Id, ego and super-ego

http://en.wikipedia.org/wiki/Sigmund_Freud

Freud proposed that the human psyche could be divided into three parts: Id, ego and super-ego. Freud discussed this model in the 1920 essay Beyond the Pleasure Principle, and fully elaborated upon it in The Ego and the Id (1923), in which he developed it as an alternative to his previous topographic schema (i.e., conscious, unconscious and preconscious).

 The id is the completely unconscious, impulsive, childlike portion of the psyche that operates on the "pleasure principle" and is the source of basic impulses and drives; it seeks immediate pleasure and gratification.^[124]

Freud acknowledged that his use of the term Id (das Es, "the It") derives from the writings of Georg Groddeck.^[125] 

The super-ego is the moral component of the psyche, which takes into account no special circumstances in which the morally right thing may not be right for a given situation.

The rational ego attempts to exact a balance between the impractical hedonism of the id and the equally impractical moralism of the super-ego;

 it is the part of the psyche that is usually reflected most directly in a person's actions. When overburdened or threatened by its tasks, it may employ defense mechanisms including denial repression, undoing, rationalization, repression, and displacement. This concept is usually represented by the "Iceberg Model".^[126] This model represents the roles the Id, Ego, and Super Ego play in relation to conscious and unconscious thought.

Freud compared the relationship between the ego and the id to that between a charioteer and his horses: the horses provide the energy and drive, while the charioteer provides direction.^[124]

Diabetes-Related Atherosclerosis

http://youtu.be/fwlLddvcBsc

Type 2 Diabetes

http://youtu.be/ZsTSoLhl3Y4

Diabetic Nephropathy

http://youtu.be/ikGl7DPXUK0

Diabetic Peripheral Arterial Disease

http://youtu.be/5UkXnEjv7x4

Insulin

http://youtu.be/n0zRiiFGGyk

Diabetes Effects on Body Animation 3D

http://youtu.be/Qi6LYIhlFdw

diabetes diet

http://en.wikipedia.org/wiki/Diabetic_diet

The American Diabetes Association in 1994 recommended that 60–70% of caloric intake should be in the form of carbohydrates. As mentioned above, this is controversial, with some researchers claiming that 40%^[11] or even less is better, while others claim benefits for a high-fiber, 75% carbohydrate diet.

Despite a common belief that table sugar contributes to the development of diabetes, it has medium (55–69) glycemic index that actually produces lower blood glucose levels than the same number of calories obtained from some other sources of carbohydrates. The Canadian Diabetes Association recommended that table sugar be included as part of the diabetes diet.^[14]

Some studies have suggested that adding vinegar to food may help to prevent carbohydrates putting up blood sugar too dramatically.^[15]

Based on the evidence that the incidence of diabetes is lower in vegetarians, some studies have investigated vegan interventions.^[19][20][21] These studies have shown that a vegan diet may be effective in managing type 2 diabetes.^[22][23] Switching diabetics to a vegan diet lowered hemoglobin A1C and LDL levels.^[22] A vegan diet may improve blood filterability.^[24] Vegan diets may lower advanced glycation endproducts.^[25]

Diabetes U.K. state that diabetes should not prevent people from going vegetarian – in fact, it may be beneficial to diabetics to go vegetarian, as this will cut down on saturated fats. Recent evidence suggests that diabetics may benefit from as many as eight portions of fruit and vegetable a day.^{[citation needed]}

Due to their high levels of dietary fibre certain foods are considered particularly beneficial for diabetics such as legumes, nuts, fruits, and vegetables.^[26]

Research has shown the Maitake mushroom (Grifola frondosa) has a hypoglycemic effect, and may be beneficial for the management of diabetes.^{[29][30][31][32][33][34]} The reason Maitake lowers blood sugar is because the mushroom naturally acts as an alpha glucosidase inhibitor.^[35] Other mushrooms like Reishi,^[36][37] Agaricus blazei,^{[38][39][40][41]} Agrocybe cylindracea^[42] andCordyceps^{[43][44][45][46][47]} have been noted to lower blood sugar levels to a certain extent, although the mechanism is currently unknown.

The Pritikin Diet consists of fruit, vegetables, whole grains, and so on, and is high in carbohydrates and roughage. The diet is accompanied by exercise.

G.I. Diet – lowering the glycemic index of one's diet can improve the control of diabetes.^[48][49] This includes avoidance of such foods as potatoes cooked in certain ways, and white bread, and instead favoring multi-grain and sourdough breads, legumes and whole grains—foods that are converted more slowly to glucose in the bloodstream.

Low Carb Diet – It has been suggested that the gradual removal of carbohydrates from the diet and replacement with fatty foods such as nuts, seeds, meats, fish, oils, eggs, avocados, olives, and vegetables may help reverse diabetes. Fats would become the primary calorie source for the body, and complications due to insulin resistance would be minimized.^[18]

• A very low carb diet to allow much tighter blood sugar control.
• For an adult, the allowed carbohydrate amounts are 6 grams for breakfast, 12 grams for lunch, 12 grams for dinner.
• Avoiding all foods with added sugar, all foods with starches, all fruits.
• Blood glucose testing up to 8 times per day.
• Target blood glucose levels that are nearly constant for the entire day.
• Weight loss for obese people with type 2 diabetes.
• Exercise for all those with type 2 diabetes.
• Basal and bolus dosing for insulin users, a technique that he invented in 1972.
• The patient takes responsibility for blood sugar control.

High fiber diet – It has been shown that a high fiber diet works better than the diet recommended by the American Diabetes Association in controlling diabetes, and may control blood sugar levels with the same efficacy as oral diabetes drugs.^[50][51][52]

Paleolithic diet – The Paleolithic diet has been shown to improve glucose tolerance in humans with diabetes type 2,^[53] humans with ischemic heart disease and glucose intolerance,^[54] and in healthy pigs.^[55] These are a limited number of studies in a limited number of subjects, but the knowledge about the benefits of the Paleolithic diet in diabetes is emerging. The scientific foundation for the Paleolithic diet and the relationship between what humans eat and diseases of the western world (including diabetes, hypertension, obesity, ischemic heart disease, stroke) is the subject of a comprehensive textbook, which is geared towards both professionals and interested laypeople alike, and which spans over 2000 references.^[56]

The diet is also known as the paleo diet, paleodiet, caveman diet, Stone Age diet, and hunter-gatherer diet.

The Paleolithic diet consists mainly of fish, grass-fed pasture raised meats, eggs, vegetables, fruit, fungi, roots, and nuts, and excludes grains, legumes, dairy products, potatoes, refined salt, refined sugar, and processed oils.^[1][2]

Vegan diet – A low-fat vegan diet improves glycemic control similar to the ADA diet.^[23]

Hyperglycemia high blood sugar

http://en.wikipedia.org/wiki/Hyperglycemia

Hyperglycemia, or high blood sugar (also spelled hyperglycaemia or hyperglycæmia, not to be confused with hypoglycemia) is a condition in which an excessive amount of glucose circulates in the blood plasma. This is generally a glucose level higher than 11.1 mmol/l (200 mg/dl), but symptoms may not start to become noticeable until even higher values such as 15–20  mmol/l (~250–300 mg/dl).

The origin of the term is Greek: hyper-, meaning excessive; -glyc-, meaning sweet; and -emia, meaning of the blood.

Chronic levels exceeding 7 mmol/l (125 mg/dl) can produce organ damage.

In general, the normal range for most people (fasting adults) is about 80 to 110 mg/dl or 4 to 6 mmol/l. (where 80 mg/dl is "optimal".) A subject with a consistent range above 126 mg/dl or 7 mmol/l is generally held to have hyperglycemia, whereas a consistent range below 70 mg/dl or 4 mmol/l is considered hypoglycemic. In fasting adults, blood plasma glucose should not exceed 126 mg/dL. Sustained higher levels of blood sugar cause damage to the blood vessels and to the organs they supply, leading to the complications of diabetes.^[3]

Chronic hyperglycemia can be measured via the HbA1c test. The definition of acute hyperglycemia varies by study, with mmol/l levels from 8 to 15.^[4]

Temporary hyperglycemia is often benign and asymptomatic. Blood glucose levels can rise well above normal for significant periods without producing any permanent effects or symptoms. However, chronic hyperglycemia at levels more than slightly above normal can produce a very wide variety of serious complications over a period of years, including kidney damage, neurological damage, cardiovascular damage, damage to the retina or damage to feet and legs. Diabetic neuropathy may be a result of long-term hyperglycemia.

In diabetes mellitus (by far the most common cause of chronic hyperglycemia), treatment aims at maintaining blood glucose at a level as close to normal as possible, in order to avoid these serious long-term complications. This is done by a combination of proper diet, regular exercise, and insulin or other medication such as Metformin, etc.

Acute hyperglycemia involving glucose levels that are extremely high is a medical emergency and can rapidly produce serious complications (such as fluid loss through osmotic diuresis). It is most often seen in persons who have uncontrolled insulin-dependent diabetes.

The following symptoms may be associated with acute or chronic hyperglycemia, with the first three composing the classic hyperglycemic triad:

• Polyphagia - frequent hunger, especially pronounced hunger
• Polydipsia - frequent thirst, especially excessive thirst
• Polyuria - frequent urination
• Blurred vision
• Fatigue (sleepiness)
• Weight loss
• Poor wound healing (cuts, scrapes, etc.)
• Dry mouth
• Dry or itchy skin
• Tingling in feet or heels
• Erectile dysfunction
• Recurrent infections, external ear infections (swimmer's ear)
• Cardiac arrhythmia
• Stupor
• Coma
• Seizures

Frequent hunger without other symptoms can also indicate that blood sugar levels are too low. This may occur when people who have diabetes take too much oral hypoglycemic medication or insulin for the amount of food they eat. The resulting drop in blood sugar level to below the normal range prompts a hunger response. This hunger is not usually as pronounced as in Type I diabetes, especially the juvenile onset form, but it makes the prescription of oral hypoglycemic medication difficult to manage.

Polydipsia and polyuria occur when blood glucose levels rise high enough to result in excretion of excess glucose via the kidneys (glycosuria), producing osmotic diuresis.

Symptoms of diabetic ketoacidosis may include:

• Ketoacidosis
• Kussmaul hyperventilation: deep, rapid breathing
• Confusion or a decreased level of consciousness
• Dehydration due to glycosuria and osmotic diuresis
• Acute hunger and/or thirst
• 'Fruity' smelling breath odor
• Impairment of cognitive function, along with increased sadness and anxiety^[5][6]

Diabetes mellitus[edit]

Chronic hyperglycemia that persists even in fasting states is most commonly caused by diabetes mellitus. In fact, chronic hyperglycemia is the defining characteristic of the disease. Intermittent hyperglycemia may be present in prediabetic states. Acute episodes of hyperglycemia without an obvious cause may indicate developing diabetes or a predisposition to the disorder.

In diabetes mellitus, hyperglycemia is usually caused by low insulin levels (Diabetes mellitus type 1) and/or by resistance to insulin at the cellular level (Diabetes mellitus type 2), depending on the type and state of the disease. Low insulin levels and/or insulin resistance prevent the body from converting glucose into glycogen (a starch-like source of energy stored mostly in the liver), which in turn makes it difficult or impossible to remove excess glucose from the blood. With normal glucose levels, the total amount of glucose in the blood at any given moment is only enough to provide energy to the body for 20-30 minutes, and so glucose levels must be precisely maintained by the body's internal control mechanisms. When the mechanisms fail in a way that allows glucose to rise to abnormal levels, hyperglycemia is the result.

Diabetic coma

• Ketoacidotic diabetic coma: intravenous fluids, insulin and administration of potassium and sodium.

• Hyperosmolar diabetic coma: plenty of intravenous fluids, insulin, potassium and sodium given as soon as possible.

• Hypoglycaemic diabetic coma: administration of the hormone glucagon to reverse the effects of insulin, or glucose given intravenously.

http://en.wikipedia.org/wiki/Diabetic_coma

Endocrine pathology: endocrine diseases (E00–E35, 240–259) Pancreas/ glucose metabolism Hypofunction Diabetes mellitus types:  type 1 type 2 MODY 1 2 3 4 5 6 complications  coma angiopathy ketoacidosis nephropathy neuropathy retinopathy cardiomyopathy insulin receptor (Rabson–Mendenhall syndrome) Insulin resistance Hyperfunction Hypoglycemia beta cell (Hyperinsulinism) G cell (Zollinger–Ellison syndrome) Hypothalamic/ pituitary axes Hypothalamus gonadotropin  Kallmann syndrome Adiposogenital dystrophy CRH (Tertiary adrenal insufficiency) vasopressin (Neurogenic diabetes insipidus) general (Hypothalamic hamartoma) Pituitary Hyperpituitarism anterior  Acromegaly Hyperprolactinaemia Pituitary ACTH hypersecretion posterior (SIADH) general (Nelson's syndrome) Hypopituitarism anterior  Kallmann syndrome Growth hormone deficiency ACTH deficiency/Secondary adrenal insufficiency GnRH insensitivity FSH insensitivity LH/hCG insensitivity posterior (Neurogenic diabetes insipidus) general  Empty sella syndrome Pituitary apoplexy Sheehan's syndrome Lymphocytic hypophysitis Thyroid Hypothyroidism Iodine deficiency Cretinism  Congenital hypothyroidism Myxedema Euthyroid sick syndrome Hyperthyroidism Hyperthyroxinemia  Thyroid hormone resistance Familial dysalbuminemic hyperthyroxinemia Hashitoxicosis Thyrotoxicosis factitia Graves' disease Thyroiditis Acute infectious Subacute  De Quervain's Subacute lymphocytic Autoimmune/chronic  Hashimoto's Postpartum Riedel's Goitre Endemic goitre Toxic nodular goitre Toxic multinodular goiter Thyroid nodule Parathyroid Hypoparathyroidism Hypoparathyroidism Pseudohypoparathyroidism Pseudopseudohypoparathyroidism Hyperparathyroidism Primary Secondary Tertiary Osteitis fibrosa cystica Adrenal Hyperfunction aldosterone: Hyperaldosteronism/Primary aldosteronism  Conn syndrome Bartter syndrome Glucocorticoid remediable aldosteronism AME Liddle's syndrome 17α CAH cortisol: Cushing's syndrome (Pseudo-Cushing's syndrome) sex hormones: 21α CAH 11β CAH Hypofunction/ Adrenal insufficiency (Addison's, WF) aldosterone: Hypoaldosteronism  21α CAH 11β CAH cortisol: CAH  Lipoid 3β 11β 17α 21α sex hormones: 17α CAH Gonads ovarian: Polycystic ovary syndrome Premature ovarian failure testicular: enzymatic  5α-reductase deficiency 17β-hydroxysteroid dehydrogenase deficiency aromatase excess syndrome) Androgen receptor (Androgen insensitivity syndrome general: Hypogonadism (Delayed puberty) Hypergonadism  Precocious puberty Hypoandrogenism Hypoestrogenism Hyperandrogenism Hyperestrogenism Height Dwarfism/Short stature  Midget Laron syndrome Psychosocial Ateliosis Gigantism Multiple Autoimmune polyendocrine syndrome multiple  APS1 APS2 Carcinoid syndrome Multiple endocrine neoplasia  1 2A 2B Progeria  Werner syndrome Acrogeria Metageria Woodhouse-Sakati syndrome M: END anat/phys/devp/horm noco (d)/cong/tumr, sysi/epon proc, drug (A10/H1/H2/H3/H5)

[hide] v t e Diabetes (E10–E14, 250) Types of diabetes Prediabetes  Impaired fasting glucose Impaired glucose tolerance Insulin resistance Conventional insulinotherapy Type 1 LADA Type 2 KPD MODY NDM  Transient Permanent Glossary of diabetes Diabetes and pregnancy: Gestational diabetes Blood tests Blood sugar Glycosylated hemoglobin Glucose tolerance test Fructosamine Diabetes management Diabetic diet Anti-diabetic drugs  Oral anti-diabetic drugs and insulin analogs Insulin therapy  Intensive insulinotherapy Pulsatile insulin Cure  Embryonic stem cells Gastric bypass surgery Artificial pancreas Complications/prognosis Diabetic comas  Diabetic hypoglycemia Diabetic ketoacidosis Hyperglycemic hyperosmolar state Diabetic angiopathy Diabetic foot  ulcer Neuropathic arthropathy Diabetic myonecrosis Diabetic nephropathy Diabetic neuropathy Diabetic retinopathy Diabetic cardiomyopathy Diabetic dermadrome  Diabetic dermopathy Diabetic bulla Diabetic cheiroarthropathy Neuropathic ulcer Other Hypoglycemia/Hyperglycemia M: END anat/phys/devp/horm noco (d)/cong/tumr, sysi/epon proc, drug (A10/H1/H2/H3/H5)