked Type-2 diabetes to tuberculosis. And the pancreatic islet amyloid deposits that they found as a by-product of systemic tubercular infection have recently been dissolved by rifampicin, a first line drug against tuberculosis. Engelbach spoke of ‘‘transitory” diabetes in TB and Karachunskii noted that patients with tuberculosis commonly wound up with insulin deficiency and persistently high blood sugars. Furthermore tubercular proteins have been shown recently not only to cause ‘‘autoimmune” Type-1 diabetes in NOD (non-obese diabetic) mice, but act as a vaccine to stop the inevitable diabetes that would otherwise materialize. The documentation of patient cases where TB has preceded and come before the development of diabetes is extensive yet underplayed. Both  Lin and Tsai’s studies speak of tuberculosis complicated by diabetes. Diabetes has been around since the first century AD, in a perpetual state of coping and managing. It is time, it is long past time, to cure diabetes. But current models as to its cause are not equipping us to do so.

 

Epidemic

In 1991, two years before The World Health Organization belatedly issued its first ever global emergency – regarding tuberculosis, a disease estimated to result in a human death every 10 seconds [1], a WHO ad hoc committee announced that an apparent epidemic of diabetes had occurred – or was occurring – in adult people throughout the world. The developing countries, as well as the minorities of disadvantaged communities in industrialized nations, particularly in the United States, seemed to be taking the brunt of the epidemic [2]. CDC maps for US Diabetes and TB at the time showed, for both diseases, a predominantly Southern US distribution, with major inroads along much of the Eastern seaboard.

 

American Diabetes: the Pimas

American Indians have some of the highest diabetes rates in the world, nearly four times greater than other Americans. In one screening study, using three geographic areas, 40–70% of American Indian adults aged 45–74 were found to have diabetes [3]. But it is within this subgroup, that the highest levels of diabetes in the world are found, in the Pima Indians of Arizona [4]. This drew investigators worldwide to grapple with questions such as why those Pimas who chose to stay in the mountains of Mexico, away from the reservations, had incredibly lower rates of diabetes.

Although Mexican Pimas have the ‘‘genes” for Type-2 diabetes, fewer than 1 in 15 get the disease. This argues against a genetic basis for the disease. Diabetes, however, was not the only problem facing the American Indians and the Pimas. For if Indian diabetes soared, their rate of TB was more than five times greater than that for other Americans, most of their children becoming tuberculin positive by the age of 10 to 15.

By 1900, tuberculosis had become the most serious health problem among North American Indians [6], as well as their leading cause of infectious death. And some of the most dreadful manifestations of tuberculosis susceptibility on record can be found when this group was compelled to change their ancestral ways and live on reservations. The first well documented outbreak of US Indian TB was among 2,800 Sioux, made US prisoners of war around 1880. Not in evidence during incarceration, and soon thereafter, TB deaths, in their most acute form occurred in the barracks, reaching, by 1913 Sioux mortalities at a level 10 times greater than any in Europe during the worst of its 19th century TB epidemics. And similar events were unfolding on other Indian Reservations. Runaway epidemics among North American Indians such as the Arizona Navajo and the Qu’Appelle Valley Canadian Indians left in their wake TB mortality rates of up to 9,000 per 100,000, the highest anywhere at any time. (Ibid)

Despite the warm, arid Arizona climate, TB still remains the greatest cause of Navajo death, a byproduct of their confinement to reservations and adopting the white man’s diet and way of life. Although tuberculosis reached the Americas with the coming of the North American Indian migrants, it only persisted at a low level of endemicity until an epidemic began 1500 years ago, thought to have originated in the Andean region of South America. Unfortunately, this epidemic did not have an opportunity to reach its apex or subside, leaving highly susceptible American Indians in the direct path of European colonizers.

The single worst disease present in European cities was tuberculosis and by 1800 it was understood that no other disease was as common, nor as deadly. Young noted that it caused one in four premature deaths in England, while major Parisian hospitals simultaneously recorded 40% of their deaths as resulting from tuberculosis. This set the backdrop for a US eastern seaboard death rate of approximately 400 per 100,000 by 1830, a reservoir with which to infect the ultra-susceptible American Indians with virulent European strains.

Perhaps the most meaningful post-mortem examination of pancreatic tissue from diabetic and non-diabetic Pima Indians ever done showed that 77% of the diabetic group had amyloidosis of the islets of the pancreas compared with only 7% in non-diabetic subjects.

Phillip schwartz and amyloidosis

As a pathologist and lead researcher, Dr. Phillip Schwarz knew all about amyloid and amyloidosis. But when no explanation of diabetes or its amyloid came close to what Schwartz, in a 50 year autopsy-driven study uncovered for the State in Warren Pennsylvania, he published. In a report of 331 autopsied cases of amyloid, ages ranging from 16 to 87, Schwartz showed tuberculous lesions somewhere in the body in practically all of them. He speculated that most of these were from childhood infection. A remarkable 224 out of 331 diabetics had, in Schwartz’s study amyloidosis of the pancreas secondary to tuberculosis. Moreover, most of those diagnosed as diabetic prior to death showed intense islet cell amyloidosis and Schwartz hypothesized that once amyloidosis of the pancreatic islet cells from tuberculosis hit a critical mass, the result was diabetes mellitus [12]. Thus, according to Schwartz, most cases of pancreatic amyloidosis, as well as the inflammatory infiltrate of the islet cells characteristic of Juvenile diabetes, ought to be considered an immunopathy induced by tuberculosis. Like Nichols, Schwartz noted that diabetes was easy enough to pick up with routine laboratory tests, TB was not, its main weapon being its insidious nature, often taking decades to discover, if then.

Schwartz knew that there were two conceivable ways in which the pancreas could be attacked by tuberculosis: First and foremost was by its toxins and inflammatory proteins, dumped into the blood. The germ need not be present and indeed could not be found in the pancreatic tissue of diabetics, which Schwartz knew would lead to “autoimmune” speculation.

The other, much less frequent means by which tuberculosis attacked was through the direct invasion of the pancreas by tubercle bacilli, either through the blood or by direct penetration of the pancreas by nearby infected lymph nodes [13]. But even in the few cases where microbes of tuberculosis were present in the pancreas, it could take up to 14 weeks to grow out in the laboratory, a practice not routinely followed.

In any scenario, Chaudhry et al. concluded, a clinical diagnosis of pancreatic tuberculosis was not possible.

To further prove the connection between tuberculosis and amyloidosis Schwartz injected M. tuberculosis into the peritoneum of 22 guinea pigs, all of whom promptly died within 28–96 days. All but four exhibited amyloidosis. Yet only one of the control animals, not injected with tuberculosis, came down with amyloidosis. Schwartz’s guinea pig experiment, supported the findings of Hass, who in a large series of rabbits, found that three out of every four animals developed amyloidosis within 15 days of being infected with bovine or cow tuberculosis. Furthermore, the injection of tuberculin, a protein derivative of tuberculosis into these animals only hastened the development of such amyloidosis.

Just as it is a well-guarded secret that glucose intolerance occurs in the setting of TB without diabetes, and is reversible following adequate anti-tuberculosis treatment so too is it glossed over that initial, pronounced, enhanced insulin secretion with TB leads to signs of relative insulin deficiency and persistent high blood sugar. It is just this higher secretion of insulin, leading in turn to lower functional insulin reserves, that sets the stage for the more frequent development of severe diabetes mellitus in patients with pulmonary tuberculosis.

Moreover, such hyperglycemia, in addition to stimulating insulin over- secretion, through the over-stimulation of pancreatic islets to release the hormone amylin, causes just the sort of destructive pancreatic islet cell amyloidosis that Schwartz regularly documented.

The ultimate importance of amyloidosis of the pancreas towards the pathogenesis of age-related diabetes shows similarities between cats and man. Thus the typical diabetic cat is obese and middle-aged, and has low but detectable circulating insulin levels. However, the most striking similarity between the species is the occurrence of islet amyloidosis (IA) in nearly all diabetic cats and in over 90% of humans with Type-2 diabetes mellitus. Even before Koch discovered the causative organism of human tuberculosis in 1882, it was recognized in dogs and cats. Up to 13% of catsharbored the disease, often unsuspected. In addition, it soon became obvious that cats were also susceptible to Avium or fowl tuberculosis.

The historical roll call referenced by Schwartz of scientists linking amyloid in man to TB is extensive and in the past amyloid’s usual precipitating cause was acknowledged to be primarily tuberculosis. However, in recent years scientific thought has shifted towards non-infectious inflammatory diseases as the most commonly associated cause of amyloidosis.

But Schwartz, studying others autopsy findings in cases of so-called ‘‘primary” or non-infectious amyloid, found important omissions in ruling out the possible presence of active or inactive tuberculosis, never stated, and most of all, never looked for.

By 1994, de Beer and Nel, studying the relationship between a major rise of serum amyloid, and having tuberculosis, saw a rapid descent in amyloid levels in patients treated with anti-tubercular drugs. Tomiyama and Asanodissolved beta-amyloid plaque with rifampin, a first line drug for TB, and one of the few agents, to this day, that is able to dissolve amyloid plaque. In 2004,Fink dissolved similar amyloid with rifampin.

 

The science of denial

A century ago diabetics were virtually doomed to die of tuberculosis, if not fatal diabetic ketoacidosis [28]. Root, in reviewing the history of the association of diabetes and tuberculosis, noted that ‘‘in the latter half of the 19th century the diabetic patient appeared doomed to die of pulmonary tuberculosis if he succeeded in escaping coma”. In 1883, Bouchardat stated ‘‘at autopsy every case of diabetes has tubercles in the lungs”. Root presented an interesting analysis of 1121 autopsied diabetics in 1934, from which he concluded that active tuberculosis occurred two to three times more frequently than expected. But because in studies like Root’s diabetes seemed to usually precede tuberculosis, it was concluded that the 5th century notion that diabetes comes first was valid. To Nichols, this came from a ‘‘peculiar consensus”, which ‘‘did not seem proper”. Even Munkner objected to Root’s conclusions, writing that one would expect a somewhat increased number of diabetics within a group of tuberculosis patients as well. Yet it was Root’s 1934 ‘‘one-sided association” between TB and diabetes, that others would blindly follow to this day. To Nichols , it was not a question of whether diabetes developed commonly in TB patients. He knew it did.

Certainly in his paper, Root’s ‘‘remarkable cases” often point more towards Nichol’s views of TB coming before diabetes, than to his own hypothesis. Were Root and others ignoring the obvious?

Not only does glucose intolerance occur in the setting of TB without diabetes, it is reversible following adequate anti-tuberculosis treatment. And lung resection of tuberculosis in patients with severe diabetes mellitus reduces the severity of their diabetes. Engelbach spoke of ‘‘transitory” diabetes in some of his TB patients prior to treatment.

By 1990, a landmark article appeared in the February issue of the  Proceedings of The National Academy of Science. Elias and Markovits carefully laid out their case. Insulin-dependent juvenile diabetes, all along thought to be from ‘‘autoimmune” destruction of the insulin-producing pancreatic islet beta cells, had been shown to be caused, in mice, by a protein by-product related to Mycobacterium tuberculosis. In the study, Elias and Markovits actually saw the onset of pancreatic beta-cell destruction occur when lymphocytes (white blood cells), developed to destroy and rid the body of these tubercular proteins called heat shock protein 65 (HSP-65). This did not occur when HSP-70, common to all bacteria, was used. Some weeks later antibodies to these HSP-65 proteins of tuberculosis also formed, along with anti-insulin antibodies. And as all of these began to decline, overt insulin-dependent diabetes developed.

The researchers also concluded that the HSP-65 manufactured by Mycobacterium tuberculosis could not only be used to induce diabetes but to serve as a vaccine against it. (Ibid) This was direct laboratory evidence that tuberculosis could indeed cause or prevent diabetes, and it was not alone. Other studies of support appeared. But the possible causative responsibility of the  tuberculosis and the mycobacteria in diabetes was still being all but ignored.

Conclusion

By 1995, the number of adults with diabetes mellitus was estimated to be 135 million worldwide; this number is expected to increase to 300 million by 2025. Diabetes has been around since the first century AD in a perpetual state of coping and managing, but with no cure in sight.

Schwartz and Haas’s studies, linking diabetes, tuberculosis and the mycobacteria, laid the foundation for such a cure and a series of studies done only within the last decade or two further solidify that link. Nichols stated outright that on the basis of his evaluation that diabetes, where it looked for, should be quite common in tuberculosis patients. The problem is, it never has been.

Thus while mankind continues its struggle to come to grips with the cause and thereby win the war against diabetes, tuberculosis and the mycobacteria continue their silent destructive path towards causing it, unobstructed by the advance of today’s science.

Recently, specific tuberculosis and mycobacterial proteins have been shown to directly cause insulitis, hyperglycemia and diabetes in mice thru the production of anti-insulin antibodies. No microbes are present in just the sort of situation that many would interpret as the ‘‘autoimmune” destruction of pancreatic islets in Type-1 diabetes. The problem is, there’s nothing ‘‘autoimmune” about the process other than the fact that you cannot recover the actual bacteria doing the damage against targeted pancreatic tissue.

That there is nothing regarding the current theory of diabetes that is set in stone has recently come to our attention. Presently under scrutiny are the long-relished, age-based categories, only first differentiated in 1957, insisting that the vast majority of children and teenagers had Type-1 diabetes (‘‘insulin dependent” or ‘‘IDDM‘‘) – a lifelong problem which occurs when cells in the pancreas fail to produce insulin, the controller of blood sugar. In contrast, experts saw Type-2 diabetes (non-insulin dependent or NIDDM) as a disease primarily of the middle-aged and elderly who no longer responded properly to insulin and have some pancreatic failure.

But, the lines between these 1957 age categories are crumbling, swiftly. If, in the US, you are now diagnosed with diabetes in your late teens or early 20’s, you are more likely to have Type-2 diabetes than Type-1. Moreover, although this increasing prevalence of Type-2 diabetes in US children is mostly in minority groups, it is fast gaining a foothold in non-minority children as well. And the same holds true in the UK where the child or adolescent need not be in a minority group to have Type-2.

Although it is conceivable that a complete eradication of tuberculosis and related mycobacteria might prevent diabetes mellitus of the aging, and perhaps the young, Schwartz preferred to leave this question open to further investigations by other authors. However such studies, although they have appeared in limited numbers and are supportive, have come at what for diabetics has been a painfully slow rate.

References

[1] Pieters J. Entry and survival of pathogenic mycobacteria in macrophages. Microbes and Infection 2001;3:249–55.

[2] King H, Rewers M. Diabetes In adults Is now a Third World problem. Wodd Health Organization Ad Hoc Diabetes Reporting Group. Ethn Dis 1993;3(Suppl):S67–74.

[3] Lee ET, Howard BV. Diabetes and impaired glucose tolerance in three American Indian populations aged 45–74 years. Diabetes Care 1995;18(5):599–610.

[4] Bogardus C, Lillioja S. Pathogenesis of NIDDM in Pima Indians. Diabetes Care 1991;14(7):685–90.

[5] Dubos R, Dubos J. The White plauge: tuberculosis, man and society. Rutgers University Press; 1987.

[6] Rieder HL. Tuberculosis among American Indians of the contiguous United States. Public Health Rep 1989;104(6):653–7.

[7] Trafzer CE. Tuberculosis death and survival among Southern California Indians, 1922–44. Can Bull Med Hist 2001;18(1):85–107.

[8] McDougall JB. Tuberculosis: a Global study in social pathology. Edinburgh: E&S Livingstone Ltd; 1950.

[9]  Daniel TM. The origins and precolonial epidemiology of tuberculosis in the Americas: can we figure them out? Int J Tuberc Lung Dis 2000;4(5):395–400.

[10] Clark A, Saad MF. Islet amyloid polypeptide in diabetic and non-diabetic Pima Indians. Diabetologia 1990;33(5):285–9.

[11]  Goto Y, Seino K. Standard sugar loading test; special reference to the possibility of differentiation of two types of diabetes mellitus and of differentiation of non-diabetics from diabetics bv sugar loading test. Tohoku J Exp Med 1957;66(2):115–24.

[12] Schwartz Ph. Amyloid degeneration and tuberculosis in the aged. Gerontologia 1972;18(5–6):321–62.

[13] Stock KP, Riemann JF, Stadler W, Rosch W. Tuberculosis of the pancreas. Endoscopy 1981;13(4):178–80.

[14] Ashino J, Ohno I, Okada S. A case of disseminated tuberculosis requiring extended period for the identification of Mycobacterium tuberculosis on culture. Kekkaku 2002;77(2):73–7.

[15] Chaudhary A, Negi SS, Sacbdev AK. Go pancreatic tuberculosis: still a histopathological diagnosis. Dig Surg 2002;19(5):389–92.

[16] Hass GM, Huntington R. Amyloid 111. The properties of amyloid deposits occurring in several species under diverse conditions. Archives of Pathology 1943;35:226–41.

[17] Basoglu OK, Bacakoglu F, Cok G, Sayiner A. The oral glucose tolerance test in patients with respiratory infections. Monaldi Arch Chest Dis 1999;54(4):307–10.

[18] Karachunskii MA, Balabolkin MI. Changes in carbohydrate metabolism in patients with tuberculosis. Vestn Ross Akad Mo Nauk 1995(7):18–21.

[19] O’Brien TD. Pathogenesis of feline diabetes mellitus. Mol Cell Endocrinol 2002;197(1–2):213–9.

[20] Blaine DP. Tuberculosis in the dog, cat and bird. Vet Rec 1913;25:677.

[21] Snider WR. Tuberculosis in canine and feline populations. Am Rev of Resp Dis 1971;104(6):877–87.

[22] Hix JW, Jones TC. Avian tubercle infection in the cat. J Am Vet Med Assoc 1961;138:641.

[23]  Jordan HL. Disseminated mycobacterial avium complex infection in three Siamese cats. Am Vet Med Assoc 1994;204(1):90–3.

[24] Malik R, Gabor L. Subcutaneous granuloma caused by Mycobacterium avium complex infection in a cat. Aust Vet J 1998;76(9):604–7.

[25] Wyngaarden JB, Smith L. Cecil textbook of medicine. 19th ed. Philadelphia: W.B. Saunders Company; 1992.

[26] de Beer FC, Nel AE. Serum amyloid A protein and C-reactive protein levels in pulmonary tuberculosis: relationship to amyloidosis. Thorax 1984;39(3):196–200.

[27] Tomiyama T, Asano S. Rifampicin prevents the aggregation and neurotoxicity of amyloid B protein in vitro. Biochem Bipohys Res Commun 1994;204(1):76–83.

[28] Schlossberg D. In: The Galaxy. Tuberculosis Praeger

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[29] Younger D, Hadley WB. In: Marble A, White P, Bradley RF, Krall LP, editors. Joslin’s diabetes mellitus. 11th ed.. Philadelphia: Lea and Febiger; 1971. p. 628–31.

[30] Root HF. The association of diabetes and tuberculosis. N Eng J Med 1934;1:210.

[31] Papaspyros NS. The history of diabetes mellitus. London: Robert Stockwell Ltd; 1952.

[32] Nichols GP. Diabetes among young tuberculous patients; a review. Am Rev of Tuberculosis 1957;76(6):1016–30.

[33] Munkner T. Incidence of pulmonary tuberculosis among diabetics in the Country of Vejle in 1944–1951. Acta Tuberc Scand 1953;28:355.

[34] Voloshyn IaM. The pulmonary resection for tuberculosis in patients with severe diabetes mellitus. Klin Khir 2000;(5):30–1.

[35] Engelbach K. Transitory diabetes mellitus in two tuberculotics. Beitr Klin Tuberk Spezif Tuberkuloseforsch 1954;110(5):470–3.

[36] Elias D, Markovits D. Induction and therapy of autoimmune diabetes in the non-obese diabetic (NOD)/Lt mouse by a 65-kDa heat shock protein. Proc Natl Acad Sci 1990;87:1576–80.

[37] Martin TC, Aguas AP. A role for CD45RBlow CD38+ T cells and co stimulatory pathways of T-cell activation in protection of non-obese diabetic (NOD) mice from diabetes. Immunology 1999;96(4):600–5.

[38]  Harada M, Kishiomoto Y. Prevention of overt diabetes andinsulitis in NOD mice by a single BCG vaccination. Diabetes Res Clin Pract 1990;8(2):85–9.

[39] Martins TC, Aguas AP. Mechanisms of Mycobacterium avium-induced resistance against insulin-dependent diabetes mellitus (IDDM) in non-obese diabetic (NOD) mice: role of Fas and Tb1 cells. Clin Exp Immunol 1999;115(2):248–54.

[40] Nomaguchi H, Yogi Y. Prevention of diabetes in non-obese diabetic mice by a single immunization with Mycobacterium leprae. Nihon Hansenbyo Gakkai Zasshi 2002;71(1):31–8.

[41] Fagot-Campagna A, Pettitt DJ, En”eJQau MM, et al. Tvoe 2 diabetes ong North American children and adolescents: an epidemiologic review and a public health perspective. J Pediatr 2000;136:664–72.

[42] American Diabetes Association. Type 2 diabetes in children and adolescents. Diabetes Care 2000;23:381–9

© 2011

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Toddlers with Diabetes: Caring for the Littlest Patients

Toddlers with diabetes are suffering from Kind one diabetes, also identified as juvenile diabetes or diabetes juvenile. The number of kids below the age of 5 currently being diagnosed with diabetes juvenile has virtually doubled in the past 5 a long time. Caring for toddlers is a challenge beneath the very best of circumstances, and toddlers with diabetes require even more unique care and attention.

Very first, if you are asking yourself no matter whether your toddler has diabetes in the initial place, right here are some indications to appear for:

•often complains of feeling thirsty
•hungry much more often
•suddenly loses fat
•urinates a lot more than normal, diapers more wet than usual
•occasional fruity smelling breath

If you observe any of these signs in your child, go over with your physician the likelihood you have a toddler with diabetes.

You or your caregiver will have to closely monitor your child’s blood sugar throughout the day to be certain it stays inside a safe range. Ideally this indicates 6-12 mmol just before meals.

Toddlers with diabetes also demand day-to-day insulin shots, which can be traumatic for you as nicely as your youngster! When administering equally finger pricks for the blood sugar assessments and the insulin shots, you really should be as fast and calm as possible about the process. If your little one is enjoying, go wherever he or she is fairly than possessing them arrive to you. That helps create the technique as just a standard component of their day.

Of course, your little one will resist these methods, and it can be challenging for mothers and fathers and caregivers to don’t forget they are carrying out this for the child’s well being. It need to be performed, even so, and you may well have to discover to restrain the child gently. It also helps to give them a huge hug and a kiss after it is completed to make certain they realize you nonetheless love them even though this hurt a bit.

One more difficulty is that toddlers with diabetes can’t tell you when they are feeling the results of reduced blood sugar, which is another purpose for watchful monitoring.
Toddlers in general can be picky eaters, and toddlers with diabetes are no different. The challenge here is in creating certain that all your alternatives fit inside a wholesome and proper diabetic diet. Have as vast a choice of these foods accessible as feasible so that when they do refuse selected meals, you can tempt them with an proper choice.

Toddlers with diabetes ought to otherwise produce the exact same way, and at the very same charge, as other young children of their age. So as lengthy as you get the necessary precautions to deal with the diabetes, and your youngster seems normal in all other methods, there’s no purpose why he or she shouldn’t be a flawlessly nutritious and pleased child.

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Pediatric Diabetes – Caring for a Diabetic Child

Despite our finest efforts as mother and father or caregivers, kids will turn into sick. One particular these illness which is turning into increasingly prevalent is pediatric diabetes. However, maintaining a diabetic little one healthful is dependent on being informed about the illness, its signs or symptoms, and remedies. Caring for the kid with diabetes is the responsibility of all persons who, at some time or other, has to get care of that little one. As these, parents want to ensure that all care givers are informed about their diabetic child’s dietary wants.

Most youngsters are inclined to have kind I diabetes, formerly known as juvenile diabetes, even though youngsters are increasingly being diagnosed with sort 2 diabetes as effectively. Kind I diabetes takes place when the pancreas does not operate and does not create any insulin. Insulin is required to aid break down sugars (glucose) in our entire body to support it perform efficiently. When this breakdown of sugars does not happen, as in the situation of sort I diabetes, the sugar stays in the blood stream.

Because insulin is essential in breaking down sugars in the body to use for vitality, insulin has to be taken to manage the illness. As a result kind I diabetes is also referred to as insulin-dependent diabetes. Physical exercise and diet are also critical supporting to manage this type of diabetes. Caring for the kid with diabetes implies that you will need to identify the signs of the illness, as effectively as any resulting reactions that can happen. The principal indicators of pediatric diabetes are:

  • Breath smelling like fruit
  • Frequent hunger
  • Pulse beating quicker than typical
  • Headaches
  • Currently being weak and dizzy
  • Trouble concentrating
  • Vision starting to be foggy
  • Skin tending to be cold and moist
  • Going through seizures

Following, you should be ready to recognize when the little one is in crisis, suffering both a hypoglycemic or hyperglycemic episode, and you must know what to do assist in possibly situation. Hyperglycemia happens when the sugar ranges are as well high. Increasing sugar ranges are normally a consequence of consuming as well considerably, not taking the appropriate quantity of insulin, or not exercising sufficient. When a kid is hyperglycemic, therapy by health-related experts is necessary. A child struggling from higher blood sugar will complain of the subsequent:

  • Weakness
  • Intense thirst
  • Needing to urinate routinely
  • Not seeing obviously
  • Not being hungry

With hypoglycemia (low blood sugar), the symptoms fluctuate from youngster to little one, but some of the typical indications include:

  • Clumsiness
  • Sudden mood modifications
  • Sweating
  • Hunger
  • Seeming perplexed
  • Trembling
  • Headache
  • Tingling feeling about the mouth

The initial course of action is to improve the child’s sugar intake by giving them something sweet to drink, this kind of as standard soda, fruit juice or glucose tablets. When the youngster is feeling greater, you need to give them one thing a lot more sound to eat. If the kid is as well weak to swallow or is unconscious, administer the proposed dosage of glucagon and call for immediate health care help. Glucagon is a medicine given by injection to rapidly boost the degree of glucose in the blood. It is usually the initial program of treatment method in serious hypoglycemia.

Diet is a key portion of keeping the diabetic little one healthful. The caregiver has the obligation to guarantee that the kid eats what is recommended. It is also important to discuss with the little one and allow them know that they will get truly sick if they consume as well numerous sweets or other meals that can pose a risk. It is also essential to let other folks, this kind of as teachers, know that a diabetic child might need to snack to enhance their sugar and vitality amounts. The child with diabetes must also have normal meals.

Exercise is crucial as well, and there is no reason why the diabetic youngster cannot take part in all typical bodily activity. Training aids to control blood sugar amounts. Nonetheless, suffering from pediatric diabetes ought to not exert on their own ahead of meal time. Also, they will need to have a snack, these as juice, crackers or a fruit, useful, as they will require to change sugar misplaced in the course of physical activity.

Most importantly, young children ought to be taught how to check their blood sugar ranges in the course of the program of the day, the moment they are in a position to do quickly their personal. This is important so that they can take insulin or eat something as necessary.

Caring for the diabetic child, whilst calling for more vigilance in terms of their eating habits can be stress totally free the moment you and others taking care of the youngster know what to do and stick to the guidelines. Also, make positive that emergency numbers are near at hand and that the child learns how to understand signs and symptoms of potential difficulty and take corrective actions.

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How Vitamin D can Help Juvenile Diabetics

Studies have shown that a large percentage, approximately 85% of adolescents with type 1 diabetes have low levels of vitamin D. Type 1 diabetes are known to have generally lower bone density and are considered at high risk of bone fractures. We know that adequate levels of vitamin D to drive stronger bones and higher bone density, which is why we have added vitamin D fortified milk year. What you may not know is that hinder the absorption of vitamin D synthesis and could have a negative effect on her child, AOS moods, sleep, stress levels, mental and cognitive abilities.

These medical conditions, race or body fat percentage, because their child to convert vitamin D into a usable form, the active hormone? The current FDA recommended daily allowance of vitamin D is 400 IU of vitamin D daily for adults, 200 units per day for adolescents. For a healthy adult, for a minimum recommended daily dose, which was to drink four glasses of 8 grams of milk per day. You can also get vitamin D from the sun.

For 400 units, which would be thirty minutes of sun during peak hours, four days a week. But there are many factors that can influence the amount of vitamin D actually obtain and use these sources. Under the sun or milk for vitamin D may not be feasible. Taking vitamins and supplements is usually required.

People with hyperparathyroidism, liver or kidney disease do not need to take vitamin D supplements because of their inability to convert into a form of active hormone, so talk with your endocrinologist if your child has any of these conditions. It should also be noted that darker skin and body higher percentage of fat you have, the vitamin D will absorb less sunlight. Also, if your child eats a diet low in fat, monounsaturated or have a condition that causes a reduction in fat absorption, also has a capacity Unable to absorb vitamin D and May need supplements. Complications of diabetes are often caused by stress. The general stress levels are kept under control by vitamin D. Moreover, levels of blood sugar affect mood and cognition. The mood swings and lack of knowledge caused by fluctuations in blood sugar can reduce and even eliminate the maintenance of adequate levels of vitamin D in the body in some cases. This is because vitamin D increases the levels of serotonin in the brain. Serotonin is a neurotransmitter that controls moods in the brain. Of vitamin D in serotonin results correct. Serotonin regulates the stress, anger, depression, aggression, appetite, behavior and more. Since stress aggravates and worsens the symptoms of diabetes and risk levels of serotonin in the control of juvenile diabetes, type 1 or type 2, can help reduce health risks.

These risks include psychosis due to sleep deprivation, depression, long-term high or low blood levels of glucose, high blood pressure, heart disease and stroke. I am your son, AM vitamin D levels checked by their doctor. If levels are low or lacking, try to work on other food sources of vitamin D, such as shrimp, salmon, cod liver oil and vitamin D fortified milk. You should consult your doctor about the use of and supplements to increase levels of vitamin D. The levels are periodic checks to monitor the absorption and the appropriate dose for your child.

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The Obesity Epidemic and Juvenile Diabetes

The growing obesity epidemic among children today is thought to be a major factor for growth of juvenile diabetes in this country today. Although not everyone agrees on the causes and affects is difficult to discuss with the continuous increase in children with type 2 diabetes are overweight. In fact, the percentage of obese children increases, so does the percentage of those afflicted with juvenile diabetes at about the same speed.

It seems there are two main reasons for this increase in type 2 diabetes among children. Most children these days have a sedentary lifestyle that revolves around watching TV, playing video games or the computer to chat with your friends by email. The second problem for many children is their eating habits and nutrition. Living the lifestyle of fast food or eat a bag of chips in a video game is one of the main reasons for the prevalence of overweight children that we see today.

For type 2 diabetes for many years was something that adults are overweight faced, especially because children have weight problems than they do now. Type 2 diabetes in an adult is also known as noninsulin-dependent diabetes. The primary treatment for this type of this disease are lifestyle changes involving diet and exercise for children and adults.

A major concern with type 2 diabetes affects children may have during the life of a child. Children with type 2 diabetes has been found that are more life-threatening complications of type 1 diabetes. Some of the smaller problems more with this type of diabetes do have heart disease, nerve damage, kidney failure, blindness and amputation of limbs, particularly the feet and calves.

The first line of defense against type 2 diabetes among young people is probably the most obvious. Maintain a healthy weight through proper diet and exercise to prevent disease. For children already diagnosed this treatment is the same if you want to avoid health complications later in life.

Childhood obesity is an epidemic all parents should take seriously. The long-term health affects all children are at stake, especially with an increased risk of juvenile diabetes, a disease that affects every child in their lifetime. By making lifestyle changes easier to focus on a healthy diet and physical activity at the onset of type 2 diabetes can be prevented or delayed in children at risk also high.

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Diabetes Symptom – You Can Do A Self – Check Of This Fatal Disease

Are finding yourself battling dizziness? You need to wake up and go to the bathroom early in the morning? It’s the yo-yo weight for no apparent reason? These are symptoms that have been associated with diabetes. If you answered yes to more than one of these questions symptoms of diabetes, you should consult your doctor. But if you answered yes to these questions, do not assume that you are diabetic. The following are some things to keep in mind when waiting to speak with your doctor.

There are two types of diabetes, a type II or have different symptoms. levels of blood sugar in the body that is a popular landmark of the disease. And the production of insulin, or rather how it is used, is what differentiates the two types. type is where there is not enough insulin produced by the body to balance blood sugar levels in the blood. Adolescents and children are common, as have the reason this is also known as juvenile. When the body tries to produce insulin and type II diabetes.

This is the most common form of the disease. Aged between 35-45 is usually when this happens. In addition, 3-5 percent of pregnant women experience gestational diabetes. Hormonal imbalance during pregnancy is the reason why this happens during the weeks 24-28 of pregnancy. There are some important considerations when you check to see if the symptoms as well and some small. However, it is important to know that the symptoms of diabetes, even minimal, if not treated can cause serious problems. Amputation and loss of vision are some problems that may occur when the main symptoms are ignored diabetes. excessive thirst is a symptom of juvenile diabetes.

 

Even after a full meal, some people still hungry. frequent urination, especially in the middle of the night is another sign that you may have diabetes. Fatigue is another thing I can point to diabetes, as a sudden change in weight. ‘The great weight gain, or more commonly, weight loss is something to talk with your doctor. Blurred vision is an example of a sign that diabetes can lead to blindness if not treated. Tingling and numbness of the hands and feet may also occur in addition to weakening the immune system. Dry skin or itching may be the result of excessive sweat glands reduced and decreased circulation.

 

Other problems can occur with any symptoms of diabetes are more or less ignored. Diabetics, for example, suffer from foot problems and poor circulation, which are urgent matters to address. When your feet are not happy in general, the rest of you are not happy either. Making a line of self-control before going to your family doctor will help you determine if there are more than a symptom of diabetes. You will find checklists and questionnaires online that can help find food.

 

We recommend that you make an appointment, when every time you fell, you must, but if the list gets too long, the appointment or not you want a necessity. Subject: There are several symptoms associated with diabetes. If you suspect this is what was bothering you, go online and find checklists and tests. Major and minor symptoms in search of diabetes are dizziness, nerve damage, blurred vision and excessive thirst and hunger.

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