Basic Health Practices

Sorry, I have an ear infection that’s driving me crazy. Started Sunday morning, and now it’s getting painful and my hearing is diminishing. I’ll run to the urgent care clinic this afternoon, and get some antibiotics, I presume, but this entry has to be brief.

Complete Breathing: When I was 16, I was fortunate to attend the Eastern Music Festival, here in Greensboro, NC, playing french horn. There, the wind players (at least) were instructed in abdominal breathing, sometimes referred to as ‘yogic breathing.’ This consists simply of breathing down, not up, as you inflate your lungs. Take a deep breath, looking at your shoulders. If they go up and your chest expands, you’re not breathing correctly. Try breathing down, so your belly expands. Your chest shouldn’t move. This is much less work also, and gets more oxygen into the bloodstream.  This is the natural way to breathe, but most of us, as children, adopt the far worse technique of breathing by swelling our chest, to look impressive, as animals do when they raise their fur to look bigger and more imposing.

The ancient Indian texts devote much space to ‘prana,’ or breath. The following is a link

http://holisticonline.com/Yoga/hol_yoga_breath_home.htm

(cut and paste into address bar) to a prana site, which covers all the basics of this yoga.

This way we get as much oxygen as possible into the bloodstream. The next step is to get as much blood as possible to the tissues. Some of my recommendations will be controversial, but please bear with me. I’ll try to continue tomorrow.

Glycosylation Reconsidered

I was going through some of the articles I intend to post here, since I have yet to figure out how to use the sidebars, and came across one that concerns a comment I made earlier, that the A1c marker  used to measure the diabetic patient’s condition, indicated the long-term attachment of glucose to the hemoglobin molecule, but that the attachment was not immediately harmful. Actually, what I asked my doctor originally, about 8 years ago, was, ‘did the attachment interfere with the hemoglobin’s ability to ferry oxygen?’ and he assured me it didn’t.  Of course, that’s not the whole story. This article,  published in 2000, concerning AGEs or Advanced Glycosylation End Products, which have severe consequences for cells exposed to high levels of sugar over long periods of time. This is why it’s so important to maintain sugars as closely to normal as possible. Here’s the article, I’ll continue below.

A.G.E. Formation - The Road To Diabetes,
Disease, & Aging
http://www.alteonpharma.com/age_backgrounder.htm
3-14-00

It appears that A.G.E. formation is an important element in solving the (aging) mystery. The same common chemical process that toughens and discolors food in storage also takes place in the human body, and apparently may play a direct role in the development of diabetic complications such as kidney failure, blindness, heart disease, and in age-related diseases such as Alzheimer’s disease.

When glucose, the most abundant sugar in the body, attaches itself to proteins without the aid of enzymes, a series of chemical reactions results in the formation and eventual accumulation of irreversible bonds, or Crosslinks, between proteins. This “molecular glue”, known as Advanced Glycosylation End-product, or A.G.E.s, causes proteins that are normally flexible and separate to become rigid and attached, making cells, tissues and organs stiff and increasingly less functional. In healthy individuals, this process occurs naturally, though slowly, as the body ages. In diabetic patients, the rate of A.G.E accumulation and the extent of protein cross-linking is accelerated, probably playing a role in many medical disorders.

The nonenzymatic reaction between glucose and proteins, known as the Maillard or browning reaction, begins when sugar carbonyl groups and protein amino groups combine, forming Schiff bases. These unstable combinations quickly rearrange into somewhat more stable substances called Amadori products. On long-lived proteins that are not normally recycled within the body for months or years, problems can develop when some of the Amadori products dehydrate. They then rearrange themselves forming A.G.E.s and eventually mediate the cross-linking of proteins.

In the early 1980s, researchers speculated that large amounts of A.G.E.s occurred in diabetic patients as a result of their elevated blood sugar levels. The A.G.E.s could be the missing link between diabetes itself and the devastating complications of the disease which occur after years of high blood sugar. Subsequent research conducted at more than 40 institutions around the world has supported this hypothesis, offering encouragement that severe diabetic complications such as kidney failure, blindness, nerve damage, hypertension, stroke, heart attack, skin ulcers and lower extremity amputations can potentially be prevented or controlled. Currently there are few viable alternatives for the prevention or treatment of diabetic complications.

The effect of diabetes on numerous organs and tissues has been described as accelerated aging because of the similarity between certain diabetic complications like cataract, joint stiffness and atherosclerosis (a build-up of plaque in the artery walls) and disorders of the elderly. Research suggests that if excess glucose hastens the onset of complications in diabetic over a relatively short time-span, normal amounts of glucose might play a part in a wide range of age-related disorders that occur much more slowly and appear only later in life. For example, studies indicate that nonenzymatic glycosylation of the eye’s lens proteins may contribute to the formation of cataracts. More recent studies implicate A.G.E.s in age-related disorders such as Alzheimer’s disease and stroke.

Similarly, scientists speculate that glucose encourages plaque formation characteristic of atherosclerosis by causing A.G.E.s to develop on the collagen in blood vessel walls. Circulating low-density lipoproteins or LDL are also subject to A.G.E. chemistry and may be trapped from the blood and accumulate to form cholesterol deposits.

Alteon’s current research and drug development focused on A.G.E. technology takes two directions: the prevention or slowing of A.G.E. formation, and the breaking of A.G.E. Crosslinks between proteins in order to prevent or reverse damage.

Obviously, glycosylation is minimized when sugars are maintained as near normal as possible.

OK, now it should be obvious that the more blood sugar is kept near or close to normal, the better you’ll be in the long run. The other major factor in staying healthy, is easy to say, but oftern hard to do:

DON’T EAT WHEN YOUR SUGAR IS HIGH!!!

Or, at least don’t consume foods which have a significant glycemic index rating. Nothing that breaks down (quickly) into sugar, in your bloodstream. That is, no carbs (bread, rice, pasta, potatoes etc.), absolutely no sweets, and probably fried food (I don’t eat fried food since I started on Humulin(TM) so I can’t speak from experience). You CAN, in moderation, eat protein like meat or fish, alone, not mixed with other things, seeds and nuts (remember, peanuts and cashews are beans, not nuts) up to a point, most (raw) root and leafy vegetables. Not beets! (Don’t eat them myself due to an unfortunate childhood experience, but it seems unlikely, since they make sugar out of them), and remember, things get sweeter as they decay. A banana that’s just past being green is barely sweet at all and has little effect on your blood sugar, but try another one a couple of days later, especially if it’s going soft, and watch your sugar skyrocket.

Part of getting to normal every day is bringing your sugar down when it stays high for more than a few hours. In my case, it usually returns to normal [on the days when it leaps up to an abnormal degree following a small breakfast, the same each day, consisting of a balanced, measured amount of carbohydrates, vegetables and protein, in that order (actually tastier than it sounds)] as my insulin activity approaches its peak 7 to 8 hours after my morning injection. Usually, although not predictably, it then drops back to normal and I eat. When it doesn’t come down in time for me to be able to eat before bed, I will resort to using a fast-acting analog, either Humalog(TM) or some of the small amount of Regular(TM) I have left. Humalog(TM), I use if I can remain awake for the action cycle of about 3 hours (actually, I like to allow up to 4), but if I need to go to sleep, Regular had become quite useful until Lilly stopped making it a few of years ago. See, when Lilly stopped making their Regular (I’ve always hated that name, you can’t say ‘my regular insulin,’ without having to explain that Regular wasn’t your regular insuline, that was something else) insulin from animals and started brewing it in vats, they changed the activity cycle from 3 hours to 9 hours. I know this, because I was keeping my insulin/food/exercise log when I needed to add a supplemental couple of units of Regular for a few days to cover a higher postprandial excursion I’d been experiencing. I showed the log to my doctor at the time,  who remarked,”that’s exactly what I’d do.” I’d been doing this when needed for years with Regular, and knew what to expect. After a few days, however, it became obvious something was different. My sugar remained very high after breakfast, didn’t come down by lunch, as it usually did, and then suddenly, 8-9 hours after the shot, plummetted. After a few days of this, I stopped taking the Regular(TM) and told my doctor about it, that its onset seemed to be delayed and started acting at the same time I was starting the NPH peak. He agreed it was curious.

I looked online and found out that was indeed the case, the activity cycle had been changed upward but no-one, it seemed had informed any doctors. The doctors I worked with at the time hadn’t heard of it. It turned out, a nine hour insulin was very convenient for the situation described above, where you have to go to bed, but need your sugar to come down while you sleep, and for those of us with HGU (hypoglycemia unawareness), having an insulin that let us go through most of the night without having to worry about blacking out in our sleep is very handy.

So, up til now we have:

GET TO NORMAL EVERY DAY (whatever it takes)

DON’T EAT WHEN YOUR SUGAR IS HIGH

In addition to these simple principles, there are a few techniques for maintaining general health, but which are especially useful for diabetics. I’ll list them now, then come back over the next few days and detail them

Breathe Completely

Eat Less

Oxygenate the Blood

Enhance Blood Flow

To be Followed

A Brief History of Hypoglycemia Unawareness

Chronology of Literature on Hypoglycemic Unawareness
(Originally Published by David G. Groves in 1992)

© 1992 David Groves
Updated 04/06/04 05:20:23 PM

1921

From the first use of insulin after its isolation by Banting and Best in 1921 in Canada, patients had problems with hypoglycemia (low blood sugars) in response to the injected medication.

1941

By 1941 it is noted by Lawrence (1) that the early warning symptoms; weakness, faintness, tremors, sweating, hot or cold feelings, palpitations, appear to be similar to the symptoms of a dose of adrenaline, and that additional symptoms of hunger, visual disturbance, diplopia and tinglings also give advance warning of hypoglycemia onset in the 50-70mg/dl blood sugar range. It is further noted that should such symptoms go unrecognized or unnoticed, they are followed by mental confusion exactly simulating alcoholic intoxication, muscular twitchings, convulsions, epileptiform seizures, transient hemiplegias, and complete coma.

Finally, this article notes the first reference to a condition now called “hypoglycemic unawareness” (HGU) and notes, “The same patient may at one time experience early premonitory warnings and at another be quite unaware of an impending [sic] attack. It is obvious that these are serious dangers.” Lawrence also observes, ” … considering the large number of stupid or careless patients on insulin treatment, serious attacks and sequelae are exceedingly rare.”

1962-1981

Various articles in various sources are published on synthetic and/or recombinant DNA means for the production of “human” insulin. D. Rabinowitz et al, report (2), “… adiposity diminishes insulin sensitivity.”

Riggs (3) reports Lilly’s $40mm investment to put human insulin in large-scale production by late 1982. Goes on to recite Keen (4) The insulin from bacteria was virtually indistinguishable from porcine insulin in lowering plasma glucose levels in normal human volunteers. Most important there were no adverse side actions.” Chance, et al, report similar findings.(20).

Sotos Raptis et al report, (5) “The feeling of hypoglycemia in the group that received the BSI [Biosynthetic Human Insulin] was significantly less intense then in the PPI [Purified Pork Insulin] group.”  The fact that this reduction of hypoglycemic symptoms was observed in a group as small as 5 healthy volunteers and 5 diabetic volunteers is of critical importance.

Gerich (6) reports, “… BHI appears to offer no advantage over presently available PPI in terms of prevention and treatment of lipodystrophy, insulin allergy and immune insulin resistance.”

Goldstein, et al, report (7), reciting from a 1977 study, that, “Hypoglycemia is considered a serious complication of insulin therapy…,” and that, ” … frequent or severe hypoglycemia occurred almost exclusively in patients with well controlled diabetes …”

July 1982

Peter J. Watkins recites (8), “Hypoglycemia is the major hazard of insulin treatment. … All diabetics on insulin who are reasonably well controlled will experience hypoglycemia at some stage. At its mildest it is no more than a slight inconvenience, but at its severest, when unconsciousness can occur, it is both a hazard and an embarrassment. … All diabetics must be carefully taught about the causes, symptoms and treatment of hypoglycemia. Ideally, new diabetics should be made to experience hypoglycemia during their initial education.”

He goes on to list “Early Warning Symptoms as, “Shaking, trembling; Sweating; Pins and needles in the lips and tongue; Hunger; Palpitations; Headache” and then proceeds as secondary and more advanced symptoms, to list, “Neutroglycopenia: Mild: Double vision; Difficulty in concentrating; Slurring of Speech — More Advanced: Confusion; Change of behavior; Truculence; Naughtiness in Children — Unconsciousness: Restlessness with Sweating; Epileptic fits, especially in children; Hemiplegia.”

He goes on to state, “Most diabetics experience the early warning symptoms of hypoglycemia and can take sugar before more serious symptoms develop. With increasing duration of diabetes … there is a tendency for early warning symptoms not to occur, and patients develop the more serious problems. Although this lack of warning has been attributed to autonomic neuropathy, I doubt whether this is generally the case…”

October 1982

R. B. Tattersall et al report (9), “Hypoglycemia is the commonest complication of treatment with insulin, but little is known about its true incidence. For example, in 1977 the argument that improved control might lead to increased morbidity and mortality from hypoglycemia could neither be refuted nor sustained since the basic information was lacking.” They go on to discuss why information on hypoglycemia is difficult to obtain and unreliable. The results show 37.4% of hospital admissions for hypoglycemia arose with no known cause, 13.7% from changes in insulin dose and 8.9% resulted from loss of awareness.

Early 1983

C. Goldgewicht et al report (10), ” … thinner patients have more severe reactions … “

January 1985

The 1985 PDR (physician’s Desk Reference) under all Lilly Humulin preparations under warnings (see additional warnings above) states amongst other things, The first symptoms of insulin reaction usually come on suddenly and may include fatigue, nervousness or shakiness, headache, rapid heart beat, nausea, and a cold sweat. A few Patients who experienced hypoglycemia after being transferred to Humulin have reported that these early warning symptoms were less pronounced than they were with animal source insulins.

[Note that this is perfectly consistent with the findings reported by Sotos Raptis et al (5) and that it is possible that Lilly had such a warning in place from the first bottle sold commercially in the US, this however was the oldest PDR your researcher could find.]

January 1986

The American Hospital Formulary Service “Drug Information ‘86 Listings” under 68:20:08 AntiDiabetic Agents at page 1564 states, under Pork Insulins, “… Cautions: … hypoglycemic reactions have also been reported in patients who were transferred from beef to pork insulin or from mixed beef or from beef to mixed beef/pork preparations. … Symptoms of hypoglycemia are usually manifested when the administered insulin reaches its peak action and may include hunger, pallor, fatigue, mild or profuse perspiration, headache, nausea. palpitation, numbness of the mouth, tingling in the fingers, tremors, muscle weakness, blurred or double vision, hypothermia, uncontrolled yawning, irritability, mental confusion, tachychardia, shallow breathing and loss of consciousness.

Early 1986

W. Berger and B. Althaus report (11) the existence of “hypoglycemic unawareness” with human insulins.

Early 1987

Fully 6 years after Raptis et al (5) have disclosed changed, reduced and therefor possibly lost advanced warning symptoms of hypoglycemia, at least 2 and more likely 3-5 years after Lilly has disclosed the potential loss of vital early warning symptoms before severe hypoglycemia, Squibb/Novo/Nordisk says nothing about the potential reduction in symptoms on changing to their Novolin. In a crass bid to invade Lilly’s US market share for human insulin they say only, the first warning symptoms of insulin reaction usually come on suddenly. They may include a cold sweat, fatigue, nervousness or shakiness, rapid heartbeat or nausea.” PPI shows last revision date of 10/86. [N.B.: the sweat symptom is totally adrenergic and this list from the Novolin insert is a fair symptom list for animal insulin but is totally incorrect for human insulin. Ed.]

April 21, 1987

8 hours after taking 11 units of Novolin Regular, which is supposed to peak in 2 hours and be totally out of the system in 8 hours, having taken the insulin in usual fashion before lunch at about 11am, David Groves falls unconscious at the wheel of his car around 7pm. Upon admission to the ER at Jackson Memorial Hospital with multiple trauma injuries from colliding with a parked car at a speed in excess of 65mph, Groves shows negative for alcohol and is revived by IV infusion of 50% dextrose, proving unconsciousness and accident must have been caused by severe insulin shock (hypoglycemic insulin reaction).

August 1987

Teuscher & Berger report (12) that based on their clinical experience with 3 cases of patients transferred from beef/pork insulin to Novo human insulins (reported in the article and presumably to Novo-Nordisk) there occurred multiple instances of, “peculiar and serious hypoglycemic reactions,” in the three patients. These adverse reactions were reported as they occurred. 3 in 1985 (including an auto accident and a switch back to porcine insulin after which normal early warning symptoms returned), 4 in 1986, the last of which was fatal, and 1 in early 1987. The presentation recites the Lilly warnings available in the US in 1987 and decries their absence in Europe. The study proceeds to examine 315 patients: 206 on human (Novo, Lilly, Nordisk) and 109 on beef/porcine or Porcine (Novo, Nordisk) between 9/86 and 2/87. 176 patients (of the 206 on human) were transferred between 1983 and 1987 and 30 had been started on human. 36% of the patients reported a loss of adrenergic early warning symptoms. The authors conclude, “Hypoglycemia unawareness with a blood glucose of 1-3mm/1 [18-54 mg/dl] was a characteristic finding in patients treated with human insulin. … The general well-being of such patients may seem to improve because of the reduced frequency of hypoglycemic symptoms. This observation is important for car drivers. …

The only universally accepted benefits of human insulin at present are the management of the few patients with insulin allergy and the possibility of the very rare insulin resistance. These seem to be small gains in comparison with the possible loss of well-being and the life threatening hazards associated with hypoglycemia unawareness. We are therefore concerned about the apparent marketing effort of manufacturers to influence physicians and patients to switch from animal to human insulin.”
Tattersall et al report (13) in a study of whether or not adrenal activity is responsible for hypoglycemia unawareness, “Our study shows that at mild levels of hypoglycemia subjects who recognized a low blood glucose were those with significant increases in circulating adrenaline and features of sympathetic nervous system activation. In contrast, 11/15 [11 of the total 15 subjects. ed.] patients who remained unaware had smaller increases in adrenaline and no symptoms or signs. …”

In the study of Sussman and colleagues (14) only 5 of 44 diabetic patients did not have a sympathetic response during insulin-induced hypoglycemia.” [NB Sussman's 44 were all on animal insulin while Tattersall's 15 were on Novo Actrapid Human, the equivalent of their US Novolin and we see 73% unawareness in the Tattersall group but only 11% unawareness in Sussman's group. The authors fail to make this observation.] They (Sussman et al.) go on to state that, “Subnormal increases in adrenaline with loss of warning during hypoglycemia are thought to occur only in long standing diabetics with autonomic neuropathy. However, most of our patients (with durations of diabetes from 3 to 33 years) had a reduced catecholamine response, suggesting that impaired sympathetic responses during hypoglycemia may be the rule in insulin treated patients…” [NB the human insulin is not postulated as the cause here, though it is the most obvious source of the major change in medical theory on HG that this article is suggesting.] They conclude, “We believe the major cause of severe hypoglycemic episodes to which diabetic patients with impaired adrenaline responses are prone (15) may be a failure to recognize a low blood glucose in time to correct it.” [NB Hypoglycemic unawareness defined yet again. ed.]

April 1989

Frank Lesser reports (16), and a month later, David Groves reads, “Preparations of ‘Human’ Insulin may put some insulin-dependent diabetics at life-threatening risk by depriving them of the warning symptoms of hypoglycemia,…” article cites a 1988 study from Balance, the Journal of the British Diabetic Association in which 53% of 158 patients transferred from animal insulin to human insulin, felt the warning of hypoglycemia less clear.

August 1989

Frank Lesser reports (17) on reports from forensic toxicologist, Dr. Patrick Toseland that deaths from hypoglycemic reaction have risen in Britain from 2 in 1985 to 9 in 1988 to 17 in the first half of 1989 and that at least half were patients who had switched to human insulin from animal insulin. The article goes on to underscore the fact that Lilly has been warning patients of this problem since at least 1987 while Novo had not but that in late 1989, Nordisk Wellcome [Squibb-Novo-Nordisk Britain] had begun issuing similar warnings after discussion in March with Britain’s Committee on Safety of Medicines (their equivalent of our FDA).

October 1989

Bill Richards, Staff Reporter for the Wall Street Journal reports (18) on the Toseland findings and states that the FDA “already requires drug manufacturers to include warnings with insulin products that symptoms of hypoglycemia are less pronounced with human insulin than with animal based products.”

R.J. Heine, et al, report (19) a statistically significant differential in Adrenergic Symptoms (p < 0.05), Tachycardia (p < 0.05), and Noradrenaline (p < 0.05) release in 8 healthy subjects. The porcine insulin causing more symptoms, faster heart rate and more noradrenaline. Their data also suggest an increase in neuroglycopenic symptoms and adrenaline production in the porcine insulin over the human insulin but these results are not countenanced since they are  (as little as) p > 0.05.

They conclude, “The physicochemical characteristics of human and porcine insulin are different. Porcine insulin is more lipophilic than human insulin and may have greater blood-brain barrier penetration. This may explain the observed difference in autonomic response.”

1990

Dr. Robert J. Moss, Pharm. D. as Associate Director, Professional Services for Novo Nordisk Pharmaceuticals Inc. issues indemnification certificates to all US Pharmacies selling Novo insulins. Indemnity covers claims or lawsuits alleging personal injury as the result of using Novo Nordisk standard insulins, subject to use and dispensation in accordance with the PPI. [Curiously issued after the split between Squibb and Novo-Nordisk and after the insertion of the FDA required warnings into the patient package insert.]

1991

A super-plenum of articles are published “proving” that human insulin is the equivalent of porcine insulins. The proofs, however, are all flawed. Several show the results we have already displayed, but discount them for their failure to achieve statistical significance (p < 0.05), most of them use hypoglycemia symptoms NOT listed in the human insulin PPI’s and some even create new symptoms or use unconsciousness itself as a symptom. Most of the “new” symptoms are symptoms that by definition the insulin-using patient would NOT be able to identify or symptoms which would tend to prevent the patient from taking appropriate corrective action.

November 1991

Eli Lilly and Company Pharmaceutical Division mails a letter to all of the Certified Diabetes Educators in the US taking the offensive against Novo Nordisk. The letter claims, inter alia, that Novo’s promotional literature for its new biosynthetic (as opposed to semi-synthetic) human insulin, violates USP approved labeling for all human insulin products.

REFERENCES

1.  “INSULIN HYPOGLYCEMIA CHANGES IN NERVOUS MANIFESTATIONS” R. D. LAWRENCE, M.D. ABERD, F.R.C.P, LANCET, Nov. 15, 1941, p.602

2. “Forearm Metabolism in obesity and its response to intra-arterial insulin. Characterization of insulin resistance and evidence of adaptive hyperinsulinism” D. Rabinowitz et al, J CLIN INVEST, 41:2173-2181

3. “Bacterial Production of Human Insulin” Arthur D. Riggs, DIABETES CARE, Vol. 4, No. 1, January-February 1981, p. 62-68

4. “Human insulin produced by recombinant DNA technology: Safety and Hypoglycemic potency in healthy men” H. Keen et al, Lancet 2: 398-401; 1980

5. “Biologic Activities of Biosynthetic Human Insulin in Healthy Volunteers and Insulin-dependent Diabetic Patients Monitored by the Artificial Endocrine Pancreas” Sotos Raptis, et al, DIABETES CARE, Vol. 4, No. 2, p. 161, March-April 1981

6. “An Appraisal of the Role of Biosynthetic Human Insulin in the Future Treatment of Diabetes Mellitus” John E. Gerich, DIABETES CARE, Vol. 4, No. 2, p. 262-63, March-April 1981

7. “A Prospective Study of Hypoglycemia in Young Diabetic Patients ” David E . Goldstein, et al, DIABETES CARE, Vol. . 4 No . 6, p. 601-605, November-December 1981

8. “ABC of Diabetes — HYPOGLYCEMIA” Peter J. Watkins, BRITISH MEDICAL JOURNAL, Vol. 285 p. 278-79, July 24, 1982

9. “Insulin-induced hypoglycemia in an accident and emergency department: the tip of an iceberg?” R. B. Tattersall, BRITISH MEDICAL JOURNAL, Vol. 285, p.1180-82, Oct. 23, 1982

10. “Hypoglycemic Reactions in 172 Type 1 (Insulin-Dependent) Diabetic Patients” C. Golgewicht et al, DIABETOLOGIA, 1983; 24: 95-99 Hypoglycemic Reactions in 172 Type 1 (Insulin-Dependent) Diabetic Patients” C. Golgewicht et al, DIABETOLOGIA, 1983; 24: 95-99

11. “Aenderungen der Hypoglykemie-Fruhsymptome bei Wechsel von tierschem Insulin auf Human insulin” W. Berger & B. Althaus, SCHWEIZ AERTZEZEIT, 1986; 67: 1130-31

12. “HYPOGLYCEMIA UNAWARENESS IN DIABETICS TRANSFERRED FROM BEEF/PORCINE INSULIN TO HUMAN INSULIN” A. Teuscher and W. G. Berger, LANCET, p. 382-85, August 15,1987

13. “INFLUENCE OF SYMPATHETIC NERVOUS SYSTEM ON HYPOGLYCEMIC WARNING SYMPTOMS” R. Tattersall, et al, LANCET, p. 359-363, August 15, 1987

14. “Failure of warning in insulin induced hypoglycemic reactions” K. E. Sussman, et al, DIABETES, 1963; 12: 38-45

15. “Identification of patients of type 1 diabetic patients at increased risk for hypoglycemia during intensified therapy” N.H. White et al, N ENG J MED, 1983; 308: 485-91

16. “‘HUMAN’ INSULIN LOSES ITS CLEAN APPEAL” Frank Lesser, NEW SCIENTIST, p. 30, April 15, 1989

17.  “HUMAN INSULIN COMES UNDER CLOSE SCRUTINY AS NUMBER OF DEATHS RISE” Frank Lesser, NEW SCIENTIST, p. 22 August 19, 1989

18. “REPORTS OF DEATHS AMONG U.K. DIABETICS USING HUMAN INSULIN STIR CONCERN HERE” Bill Richards, WALL STREET JOURNAL, Metro DC edition sometime in or near the week of 10/23-30/1989

19. “RESPONSES TO HUMAN AND PORCINE INSULIN IN HEALTHY SUBJECTS” R.J. Heine, et al, LANCET, p. 946-49, October 21,1989

20. “Clinical, physical and biological properties of biosynthetic human insulin” R.E. Chance, et al, DIABETES CARE, 1981; 4: 147-54

Dave Groves dggroves@earthlink.net

Note: David died a few years ago, so the above address is probably no longer valid–Michael

Blackouts and Basics

I’m afraid I’ve left it a bit late to post today, I work from 5:30 until 11:30 pm, which means (although I like it) sleeping until around 4:00pm because I have to squeeze in work before my insulin, that is Humulin(TM) starts to peak (in 7 to 8 hours, but the timing always varies. (Important Digression; main thread continues below) And I have to let the Humulin(TM) get going in my system for at least an hour, so it’s at least somewhat active soon after eating, waiting most of the hour to eat, if eating is at all possible [checking the log, I see I ate breakfast (2-5 oz. of a pasta, vegetable, meat mix, I eat at least twice a day, to minimize variables) every day this week, m-f, which means I began every day with a normal or near normal blood sugar. That’s a pretty good week, because reaching euglycemia, or normal blood sugar at least once every day will ensure you will not experience (with the exception of unusual circumstances, such as illness) ketoacidosis, period. This is one of the pillars of my technique: GET TO NORMAL EVERY DAY)

I can’t stress this enough, the only target for your blood sugar is normal blood sugar. This is the only way to avert complications down the road. The downside to this is that You will experience hypoglycemias. I know, even for those receiving adequate warning, reactions can be terrifying,  Twenty seven years ago, in between school I worked with a lady who remarked on the equanimity with which I endured and remedied insulin reactions. She told me her diabetic husband was terrified of them. Her husband was a very large, strong and thoroughly imposing guy and you wouldn’t expect that sort of response, so I know how scary insulin shock can be. Think how bad it is for someone who can’t tell, most of the time, that it’s even happening!  I see doctors, who are trying to help their patients avoid these events, encourage patients to maintain their sugar at what I consider alarmingly high levels. My friend Fred, with a diabetic daughter, told me that once at a support group meeting, he was talking to a woman who said her sugar hadn’t been under 200mg/dl in 6 months. I was horrified, I said ‘Fred she needs to be under a doctor’s care!’ He replied, ‘What are you talking about, Mike? She IS under a doctor’s care!”

The problem is, in a few years, she’ll be experiencing gradually increasing complications, cardiovascular and renal (kidneys). Her eyesight will be rapidly deteriorating (I’ll show you how to prevent that later) and she’s going to end up blind, ischemic (interruptions of blood supply) and on dialysis. THIS IS NOT A GOOD TRADE-OFF! Hypoglycemias can, in most cases, be dealt with easily and quickly (although for the elderly patient, already advanced in years, the equation might be re-examined), and this is a much simpler and easier process than living on dialysis or being blind, Then, of course there are the other commonplace results of perpetual high blood sugars, such as  losing limbs, not fun.

(This is not intended to be unfairly critical of doctors. By far, most doctors are very hardworking and immensely compassionate, especially my last three doctors, people. They’re in a hopeless position, trapped between loyalty to their patient and the draconian dictates of “managed” care accountants.

On top of that they’re being lied to, yes, I said it, by pharmaceutical drug dealers interested only in perpetuating, not curing conditions which garner them billions every year. Rezulin (troglitazone) springs to mind, the TZD (thiazolidinediones: http://en.wikipedia.org/wiki/Thiazolidinedione) medication, reported on by 60 Minutes, in which pharmaceutical representatives state that when briefing doctors on Rezulin, if asked about  possible adverse effects, they were instructed to ’steer the conversation to another topic.’ Rezulin killed at least 63 people, although I’m pretty sure NPR revised that number upward more recently.    http://www.yourlawyer.com/topics/overview/rezulin)

Thread Coninues:– because that is when most of my hypoglycemias or blackouts occur, although they can and have occurred pretty much every hour of the day. Naturally, they tend to correlate with the rise and fall of the insulin activity. Anyway, I’m awake all night and  had a friend come over, I hadn’t entertained in a long time, so with one thing and  another, it’s already bedtime. But I would like to at least post links to some of the articles I’ve been collecting over the last 8 years, if I can figure out how, hang on. Also, I wanted to mention some of the other topics I intend to discuss, including the structure of insulin, why Humulin(TM) is NOT insulin, the role of Big Pharma in the selection and editing of research on a number of products, including insulin and the relationship between Humulin(TM) and osteoporosis     (Daniels, Stephen R. M.D. , Ph.D. The Journal of Pediatrics, Vol. 144, Issue 1, Jan. 2004, page A3 — “Type 1 Diabetes and Osteoporosis”). At the same time, along, hopefully, the left edge, I’ll post the hourly log, I keep every day, and have for nine years, since shortly after I was forced to go to Humulin(TM). One of the purposes of this blog is to shed light on the existence of persons living with Hypoglycemic Unawareness (from now on, I’ll just type ‘HU) and having to depend on a synthetic drug which behaves for over 10%  of the people using it, extremely erratically, causing blood sugar to skyrocket even without food and nearly always after a very small amount of food, then plunging precipitously with the space of minutes to an hour. Source:(http://members.tripod.com/diabetics_world/symptoms_of_synthetics.htm) That is, except for the days when it doesn’t do that

There will be criticisms of the technique described, I know, because of my nearly exclusive use of reagent strips for estimated blood glucose measurement. I yield willingly to these anticipated critiques, I would love to be able to use one of my many glucometers whenever I liked, but the cost of strips is prohibitively expensive for a person who, because of his condition, has to work a little more than part time (up to 30 hours/week so I can get back before the peak gets going).  Also, digressing again for a moment, sometimes it’s not necessary to know exactly where your blood sugar is as long as you know it’s still high, and you need to wait to eat, or it’s not above normal and you CAN eat. People are far more likely to check their sugars more often if all they have to do is pee on a strip. Guys of course have an advantage.    (Insert: I would like to stress that the data I get from reagent tapes is carefully phrased, the color ranges are assigned values which have been repeatedly correlated with one or more (occasionally) glucometers. The data extracted from reagent strips is limited to “110mg/dl or lower” to “160 mg/dl or higher”  or points in between. Also, after years of experience, I can estimate correctly to within 10 milligrams (mg) blood sugars up to 200mg/dl (deciliter or one tenth of a liter). Again I would use a glucometer more often, especially during the peak, if I could afford the test strips. Because of the rapid change in glucose level around the activity peak, when it’s most effective, the 15 minute minimum delay of the reagent reading (only reflects averaged blood glucose for the period since last urination no closer than fifteen minutes earlier–you pee on the end of the strip) blood sugar can drop very low while waiting for the urine to clear. At times like that a glucometer strip is the way to go with a current reading of blood glucose.  On animal insulin, I worked full-time almost exclusively for over twenty years, starting out as a clerk in a bookstore, then manager, then owning my own ten years in, eventually selling the last one, after I started waking up on the floor, confused and missing  a couple of hours (during the first six months I spent on Humulin(TM), before I switched myself back, and all the aforementioned symptoms ceased).  One of the best sites on the web for more information about all aspects of adverse reactions to insulin, including scientific studies, personal accounts and news about diabetes in general, is the website, founded by the late David Groves, who was experiencing the same symptoms I do, but many years earlier, called the Diabetic International Foundation, here is a link to their main page. Theyve been working on this page for several years now, but if you click on ‘the old table of Contents’ link, and scan the long list of articles, you’ll find a great deal of fascinating and infuriating material:

http://members.tripod.com/diabetics_world/

I don’t think these are displaying as links, so you may have to drag, copy and paste into the address bar, I’d open a new tab so you can flip back and forth.

Before I go, I want to post another very valuable link:http://www.childrenwithdiabetes.com

That’s the main site, but here is the page with the Daily News Summary, all the research published that day on diabetes. Scan it, just to get an idea of what’s available:

http://www.childrenwithdiabetes.com/d_0j_200.htm

This is an immensely useful site for anyone researching diabetes, and they’ve kept it up for years. This is a daily log of basically all the published research on diabetes every day for that day.  Statistical extrapolations may also be performed on this database of research, for example, as far back as this log ran, when I first accessed about six years ago, which was the mid 90s, there were, at that time, only two studies (I believe, it was a long time ago, but that was pretty much it) on hypoglycemic reactions, as Humulin(TM) permeated the market, the number of log entries concerning hypoglycemia steadily increased. The correlation is clear.

The entire Children With Diabetes site is well worth a look, especially for families with diabetic children. Will return…

A Diabetic’s Story

7/18/08

(Before we get going, let me first say I am not a doctor and I have had no formal medical training. Nothing you read here should be construed as traditionally informed medical advice. Any inferences are made solely by the reader and any action taken by the reader is entirely that person’s responsibility. Everything I say here is based entirely and solely on my own experiences and research, for which I will, as much as possible, cite my references. Also, it should be noted that the commercial insulins referred to herein are all trademarked products, and if you don’t see a trademark insignia, it should be assumed to be present. I also want to point out that even for a non-diabetic, I am in excellent health still, showing almost none of the usual complications of diabetes, such as retinopathy, the uncontrolled growth of blood vessels over the retina which is the reason diabetes is the leading cause of blindness in the US. This is my 1st blog and it is presently under construction, so please bear with me. In the near future I intend to post a photo of myself, showing as much skin as possible, so you can see for yourself what kind of shape I’m in. I am also going to detail how to prevent retinopathy and other measures for maintaining health, particularly beneficial for diabetics, but also for the general public. It will take probably a few weeks to get it all together.)

My name is Michael Damian Dana, I am now 52 years old. I was diagnosed as a type 1 diabetic (juvenile onset) in June, 1974. This was almost immediately before starting college, and I pretty much ignored the condition, save for taking my daily insulin injections each morning. I was given no further instructions beyond that, and I ate almost anything I wanted, with the sole exception of avoiding sugar. Amazingly, it was three years before I ended up in DKA (diabetic ketoacidosis). I had actually stopped taking shots for several weeks, the previous year, while I backpacked much of the southern end of the Appalachian Trail, from Georgia to Virginia, believing that the exercise I was getting every day would allow me to do this, as indeed, it did. I resumed shots, with no complications, when I reached my destination, visiting close friends in Glasgow, Va. Although a year after being diagnosed, I’m now fairly sure I was still in the “honeymoon” period,” that often follows the initial diagnosis, which allowed me to be more relaxed than I could be thereafter in following the usual treatment guidelines. Also, in college, I was studying martial arts three nights a week, taking archery, some dance and riding a bicycle as my principal means of transportation. So I was getting plenty of exercise. This was probably what allowed me to eat large quantities of food daily, without causing extreme sugar ‘excursions,’ as high blood sugars are referred to in the textbooks. That is not to say that they didn’t occasionally happen, but when I felt my sugar to be high, I would stop eating for a few hours, until my insulin caught up with my sugar and brought it back down. Taking care of low blood sugars was even easier, since I would quickly start experiencing the symptoms of insulin shock when my sugar dropped below 90, in plenty of time to eat some sugar or sweet food. (This is no longer the case for me, and this insensitivity to low blood sugar, called “hypoglycemia unawareness” has been one of the worse consequences of Lilly’s decision to stop making animal insulins.) During this time, my doctor at the time had not informed me there were more varieties of insulin than the 24 hour NPH (from beef and pork insulin) I was taking, probably believing that since I was doing fairly well, making me aware of faster-acting insulins, such as Regular insulin (now no longer available) which onset, peaked and offset in only 3 hours, would only result in complications.

Inevitably, this caught up with me and in spring 1977, I had my first (and last) experience with acidosis, an elctrolyte imbalance caused by the metabolism of fat for fuel by the body’s cells as a result of being unable to access the blood glucose normally used for energy. After a period of time, usually (but not always) a few days, this typically results in coma or death by cerebral edema, or swelling of the brain. While the condition progresses, the brain is unable to properly receive or transmit signals, and let me tell you, this is a truly terrifying experience. You know something’s badly wrong, but you can’t think well enough to understand what it is or take action ( like taking more insulin) to remedy it. The night this happened, I was eventually able, with my roommate’s help, to telephone my doctor and ask him if I should take more insulin. He agreed, although I now know it was probably more as a psychological aid than anything else, since the 24 hour NPH insulin would do very little to relieve my immediate condition, taking 1.5 hours to onset and not peaking for 8 hours, by which time I would see him, as I did the next morning. Fortunately, his office was only a short walk from my apartment and I was there as soon as it opened. He immediately reserved a hospital bed for me, and my roommate took me there that afternoon. With the appropriate insulin, he quickly brought down my sugar, but kept me there several days for observation.

While I was there, my food intake was measured and it turned out I was eating more than 2,500 calories a day. This may not be that much for a large person, but I’m only 5′3″ and at that time even skinnier than I am now. For more than the last twenty years, my daily caloric intake has been only around 900 calories, and after the substitution of Humulin (TM) for insulin, often far less. My weight, however has remained fairly constant, now, 128 lbs, and at that time, 115lbs.

(One of my science heroes is the late Dr Roy Walford [http://en.wikipedia.org/wiki/Roy_Walford], whose research into gerontology, the study of aging, led me in the mid 80s to drastically reduce my caloric consumption. This reduction in food intake is one of the things that has kept me so healthy, and I believe, although I can’t yet prove, is one of the main reasons my hair is still very dark, as a result of the reduction of free radical generation). Hey, I just looked it up, and it seems I’m not alone in that opinion, check out this site:http://ask.yahoo.com/20020926.html

I was released from hospital a few days later, having been informed by doctor about the existence of fast-acting insulins, and Lente insulin, also a 24 hour activity cycle, but which allowed me to mix, if necessary, Regular and Lente in the same syringe. It was at this time, I began looking for my own answers about my condition, and I found them! Over the next few years I came to conclusions, sometimes not shared by doctors, which allowed me from then until animal insulins were removed by Lilly and Novo, the only two major manufacturers of insulin worldwide, to keep my sugar so closely under control, that when, in 1996, I was given my 1st HbA1c test (glycosylated hemoglobin, a marker indicating the attachment of sugar to hemoglobin molecules, itself  not immediately dangerous [see 'Glycosylation Reconsidered' below], but which act as a marker for the control of diabetes) the doctor who examined me was amazed to find it was only 4.5%, when the normal, non-diabetic level is 4%. The word he used was ‘astonishing’. Even now, the ADA (American Diabetic Association), only recommends it be kept under 7%, in my opinion, way too high. I did discover, a few years ago, a (then) small company in England, where I was born, CP Pharmaceuticals, which continued to make animal insulins. They have since been bought out by an Indian (I believe) company and are now known as Wockhardt, UK. (http://www.wockhardt.co.uk/). Unfortunately, the US government has thrown up immense roadblocks to the importation of animal insulins from overseas (and even Canada), at at last count (this is some years ago) less than 50 of the tens of thousands of type 1 diabetics in this country that need animal insulin, have actually been able to import it. (Megan Romano, Genewatch magazine, 2003: http://www.gene-watch.org/genewatch/articles/16-6romano.html.

(9/5/08 I’ve posted these links and others to follow, in the blogroll at top right)

I’m going to stop now and go to bed, but I’ll pick this up again tomorrow. In the days to come, I intend to create sidebars devoted to particular topics, with links to sites, both scientific and personal, that will provide shortcuts to essential articles.  I will also state the four essential principles I believe will allow most or all type 1s to maintain their health, it’s just too late right now. This isn’t just for diabetics, anybody can benefit from these practices. One of them is the means of preventing retinopathy, another is the cure for osteopenia/osteoporosis (without having to pay for a biophosphonate such as (TM) Fosamax, a hideously expensive, and basically unnecessary moneymaker for Big Pharma ( the collective name given to the united organization of pharmaceutical companies). ( I was diagnosed with osteoporosis in 2001, saw a specialist who assured me I would develop a hump (and he was a very good doctor and person, no criticism of him is implied, he just said what he’d been told was true), and yet not only do I not have a hump, but was able to replace about 4/5 of the spinal disintegration I had experienced, that is regained 2.5″ of the 3″ I had lost in height! More will follow, stay tuned.