History of Diabetes

insulin kit

Diabetes History

Diabetes has been with us for a long time. Here is diabetes history in a convenient timeline:

1552 BC – Written on a 3rd Dynasty Egyptian papyrus, physician Hesy-Ra mentions frequent urination as a symptom. This is the earliest known record of diabetes.

1500 BC — Ancient Hindu writings note that ants are attracted to the urine of people with a mysterious emaciating disease.

500 BC — The first descriptions of sugar in the urine and its occurrence in obese individuals.

250 BC — Apollonius of Memphis is credited with coining the term “diabetes”, meaning to go through, or siphon, for a disease that drains patients of more fluid than they can consume.

1st Century AD – The Greeks describe the disease as “a melting down of the flesh and limbs into urine.”

164 AD – Greek physician, Galen of Pergamum, diagnoses diabetes as a kidney ailment.

Up to 11th Century – Since the urine of people with diabetes is thought to be sweet tasting, diagnosis is often made by “water tasters” who drink the urine of those suspected of having diabetes. Mellitus, the Latin word for honey, is added to the term “diabetes”.

16th Century – Paracelsus identifies diabetes as a serious general disorder.

For thousands of years, no one knows how to live with diabetes, let alone treat or cure it. Children with diabetes often die within days of onset and older people deal with devastating complications. Remedies range from herbs to bleeding.

1776 – Dobson finds a substance like brown sugar in appearance and taste when diabetic urine evaporates. He also notes a sweetish taste of sugar in the blood of diabetics. He observes that, for some people, diabetes is fatal in less than five weeks and, for others, is a chronic condition. This is the first time that a distinction between Type 1 and Type 2 has been made.

1797 – Dr. John Rollo—a surgeon in the British Royal Artillery—published a book entitled An Account of Two Cases of the Diabetes Mellitus.  He discussed his experience treating two diabetic Army officers with a high-fat, high-meat, low-carbohydrate diet. .

1798 – Rollo documents excess sugar in the blood, as well as the urine.

Early 1800′s – Researchers develop the first chemical tests to indicate and measure the presence of sugar in the urine.

1848 – Bernard discovers that glycogen is formed by the liver and speculates that this is the same sugar found in the urine of diabetics. This is the first linking of diabetes and glycogen metabolism.

Late 1850s – The French physician, Priorry, advises diabetes patients to eat extra large quantities of sugar as a treatment. Oops! This won’t be the last time that strange and unhelpful treatments for diabetes will be tried.

1869 – Langerhans, a German medical student, announces the pancreas contains two types of cells – one set secretes the normal pancreatic fluids, while the function of the other is unknown. Later, these cells are identified as the “islets of Langerhans”, which help produce the hormone insulin.

1870s – French physician, Bouchardat, notices the disappearance of sugar in the urine of his diabetes patients during the food rationing in Paris during the Franco-Prussian War and formulates the idea of individualized diets.

1889 – Minkowski and von Mering, at the University of Strasbourg, France, remove the pancreas from a dog to determine the effect on digestion and discover that diabetes develops.

In 1897, the average life expectancy for a 10-year-old child with diabetes is about 1 year. Diagnosis at age 30 carries a life expectancy of about 4 years. A newly diagnosed 50-year-old might live 8 more years.

1908 – Zuelzer extracts a pancreatic “substance” and injects it into five diabetes patients. Although sugar in the urine is reduced or disappears, the side effects of treatment are extreme and unacceptable.

1909 – de Meyer of Belgium proposes the name “insulin” (Latin: insula, island) for the unknown pancreatic substance.

1911 – Benedict devises a new method to measure urine sugar (Benedict’s Solution).

1900-1915 – Diabetes treatment includes: the “oat-cure” (daily allowance is approximately eight ounces of oatmeal mixed with eight ounces of butter, eaten every two hours), the milk diet, the rice cure, “potato therapy”, opium, and overfeeding to compensate for the loss of fluids and weight.

1913 – Allen’s book, Studies Concerning Glycosuria and Diabetes, stimulates a revolution in diabetes therapy.

1910-1920 – Allen and Joslin are considered the two leading diabetes specialists in the United States. Joslin believes that diabetes is “the best of the chronic diseases” because it was “clean, seldom unsightly, not contagious, often painless and susceptible to treatment”.

1916 – Allen promotes a strict diet regimen, which is soon widely adopted. Allen believes that the diabetic’s body cannot use food, so he limits the amount of food allowed patients. Patients were admitted to the hospital and given only whiskey mixed with black coffee (or clear soup for teetotalers) every two hours from 7 am to 7 pm. This diet is followed until there is no sign of sugar in the urine – usually 5 days or less. A strict diet follows. Outcomes are better than ever seen before for those with Type 2 diabetes. Unfortunately, those patients with Type 1 commonly die during the treatment, likely from starvation. A few young people do survive and become the first insulin users.

1919 – Allen publishes Total Dietary Regulation in the Treatment of Diabetes, with exhaustive case records and observations of 76 of his 100 diabetes patients. He becomes the director of diabetes research at the Rockefeller Institute.

1920 – Banting conceives of the idea of insulin after reading Moses Barron’s The Relation of the Islets of Langerhans to Diabetes with Special Reference to Cases of Pancreatic Lithiasis in the journal: Surgery, Gynecology and Obstetrics. With help from Best, Collip and Macleod, Banting continues experimenting with different pancreatic extracts on de-pancreatized dogs.

1921 – Paulescu, a distinguished Romanian scientist, publishes an article describing his successful isolation of “pancreine” – insulin.

1921 – Insulin is “discovered”. A de-pancreatized dog is successfully treated with insulin.

1921 – Banting presents The Beneficial Influences of Certain Pancreatic Extracts on Pancreatic Diabetes, summarizing his work at a session of the American Physiological Society at Yale University.

1922 – In Toronto, one of Collip’s insulin extracts is tested on a human being, a 14-year-old boy named Leonard Thompson. This test is considered a success by the end of the following February.

1922 – Eli Lilly and the University of Toronto strike a deal for the mass production of insulin in North America.

1923 – Banting and his colleague, Macleod, are awarded the Nobel Prize in Physiology or Medicine. Banting shares his award with Best; Macleod shares his with Collip.

While insulin can prevent early death from diabetic coma, insulin treatment does not prevent the chronic, disabling and sometimes deadly complications of the disease.

1923 – Eli Lilly begins commercial production of insulin. The Toronto group calls the substance “insulin”; Eli Lilly calls their product “Isletin Insulin.”

1925 – Home testing for sugar in the urine is introduced. Eight drops of urine is mixed in a test tube with 6 cc of Benedict’s solution provided by the doctor. The tube is put into boiling water for five minutes. The color of the liquid indicates the presence of sugar: greenish (light sugar), yellow (moderate) or red/orange (heavy).

1930s – Insulin is further refined. Protamine zinc insulin, a long acting insulin that provides greater flexibility for diabetics, is introduced. (It actually remained on the market until several years ago.)

1936 – Research by Himsworth (UK) divides diabetics into two types based on “insulin sensitivity.”

1940′s – The connection is made between diabetes and long-term complications such as kidney and eye disease.

1944 – A uniform insulin syringe is developed and diabetes management becomes more standardized.

By 1945, a newly diagnosed 10-year-old has a life expectancy of 45 years; a 30-year-old has 30.5 more years; and a 50-year-old might have 16 more years to live.

1948 – Joslin writes about the “unknown diabetic” in Postgraduate Medicine. Although a million people are known to have diabetes, he speculates a million more have it but don’t know it. He is the first expert to emphasize that insulin alone cannot solve all diabetes-related issues.

Late 1940′s – Helen Free develops the “dip-and-read” urine test (Clinistix), allowing instant monitoring of blood glucose levels.

1950s – Specialists still recommend against marriage for people “with hereditary diabetes”.

1951 – Lawrence and Bornstein measure the amount of insulin in the blood. They find that older and obese patients with diabetes do have insulin, but those who are young have none.

1955 – Oral drugs that help lower blood glucose levels are introduced.

1959 – Two major types of diabetes are recognized: Type 1 (insulin-dependent) diabetes and Type 2 (non-insulin-dependent) diabetes.

1960′s – Home testing for glucose levels in the urine increases the level of control for people with diabetes.

1964 – The first strips for testing blood glucose are used. A drop of blood is placed on the paper strip for 1 minute, and then washed off. Comparing the color to a color chart provides a rough indication of blood glucose levels.

1965 – Instant glucose is developed.

1966 – Doctors at the University of Manitoba perform the first pancreas transplant.

1970 – First blood glucose meter (Ames) is introduced. It is intended for use in doctors’ offices and costs around $500.

1970 – Insulin pumps are developed.

The development of testing equipment and supplies provides patients with much greater control and flexibility in the management of their diabetes.

1970 – Laser therapy is used to help slow or prevent blindness resulting from diabetes.

1973 – U-100 insulin is introduced.

1976 – HbA1c test is introduced.

1978 – Testing of the first recombinant DNA insulin is announced.

Until this date manufacturers of insulin have had to stockpile animal pancreatic tissue. This changes dramatically with the development of DNA technology that allows the manufacturing of a genetically engineered “human” type of insulin.

1978 – The National Diabetes Information Clearinghouse (NDIC) is established to increase knowledge and understanding about diabetes among patients, health care professionals and the general public.

1983 – The first biosynthetic human insulin is introduced.

1983 – “Reflolux”, later known as “Accu-Chek”, is introduced allowing relatively easy and accurate blood glucose self-monitoring.

1986 – Insulin pen delivery system is introduced.

1990 – Defeat Diabetes Foundation established to address the issue of prevention, which was not being met by existing diabetes related organizations.

1993 – The landmark clinical trial Diabetes Control and Complications Trial (DCCT) publishes its report. The study clearly demonstrates that more active self-management through nutrition, activity and monitoring of glucose levels (and adjustments) delays the onset and progression of long-term complications in Type 1 individuals. The study results shows proper management reduces risk complications significantly for eye disease (76%), kidney disease (50%) and nerve disease (60%).

1993 – Instant Glucose tablets are introduced.

1996 – The FDA approves the first recombinant DNA human insulin analogue, lispro (Humalog).

1990-1997 – External insulin pumps allow closer control and freedom from multiple injections. More sophisticated insulin analogues are introduced which offer faster action, less risk of reactions and more flexibility for diabetes management.

More than 300 insulin analogues have been identified, including 70 animal insulin’s, 80 chemically modified insulin’s and 150 biosynthetic insulin’s. These allow physicians the ability to customize treatment, reduce side effects and have improved outcomes.

2003 – The names Insulin Dependent Diabetes Mellitus (IDDM) for Type 1 and Non Insulin Dependent Diabetes Mellitus (NIDDM) for Type 2 diabetes are formally dropped.

The life expectancy for people with diabetes in 2004 is still lower than that for the general population by about 15 years.

2014 – 26 million Americans have diabetes and 1 in 3 of them don’t know it. Another 79 million Americans are categorized as “pre-diabetic” and are at risk of developing diabetes in the next ten years if they don’t make appropriate lifestyle changes.

Sources

http://www.britannica.com/eb/article?tocId=45578

http://www.cygn.com/overview/history.html

http://diabetes.about.com/library/blNIHdiabetesoverview8.htm

http://www.diabetes.ca/Section_About/timeline.asp

http://inventors.about.com/gi/dynamic/offsite.htm?site=http://web.mit.edu/invent/iow/free.html

http://www.postgradmed.com/issues/1997/04_97/diabetes.htm

http//www.DefeatDiabetes.org

– See more at http://dartmed.dartmouth.edu/winter08/html/diabetes_detectives.php

Medicines that will burn out your pancreas (Sulfonylureas)

Beta-Cell-Burnout

There is a growing trend I am seeing that is extremely disturbing. We are finding many doctors not adequately explaining or giving no explanations of the dangers of some of the medicines they are proscribing.

Someone had the bright idea some time ago to use a drug to “stimulate” the pancreas into making extra insulin. Not let put this into an example that will be easier to understand.

Let’s say you have a little car with a small engine and you try to race someone with a much larger car and engine. To even have a chance of beating them you are going to have to run your engine much harder than is safe. As the RPM’s climb in your little engine it has a greater chance of having any type of failure due to the heavy-handed use of it. Even the drag racer knows this concept and many of them will rebuild their engines after each run to make sure they don’t fail.

Now, applying that to your pancreas and beta cells. (the beta cells are the cells that produce insulin) We do not yet have the technology to rebuild our pancreas. Or replace the lost beta cells. Yet.

Eventually, we should be able to duplicate the live beta cells (clone) and install them back in our pancreas, thereby curing our diabetes. However, those of us that have burnt out our beta cells in our pancreas so there is nothing left by taking these medicines will be unable to have this beta cell transplant.

So you have to ask yourself, do you want to save some of your beta cells so that you can benefit from the future technology? Or take this medicine so much that you become insulin dependant for the rest of your life?

One thing I have not mentioned yet is how these drugs work. They stimulate the vagus nerve that leads to the pancreas. Another problem that has occurred is that this same vagus nerve stimulates the heart. In some cases there have been heart issues from this “overclocking”.

Here are several links that will explain more and list the names of the medicines. YOU are YOUR best advocate for YOUR health. Inquire to your MD about the long term ramifications of the meds you are on.

Sulfonylureas

Dangers of Sulfonylureas for Diabetes

Heart Attack from Sulfonylureas

Januvia Virtually Identical to Glipizide

The Declining Role of Sulfonylureas as Add-on Therapy

Glycemic Index and Glycemic Load

Glycemic Load (GL) is a ranking system for carbohydrate-rich food that measures the amount of carbohydrates in a serving of food.

Foods with a glycemic load (GL) under 10 are considered low-GL foods and have little impact on your blood sugar; between 10 and 20 moderate-GL foods with moderate impact on blood sugar, and above 20 high-GL foods that tend to cause blood sugar spikes.

Glycemic Index (GI) indicates how rapidly a carbohydrate is digested and released as glucose (sugar) into the blood stream. In other words, how quickly foods break down into sugar in your bloodstream. A food with a high GI raises blood sugar more than a food with a medium to low GI.

But the glycemic index does not take into account the amount of carbohydrate in a food. So glycemic load is a better indicator of how a carbohydrate food will affect blood sugar.

If a food has a high glycemic index and a low glycemic load — like graham crackers have a GI of 74 and a GL of 8.1 — how will that affect your blood sugar?

Food ranked high on the GI may represent a huge portion of a food because GI is not based on standard serving sizes. Basically, if a food is ranked high on the glycemic index it has readily available carbohydrate for quick absorption. However, the same food can have a low glycemic load because there may not actually be much total carbohydrate in a given serving of that food. A low GL is the better indicator that a food won’t have much impact on blood glucose levels.

Here are two examples: Watermelon has a high GI of 72, yet a low GL of 7.21. The high GI is based on 5 cups of watermelon, not an actual serving size of 1 cup. The low GL means one serving of watermelon doesn’t contain much carbohydrate, because it is actually mostly water. The low GL indicates that a serving of watermelon won’t have much impact on your blood sugar.Carrots are another example of a low GL food that many people think will raise their blood sugar a lot — but it’s not true. That’s because carrots have a high GI of 71. However, what most people don’t know, is that the GL for carrots is only 6. Therefore, unless you’re going to eat a pound and a half of carrots in one sitting, an average serving of carrots will have very little impact on blood glucose levels. That said, juicing carrots — which means consuming more carrots at once — will have a greater impact on blood glucose.

How can knowing the glycemic load and glycemic index of foods be used to make healthier eating choices?

Everyone can benefit by eating a balanced diet of protein and fat, and foods that are lower on the GL and GI index. Foods with a lower GL and GI typically are high in fiber and nutrients and sustain your energy better throughout the day.

Also, knowing the GL of a food is a better indicator of whether that food will cause your blood sugar to spike. When your blood sugar spikes, the body releases extra insulin to bring down your blood sugar. If your body is asked to release extra insulin on a regular basis, it begins to lead to insulin resistance for many people and diabetes — especially if diabetes is in your family.

Can knowing the glycemic load of foods help people lose weight?

Yes. Consuming low GL and GI foods keeps us satiated longer because these foods are more slowly broken down for glucose utilization. The result is that you feel fuller for longer.

When you consume high GL and GI foods, blood sugar levels spike which causes a short-term feeling of fullness, but then blood sugars plummet which causes you to crave food again and you ultimately end up consuming excess calories, which contributes to weight gain.

This is particularly dangerous for diabetics, when they treat the spike to lower their blood sugar and the spike goes away it can cause a low blood sugar event.

Here are some foods and some values:

Food GI Serving Size (g) GL
CANDY/SWEETS
Honey 87 1 Tbs 3
Jelly Beans 78 1 oz 22
Snickers Bar 68 60g (1/2 bar) 23
Table Sugar 68 2 Tsp 7
Strawberry Jam 51 2 Tbs 10.1
Peanut M&Ms 33 30 g (1 oz) 5.6
Dove Dark Chocolate Bar 23 37g (1 oz) 4.4
BAKED GOODS & CEREALS
Corn Bread 110 60g (1 piece) 30.8
French Bread 95 64g (1 slice) 29.5
Corn Flakes 92 28g (1 cup) 21.1
Corn Chex 83 30g (1 cup) 20.8
Rice Krispies 82 33g (1.25 cup) 23
Corn pops 80 31g (1 cup) 22.4
Donut (lrg. glazed) 76 75g (1 donut) 24.3
Waffle (homemade) 76 75g (1 waffle) 18.7
Grape Nuts 75 58g (1/2 cup) 31.5
Bran Flakes 74 29g (3/4 cup) 13.3
Graham Cracker 74 14g (2 sqrs) 8.1
Cheerios 74 30g (1 cup) 13.3
Kaiser Roll 73 57g (1 roll) 21.2
Bagel 72 89g (1/4 in.) 33
Corn tortilla 70 24g (1 tortilla) 7.7
Melba Toast 70 12g (4 rounds) 5.6
Wheat Bread 70 28g (1 slice) 7.7
White Bread 70 25g (1 slice) 8.4
Kellogg’s Special K 69 31g (1 cup) 14.5
Taco Shell 68 13g (1 med) 4.8
Angel food cake 67 28g (1 slice) 10.7
Croissant, Butter 67 57g (1 med) 17.5
Muselix 66 55g (2/3 cup) 23.8
Oatmeal, Instant 65 234g (1 cup) 13.7
Rye bread, 100% whole 65 32g (1 slice) 8.5
Rye Krisp Crackers 65 25 (1 wafer) 11.1
Raisin Bran 61 61g (1 cup) 24.4
Bran Muffin 60 113g (1 med) 30
Blueberry Muffin 59 113g (1 med) 30
Oatmeal 58 117g (1/2 cup) 6.4
Whole wheat pita 57 64g (1 pita) 17
Oatmeal Cookie 55 18g (1 large) 6
Popcorn 55 8g (1 cup) 2.8
Pound cake, Sara Lee 54 30g (1 piece) 8.1
Vanilla Cake and Vanilla Frosting 42 64g (1 slice) 16
Pumpernickel bread 41 26g (1slice) 4.5
Chocolate cake w/chocolate frosting 38 64g (1 slice) 12.5
BEVERAGES
Gatorade Powder 78 16g (.75 scoop) 11.7
Cranberry Juice Cocktail 68 253g (1 cup) 24.5
Cola, Carbonated 63 370g (12oz can) 25.2
Orange Juice 57 249g (1 cup) 14.25
Carrot juice (freshly made) 43 250g 10
Hot Chocolate Mix 51 28g (1 packet) 11.7
Grapefruit Juice, sweetened 48 250g (1 cup) 13.4
Pineapple Juice 46 250g (1 cup) 14.7
Soy Milk 44 245g (1 cup) 4
Apple Juice 41 248g (1 cup) 11.9
Tomato Juice 38 243g (1 cup) 3.4
LEGUMES
Baked Beans 48 253g (1 cup) 18.2
Pinto Beans 39 171g (1 cup) 11.7
Lima Beans 31 241g (1 cup) 7.4
Chickpeas, Boiled 31 240g (1 cup) 13.3
Lentils 29 198g (1 cup) 7
Kidney Beans 27 256g (1 cup) 7
Soy Beans 20 172g (1 cup) 1.4
Peanuts 13 146g (1 cup) 1.6
VEGETABLES
Potato 104 213g (1 med) 36.4
Parsnip 97 78g (1/2 cup) 11.6
Carrot, raw 92 15g (1 large) 1
Beets, canned 64 246g (1/2 cup) 9.6
Corn, yellow 55 166g (1 cup) 61.5
Sweet Potato 54 133g (1 cup) 12.4
Yam 51 136g (1 cup) 16.8
Peas, Frozen 48 72g (1/2 cup) 3.4
Tomato 38 123g (1 med) 1.5
Broccoli, cooked 0 78g (1/2 cup) 0
Cabbage, cooked 0 75g (1/2 cup) 0
Celery, raw 0 62g (1 stalk) 0
Cauliflower 0 100g (1 cup) 0
Green Beans 0 135g (1 cup) 0
Mushrooms 0 70g (1 cup) 0
Spinach 0 30g (1 cup) 0
FRUIT
Watermelon 72 152g (1 cup) 7.2
Pineapple, raw 66 155g (1 cup) 11.9
Cantaloupe 65 177g (1 cup) 7.8
Apricot, canned in light syrup 64 253g (1 cup) 24.3
Raisins 64 43g (small box) 20.5
Papaya 60 140g (1 cup) 6.6
Peaches, canned, heavy syrup 58 262g (1 cup) 28.4
Kiwi, w/ skin 58 76g (1 fruit) 5.2
Fruit Cocktail, drained 55 214g (1 cup) 19.8
Peaches, canned, light syrup 52 251g (1 cup) 17.7
Banana 51 118g (1 med) 12.2
Mango 51 165g (1 cup) 12.8
Orange 48 140g (1 fruit) 7.2
Pears, canned in pear juice 44 248g (1 cup) 12.3
Grapes 43 92g (1 cup) 6.5
Strawberries 40 152g (1 cup) 3.6
Apples, w/ skin 39 138g (1 med) 6.2
Pears 33 166g (1 med) 6.9
Apricot, dried 32 130g (1 cup) 23
Prunes 29 132g (1 cup) 34.2
Peach 28 98g (1 med) 2.2
Grapefruit 25 123g (1/2 fruit) 2.8
Plum 24 66g (1 fruit) 1.7
Sweet Cherries, raw 22 117g (1 cup) 3.7
NUTS
Cashews 22
Almonds 0
Hazelnuts 0
Macademia 0
Pecans 0
Walnuts 0
DAIRY
Ice Cream (Lower Fat) 47 76g (1/2 cup) 9.4
Pudding 44 100g (1/2 cup) 8.4
Milk, Whole 40 244g (1 cup) 4.4
Ice Cream 38 72g (1/2 cup) 6
Yogurt, Plain 36 245g (1 cup) 6.1
MEAT/PROTEIN
Beef 0
Chicken 0
Eggs 0
Fish 0
Lamb 0
Pork 0
Veal 0
Deer-Venison 0
Elk 0
Buffalo 0
Rabbit 0
Duck 0
Ostrich 0
Shellfish 0
Lobster 0
Turkey 0
Ham 0

Just remember your results as a diabetic may vary, so always test, test, test!