Making Healthy Food Choices!!

Knowing what to eat can be confusing.

Everywhere you turn, there is news about what is or isn't good for you. Some basic principles have weathered the fad diets, and have stood the test of time.

Here are a few tips on making healthful food choices for you and your entire family.

1. Eat lots of vegetables and fruits. Try picking from the rainbow of colors available to maximize variety.
2. Eat non-starchy vegetables such as spinach, carrots, broccoli or green beans with meals.
3. Choose whole grain foods over processed grain products. Try brown rice with your stir fry or whole wheat spaghetti with your favorite pasta sauce.
4. Include dried beans (like kidney or pinto beans) and lentils into your meals.
5. Include fish in your meals 2-3 times a week.
6. Choose lean meats like cuts of beef and pork that end in "loin" such as pork loin and sirloin. Remove the skin from chicken and turkey.
7. Choose non-fat dairy such as skim milk, non-fat yogurt and non-fat cheese.
8. Choose water and calorie-free "diet" drinks instead of regular soda, fruit punch, sweet tea and other sugar-sweetened drinks.
9. Choose liquid oils for cooking instead of solid fats that can be high in saturated and trans fats. Remember that fats are high in calories. If you're trying to lose weight, watch your portion sizes of added fats.
10. Cut back on high calorie snack foods and desserts like chips, cookies, cakes, and full-fat ice cream.

Eating too much of even healthful foods can lead to weight gain. Watch your portion sizes.

CRITICISMS TO CONCEPT OF GLYCEMIC INDEX!!

If a person consumes 50% of his or her calories from carbohydrates, the glycemic index can enable him or her to consume the same number of calories and have lower, more stable glucose and insulin levels. The use of the glycemic index, however, is limited by several factors:

The glycemic index does not take into account other factors besides glycemic response, such as insulin response, which is measured by the insulin index and can be more appropriate in representing the effects from some food contents other than carbohydrates.

The glycemic index is significantly altered by the type of food, its ripeness, processing, the length of storage, cooking methods, and its variety (white potatoes are a notable example, ranging from moderate to very high GI even within the same variety


The glycemic response is different from one person to another, and even in the same person from day to day, depending on blood glucose levels, insulin resistance, and other factors.

The number of grams of carbohydrate impacts blood sugar levels more than the glycemic index. Lowering glycemic index leads to small improvements in the blood sugar level, but consuming fewer calories, losing weight, and carbohydrate counting would benefit the blood sugar level more.Carbohydrate impacts glucose levels most profoundly, and two foods with the same carbohydrate content are, in general, comparable in their effects on blood sugar. A food with a low glycemic index may have a high carbohydrate content or vice versa; this can be accounted for with the glycemic load. Consuming carbohydrates with a low glycemic index and calculating carbohydrate intake would produce the most stable blood sugar levels.

Most of the values on the glycemic index do not show the impact on glucose levels after two hours. Some diabetics may still have elevated levels after four hours.

The GI of foods is determined under experimental conditions after an overnight fast, and might not apply to foods consumed later during the day because glycemic response is strongly influenced by the composition of the previous meal, particularly when meals are consumed within an interval of few hours. Indeed, it has been shown that a high-GI breakfast cereal (GI = 124) elicited a lower increase in blood glucose concentrations at lunch than at breakfast. Also, the difference in glycemic responses induced by the low- and the high-GI breakfast cereals at lunch were lower than that predicted by the large difference in their GI, which was determined at breakfast.

GLYCEMIC INDEX

The glycemic index, glycaemic index, or GI is a measure of the effects of carbohydrates on blood sugar levels. Carbohydrates that break down quickly during digestion and release glucose rapidly into the bloodstream have a high GI; carbohydrates that break down more slowly, releasing glucose more gradually into the bloodstream, have a low GI. The concept was developed by Dr. David J. Jenkins and colleagues in 1980–1981 at the University of Toronto in their research to find out which foods were best for people with diabetes.

A lower glycemic index suggests slower rates of digestion and absorption of the foods' carbohydrates and may also indicate greater extraction from the liver and periphery of the products of carbohydrate digestion. A lower glycemic response usually equates to a lower insulin demand but not always, and may improve long-term blood glucose control and blood lipids. The insulin index is also useful, as it provides a direct measure of the insulin response to a food.

The glycemic index of a food is defined as the area under the two hour blood glucose response curve (AUC) following the ingestion of a fixed portion of carbohydrate (usually 50 g). The AUC of the test food is divided by the AUC of the standard (either glucose or white bread, giving two different definitions) and multiplied by 100. The average GI value is calculated from data collected in 10 human subjects. Both the standard and test food must contain an equal amount of available carbohydrate. The result gives a relative ranking for each tested food.

The current validated methods use glucose as the reference food, giving it a glycemic index value of 100 by definition. This has the advantages of being universal and producing maximum GI values of approximately 100. White bread can also be used as a reference food, giving a different set of GI values (if white bread = 100, then glucose ≈ 140). For people whose staple carbohydrate source is white bread, this has the advantage of conveying directly whether replacement of the dietary staple with a different food would result in faster or slower blood glucose response. The disadvantages with this system are that the reference food is not well-defined and the GI scale is culture dependent.

FLATBUSH DIABETES - TYPE 1 or TYPE2??

Flatbush diabetes is named after an area in New york where it was described some years ago.

Etiology

Exact etiology is not clear as of now. it has been suggested that some patients may develop Flatbush diabetes as they are extremely sensitive to transient damage to Beta cells by Glucotoxicity & Lipotoxicity. when this condition is reversed with diet , oral hypoglycemic agents or Insulin the beta cells are able to recover.

Why is the knowledge about Flatbush Diabetes important??

There is a lot we do not know about flatbush diabetes but the more we are aware that such a form of diabetes exists ,the more our physicians will be apt to spot patients who have it, and the more patients are correctly Diagnosed, the better their treatment will be!!

Characteristics of Flatbush Diabetes

Patients present with very high blood sugars (>700mg/dl)

No antibodies as seen in type 1 Diabetes

Ketosis might be present

Obesity

family history of type2 diabetes

patients have signs of insulin resistance

Patients respond well to OHA ( oral hypoglycemic agents) 

Hypoglycemic agents - Extinct, Present & Future

Sensitizers

Biguanides -Metformin, Buformin ( withdrawn from market),Phenformin ( withdrawn from market)
TZDs (PPAR) - Pioglitazone, Rivoglitazone ( in clinical trials), Rosiglitazone ( about to be withdrawn from market), Troglitazone ( withdrawn from market)
Dual PPAR agonists - Aleglitazar ( in clinical trials), Muraglitazar ( dropped during clinical trials), Tesaglitazar ( dropped during clinical trials)

Secretagogues

Sulfonylureas - 1st generation: Acetohexamide, Carbutamide, Chlorpropamide ,Gliclazide, Tolbutamide, Tolazamide.
2nd generation: Glibenclamide (Glyburide),Glipizide, Gliquidone, Glyclopyramide
3rd generation: Glimepiride

Meglitinides/"glinides" - Nateglinide, Repaglinide, Mitiglinide

GLP-1 analogs -Exenatide, Liraglutide, Taspoglutide( in clinical trials), Albiglutide ( in clinical trials)

DPP-4 inhibitors - Alogliptin ( in clinical trials), Linagliptin( in clinical trials), Saxagliptin, Sitagliptin, Vildagliptin

Analogs/other insulins -
Fast acting (Insulin lispro, Insulin aspart, Insulin glulisine)
Short acting (Regular insulin)
Long acting (Insulin glargine , Insulin detemir)
Inhalable insulin (Exubera)- withdrawn from market
NPH insulin

Alpha-glucosidase inhibitors -Acarbose, Miglitol , Voglibose

Amylin analog - Pramlintide

SGLT2 inhibitors - Canagliflozin ( in clinical trials) , Dapagliflozin ( in clinical trials) , Remogliflozin( in clinical trials) , Sergliflozin( in clinical trials)

Others - Benfluorex , Tolrestat ( withdrawn from market)

Insulin tolerance test

An insulin tolerance test (ITT) is a medical diagnostic procedure during which insulin is injected into a patient's vein to assess pituitary function, adrenal function, and sometimes for other purposes.

Insulin injections are intended to induce hypoglycemia. In response, Adrenocorticotropic hormone (ACTH) and Growth Hormone (GH) are released as a part of the stress mechanism. ACTH elevation causes the adrenal cortex to release cortisol. Normally, both cortisol and GH serve as Counterregulatory hormones, opposing the action of insulin.

Thus ITT is considered to be a Gold standard for assessing the integrity of the hypothalamo-pituitary-adrenal axis. Sometimes ITT is performed to assess the peak adrenal capacity, e.g. before surgery. It is assumed that the ability to respond to insulin induced hypoglycemia translates into appropriate cortisol rise in the stressful event of acute illness or major surgery.

Side Effects

Side effects include sweating, palpitations, loss of consciousness and rarely convulsions due to severe hypoglycemia which may cause coma. If extreme symptoms are present, glucose should be given intravenously. In subjects with no adrenal reserve an Addisonian crisis may occur. For cortisol stimulation, the ACTH stimulation test has much less risk

Contraindications to ITT

Age > 60 years
This test should not be performed on children outside a specialist pediatric endocrine unit
Ischemic heart disease
Epilepsy
Severe panhypopituitarism, hypoadrenalism
Hypothyroidism impairs the GH and cortisol response. Patients should have corticosteroid replacement commenced prior to thyroxine as the latter has been reported to precipitate an Addisonian crisis with dual deficiency. If adrenal insufficiency is confirmed, the need for a repeat ITT may need to be reconsidered after 3 months thyroxine therapy.

Interpratation -

The test cannot be interpreted unless hypoglycaemia (< 2.2 mmol/L) is achieved.

Hypopituitarism

An adequate cortisol response is defined as a rise to greater than 550 nmol/L. Patients with impaired cortisol responses (less than 550 but greater than 400 nmol/L) may only need steroid cover for major illnesses or stresses. An adequate GH response occurs with an absolute response exceeding 20 mU/L.

Cushing's syndrome

There will be a rise of less than 170 nmol/L above the fluctuations of basal levels of cortisol.

Physiological Effects Of Insulin!!

Insulin binds to its receptor, which in turn starts many protein activation cascades.

These include-

Translocation of Glut-4 transporter to the plasma membrane and influx of glucose, glycogen synthesis, glycolysis and fatty acid synthesis.

The actions of insulin on the human metabolism level include:

Control of cellular intake of certain substances, most prominently glucose in muscle and adipose tissue (about ⅔ of body cells).
Increase of DNA replication and protein synthesis via control of amino acid uptake.
Modification of the activity of numerous enzymes.

The actions of insulin on cells include:

Increased glycogen synthesis – insulin forces storage of glucose in liver (and muscle) cells in the form of glycogen; lowered levels of insulin cause liver cells to convert glycogen to glucose and excrete it into the blood. This is the clinical action of insulin, which is directly useful in reducing high blood glucose levels as in diabetes.
Increased fatty acid synthesis – insulin forces fat cells to take in blood lipids, which are converted to triglycerides; lack of insulin causes the reverse.
Increased esterification of fatty acids – forces adipose tissue to make fats (i.e., triglycerides) from fatty acid esters; lack of insulin causes the reverse.
Decreased proteolysis – decreasing the breakdown of protein.
Decreased lipolysis – forces reduction in conversion of fat cell lipid stores into blood fatty acids; lack of insulin causes the reverse.
Decreased gluconeogenesis – decreases production of glucose from non-sugar substrates, primarily in the liver (remember, the vast majority of endogenous insulin arriving at the liver never leaves the liver); lack of insulin causes glucose production from assorted substrates in the liver and elsewhere.
Decreased autophagy - decreased level of degradation of damaged organelles. Postprandial levels inhibit autophagy completely.
Increased amino acid uptake – forces cells to absorb circulating amino acids; lack of insulin inhibits absorption.
Increased potassium uptake – forces cells to absorb serum potassium; lack of insulin inhibits absorption. Insulin's increase in cellular potassium uptake lowers potassium levels in blood.
Arterial muscle tone – forces arterial wall muscle to relax, increasing blood flow, especially in micro arteries; lack of insulin reduces flow by allowing these muscles to contract.
Increase in the secretion of hydrochloric acid by Parietal cells in the stomach.

Question for All...

does anybody have information on DEGLUDEC ?
Any information on new gliptins in the pipeline?