Diabetes Information
Basal Testing PDF Print E-mail
Written by Lloyd   
Sunday, 20 June 2010 01:53

Simply put, basal insulin is the insulin you take for your basic metabolic processes.  It is insulin that an insulin dependent diabetic must have, even when they do not eat.  Do not exercise during the specific times you are testing, that can skew the results drastically.

To test whether you are getting the correct amount of basal insulin (lantus or levimir if injected; apidra, novorapid(novolog) or humalog if infused by a pump), you need to test your glucose in a way that will be not affected by food you eat.

For most diabetics, by 3 hours or so after eating, your glucose has settled down, at least if you have not had a large amount of carbohydrates.

To get a complete picture, you really need testing 24 hours a day, just not in one day, but spread out over several days.

One way is to skip a meal (but only one).  If you skipped breakfast, you could test from the time you woke up until you had lunch.  Then you could test again at something like 3 hours after lunch until supper, and 3 hours after supper you could start again and test until you go to bed (providing you don't have a snack).

An alternative I find that works well for me, is to delay meals instead of skipping them.  If I had breakfast at 6 am, I could test from 9am to lunch.  The next day, if I had a 9 am breakfast, I could test from 6 am to 9 am.  In this way, you can build up a picture of how your basal rates are at all times of the day.

Night time is a tough one.  You need to test at least once an hour, one way would be to stay up late one night, and get up early another.

The best way, by far, is to use a continuous glucose monitor.  Sometimes doctors can get you the use of one for a few days.  Then all you need to do is vary your mealtimes and make a record of what you eat and exercise.

I use a pump, my goal is to have the basal set so that if I skip a meal, my glucose remains very steady for at least 6 hours or until the next meal.

With injections, this goal would be hard to achieve, but none-the-less, it is what you are trying for.  The idea is if a meal is an hour early or an hour late, you can avoid lows due to not eating, if your basal amount is right on.

-Lloyd

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Testing on a Budget PDF Print E-mail
Written by Alan   
Thursday, 10 June 2010 19:44

I'm very lucky to be in a country where diabetics in the past have successfully lobbied for specific support within the government health system to assist good diabetes control. I'm eternally grateful for the pioneers who created Australian medicare and the NDSS.

However, I'm daily reminded that others overseas are not so fortunate. Consequently, some have difficulty following the full Test, Test, Test regimen as Jennifer suggests because of strip cost.

For them, I suggest a "one strip a day" method. This works more slowly than following Jennifer's advice completely - but it can still work. When I say "one strip a day" I'm not counting the FBG or other tests the doctor wants - discuss with the doc if you can cut back there. In hard economic circumstances I can't see that doing FBG every second or even third day is going to be a problem for the doc - but check to be sure. Let's face it, the "average" type 2 out there is testing FBG maybe once per week, doing absolutely nothing with the result, and wondering why their A1c goes up every 3-6 months.

This other daily test strip is purely to let YOU know what's happening when you eat.

First, it will take a few extra BG tests for two or three days to discover when your peak timing is. Once you know that for each meal, you can focus on that timing. Some reckon you also need to test before meals to see what the rise was; in these circumstances I would see the pre-meal test as a waste of a strip. Just concentrate on the absolute peak level. Target one meal per week. Most of us have problems with breakfast, so I'd recommend starting there.

Test at the peak spike time, just for breakfast, until you have modified your breakfast to the point where the spikes are acceptable to you. I use Jennifer's guidelines, which are similar to the AACE, but check with your doctor if in doubt. Concentrate on that meal for one week, by that time you should have something workable. I've given some alternative breakfast ideas here, but think outside the square and find what works for you. There is no law that decrees cereal, juice, milk or toast before noon. I just finished a kransky sausage with one dry-fried egg before typing this (it's 7:40am here:-) That will be followed with black, cinnamon-infused coffee.

Then concentrate on Lunch for week two, Dinner for week three and so on. Then repeat over the next three weeks. Over time you will find a range of foods that are OK - and a range of foods that aren't - and slowly build a safe menu base.

Cheers, Alan

Republished with kind permission of the author from the original: http://loraldiabetes.blogspot.com/2007/04/teting-on-budget.html

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Diabetic Peripheral Neuropathy PDF Print E-mail
Written by Jim Hartmann   
Tuesday, 08 June 2010 20:38

Diabetic Peripheral Neuropathy

Neuropathy is disease of the nerves. In a diabetic, it takes two forms: Autonomic Neuropathy and Peripheral Neuropathy.

Autonomic Neuropathy

The autonomic nervous system is the one that operates in the background, controlling things like breathing, heartbeat, stomach emptying, etc.

The most common diabetes-related autonomic neuropathy is gastroparesis, or delayed/irregular stomach emptying. Many longtime Type-1s can tell you how this can make insulin bolus dosing a nightmare. Other symptoms are aberrations in sweating, postural hypotension, bladder control, abnormal febrile responses, impotence, diarrhea, nausea, and on and on.

You can do a simple test for autonomic neuropathy simply by taking your pulse. This is called the R-R Interval. Take your pulse and note the (hopefully) regular beat when inhaling. Your pulse will normally slow when exhaling. If it doesn't, it may be an indication of autonomic neuropathy which should be checked with your doc.

Peripheral Neuropathy

One of the first complications noted by many diabetics is a tingling, pain, or loss of sensation in the toes and feet. This is often a symptom of Diabetic Peripheral Neuropathy or DPN.

Not every ache, pain, or numb feeling is DPN. It should not be confused with numbness on one side only, as it most often presents bilaterally (on both sides of the body) and tends to start in areas farthest from the heart, i.e., in the toes, feet and fingers. If you have one-sided symptoms, it is more likely a pinched nerve, sprained or strained muscle, tendon or ligament, carpal tunnel or something else completely unassociated with diabetes. It could also be a symptom of a blocked blood vessel, which is a potentially life threatening condition. Only your doctor can diagnose the cause, so it is wise to seek medical attention as soon as possible. You might have to visit a neurologist for specialized tests described below.

Causes of DPN

The current theory seems to be that there are two potential causes DPN. They are Advanced Glycation Endproducts [AGE] and what is being called "Oxidative Stress."

Glycation is the attachment of glucose. AGEs are the result of the glycation of proteins, a particular problem in diabetics due to our hyperglycemia. Like the glycation of hemoglobin (measured as HbA1c) or the glycation of albumin (measured as fructosamine), other proteins can become glycated. One course of study centers around the glycation of lipoproteins, like HDL, LDL, and triglycerides. It is thought that this glycation makes the proteins sticky, causing aggregation in the blood vessels, and hence the formation of plaque in the arteries, and the subsequent increased cardiac risk. Since it is believed that a major contributor to this process is free radicals, the use of antioxidants is being studied to scavenge the free radicals.

Oxidative Stress is thought to be part of the process related to diabetic neuropathy and retinopathy. Again, the free radicals apparently cause damage to the vessels and nerves. There is still much research to be done, and we do not have all the answers yet, but even the most pessimistic should agree that this line of research has potential.

Symptoms of DPN

Most diabetics who are experiencing DPN have shooting pains, burning pains, hyper-sensitivity, or numbness in their toes and feet. Untreated, this can eventually spread up the legs and also cause similar symptoms in the fingers and hands. Some report that they feel like they are wearing socks when they aren't, or that they feel a non-existent fold or crease in the socks they are wearing.

Testing for DPN

Common tests for DPN can be carried out in your doctor's office using two simple tools: monofilament, and a tuning fork. Monofilament is a short piece of common fishing line. By using a specific length of a specific diameter of monofilament, your doctor will touch the skin of your toes and feet and ask you when you feel the touch. Similarly, the doctor will strike the tuning fork to start it vibrating and hold it to your foot, asking you to report when you can no longer feel the vibration. Depending on your doctor's interpretation of these tests, you may be referred to a neurologist for additional testing.

A neurologist will probably want to do two somewhat more complex tests, called NCV and EMG.  Nerve conduction velocity (NCV) tests the speed of conduction of impulses through a nerve. The nerve is stimulated, usually with patch-like electrodes on the skin (similar to those used for ECG) over the nerves at various locations. One electrode stimulates the nerve with a very mild electrical impulse. The resulting electrical activity is recorded by the other electrodes. The distance between electrodes and the time it takes for electrical impulses to travel between electrodes are used to calculate the nerve conduction velocity.

The second test is called Electromyography (EMG). For an EMG, a needle electrode is inserted through the skin into the muscle. The electrical activity detected by this electrode is displayed on an oscilloscope, and may be heard through a speaker.

After placement of the electrodes, you may be asked to contract the muscle (for example, by flexing your foot). The presence, size, and shape of the wave form produced on the oscilloscope provide information about the ability of the muscle to respond when the nerves are stimulated.

Treatment of DPN

The first, best, and most important step in treating DPN is to reestablish normal blood sugars.

In addition, your doctor has pharmaceutical tools, such as small doses of tri-cyclic antidepressants like amitriptyline, or the more potent anti-seizure meds like Tegetrol (carbamazepine), Dilantin (phenytoin), and Neurontin (gabapentin). These will mask the symptoms, but do nothing to address the underlying pathology.

Another approach attempts to treat the underlying causes of DPN, i.e., Advanced Glycation Endproducts and Oxidative Stress through the use of antioxidants, specifically Alpha Lipoic Acid, which is also known as Thioctic Acid, and Gamma Linolenic Acid.  Probably the most leading-edge work is being done in Germany, and has been reported in the DEKAN Study (see footnote below).

The DPN Cocktail

The following is a recommendation for treatment of DPN by use of anti-oxidants, and is based on the research of Stan Angilley. It has been used successfully by many diabetics to reduce or even eliminate DPN. Before starting on this regimen, you should discuss it with your doctor, as you may have other medical issues which would contraindicate its use. It is likely that your doctor will have heard little or nothing about this approach, so we have provided citations to applicable literature below.

The DPN cocktail has three components: Alpha Lipoic Acid (ALA), Gamma Linolenic Acid (GLA) as contained in Evening Primrose Oil (EPO), and Vitamin C. These components are available from many sources, including pharmacies, health food stores, and over the internet. The ALA component is somewhat expensive, so we will provide some internet sources that many have used successfully. We have no profit motive here, and suggest that you research sources to find your best buy. The unique properties of the components make this cocktail synergistic, in other words, the parts work together to reinforce and replenish each other.

Alpha Lipoic Acid (ALA), also known as thioctic acid, has a short plasma half-life of about 30 minutes. It is also both water and fat soluble, which assists in its transport in the body. It also isn't cheap, so to get the maximum benefit use only Extended Release versions. This used to limit you to formulations from the Lipoic Foundation and Jarrow. Nowadays, it is made by a couple of others.  ALA is a sulfur based compound, so expect your urine to have a sulfur smell.  ALA is also known to assist in the reduction of blood glucose, likely by decreasing peripheral insulin resistance. You should carefully monitor its effect on your BG to avoid potential hypos.

Gamma-linolenic acid (GLA) is an n-6 (omega-6) polyunsaturated fatty acid commonly contained in Evening Primrose Oil (EPO) and Borage Oil (BO). EPO typically contains more GLA than BO. Depending on the method of extraction from the plants, EPO can contain varying amounts of GLA. Buy a brand of EPO that contains at least 10% GLA. For example, choose a 1300mg EPO tablet that contains at least 130mg of GLA.

The last component is Vitamin C. There is nothing special required in selecting a specific form of Vitamin C, so you can choose generic, Rosehips, or Ester C.

The components of the cocktail are:

  • 300mg Slow Release Alpha Lipoic Acid
  • 1300mg Evening Primrose Oil
  • 500mg Vitamin C

Starting off, take one cocktail morning and night. After you get relief from the neuropathy feelings, you should be able to reduce this to a maintenance dose of once a day. Most report improvements in DPN after about 3 months of use. Some report stomach upset from the cocktail, so taking it with a meal may help. No other serious adverse reactions have been reported.

Again, we have no vested interest in where you get the components. Here are several internet sources should you have difficulty in obtaining them from your local pharmacy or health food store. Prices change, so research your best buy.

Citations to Literature for Your Skeptical Doctor

http://www.medscape.com/viewarticle/547879

Alpha-Lipoic Acid Improves Symptomatic Diabetic Polyneuropathy

Diabetes Care 2006;29:2365-2370.

Alpha-lipoic acid (ALA) given orally improves symptoms in patients with diabetic polyneuropathy, according to a report in the November issue of Diabetes Care.

A recent meta-analysis showed that daily intravenous treatment with ALA could reduce pain, paresthesia, and numbness in diabetic patients, the authors explain, but little work has been done to investigate the use of oral ALA.

Dr. Dan Ziegler from Heinrich Heine University, Duesseldorf, Germany and colleagues compared three doses of oral ALA to placebo in 166 patients with symptomatic diabetic polyneuropathy.

Mean total symptom scores and stabbing/lancinating and burning pain subscores were significantly reduced after 5 weeks in all active treatment arms compared with the placebo arm, the authors report.

ALA treatment had no measurable effect on paresthesia and numbness, the results indicate.

Symptoms improved significantly as early as 1 week with the highest ALA dose (1800 mg daily) and within 2 weeks with the other doses (600 mg and 1200 mg daily), the researchers note, and there were no significant differences among the three ALA groups for changes in mean total symptom score at any time point.

The findings were similar when Neurology Symptoms and Change Score was used instead of mean total symptom score, the report indicates.

Nausea, vomiting, and vertigo were more common with ALA treatment than with placebo treatment, the investigators say.

"Whether the observed favorable short-term effect of ALA on neuropathic symptoms and deficits can be translated into slowing the progression of diabetic polyneuropathy in the long term is unknown," the authors write. "However, our finding that neuropathic deficits such as impaired sensory function were improved is encouraging, because these are major risk factors in the development of neuropathic foot ulcers."

"In the absence of a dose response and because the higher doses resulted in increased rates of gastrointestinal side effects, 600 mg once daily seems to be the most appropriate oral dose," the researchers add.

http://tinyurl.com/ofqag

Effects of treatment with the antioxidant alpha-lipoic acid on cardiac autonomic neuropathy in NIDDM patients. A 4-month randomized controlled multicenter trial (DEKAN Study). Deutsche Kardiale Autonome Neuropathie.

Ziegler D., Schatz H, Conrad F., Gries FA, Ulrich H, Reichel G Diabetes-Forschungsinstitut an der Heinrich-Heine-Universitat, Dusseldorf, Germany.

OBJECTIVE: To evaluate the efficacy and safety of oral treatment with the antioxidant alpha-lipoic acid (ALA) in NIDDM patients with cardiac autonomic neuropathy (CAN), assessed by heart rate variability (HRV). RESEARCH DESIGN AND METHODS: In a randomized, double-blind placebo-controlled multicenter trial (Deutsche Kardiale Autonome Neuropathie [DEKAN] Study), NIDDM patients with reduced HRV were randomly assigned to treatment with daily oral dose of 800 mg ALA (n = 39) or placebo (n = 34) for 4 months. Parameters of HRV at rest included the coefficient of variation (CV), root mean square successive difference (RMSSD), and spectral power in the low-frequency (LF; 0.05-0.15 Hz) and high-frequency (HF; 0.15-0.5 Hz) bands. In addition, cardiovascular autonomic symptoms were assessed. RESULTS: Seventeen patients dropped out of the study (ALA n = 10; placebo n = 7). Mean blood pressure and HbA1 levels did not differ between the groups at baseline and during the study, but heart rate at baseline was higher in the group treated with ALA (P < 0.05). RMSSD increased from baseline to 4 months by 1.5 ms (-37.6 to 77.1) [median (minimum-maximum)] in the group given ALA and decreased by -0.1 ms (-19.2 to 32.8) in the placebo group (P < 0.05 for ALA vs. placebo). Power spectrum in the LF band increased by 0.06 bpm2 (-0. 09 to 0.62) in ALA, whereas it declined by -0.01 bpm2 (-0.48 to 1.86) in placebo (P < 0.05 for ALA vs. placebo). Furthermore, there was a trend toward a favorable effect of ALA versus placebo for the CV and HF band power spectrum (P = 0.097 and P = 0.094 for ALA vs. placebo). The changes in cardiovascular autonomic symptoms did not differ significantly between the groups during the period studied. No differences between the groups were noted regarding the rates of adverse events. CONCLUSIONS: These findings suggest that treatment with ALA using a well-tolerated oral dose of 800 mg/day for 4 months may slightly improve CAN in NIDDM patients.

http://www.mayoclinic.org/news2003-rst/1733.html

Mayo Clinic in Rochester

Monday, April 07, 2003

Antioxidant Alpha Lipoic Acid (ALA) Significantly Improves Symptoms of Diabetic Neuropathy

ROCHESTER, Minn. -- A collaborative study between Mayo Clinic and a medical center in Russia found that alpha lipoic acid (ALA) significantly and rapidly reduces the frequency and severity of symptoms of the most common kind of diabetic neuropathy. Symptoms decreased include burning and sharply cutting pain, prickling sensations and numbness.

The findings appear in the March 2003 issue of Diabetes Care, http://care.diabetesjournals.org/.

Diabetes 1997 Sep;46 Suppl 2:S62-6
Alpha-lipoic acid in the treatment of diabetic peripheral and cardiac autonomic neuropathy.

Ziegler D, Gries FA  Diabetes Research Institute at the Heinrich Heine University,
Dusseldorf, Germany.

Antioxidant treatment has been shown to prevent nerve dysfunction in
experimental diabetes, providing a rationale for a potential therapeutic
value in diabetic patients. The effects of the antioxidant alpha-lipoic
acid (thioctic acid) were studied in two multicenter, randomized,
double-blind placebo-controlled trials. In the Alpha-Lipoic Acid in
Diabetic Neuropathy Study, 328 patients with NIDDM and symptomatic
peripheral neuropathy were randomly assigned to treatment with
intravenous infusion of alpha-lipoic acid using three doses (ALA 1,200
mg; 600 mg; 100 mg) or placebo (PLAC) over 3 weeks. The total symptom
score (TSS) (pain, burning, paresthesia, and numbness) in the feet
decreased significantly from baseline to day 19 in ALA 1,200 and ALA 600
vs. PLAC. Each of the four individual symptom scores was significantly
lower in ALA 600 than in PLAC after 19 days (all P < 0.05). The total
scale of the Hamburg Pain Adjective List (HPAL) was significantly
reduced in ALA 1,200 and ALA 600 compared with PLAC after 19 days (both
P < 0.05). In the Deutsche Kardiale Autonome
Neuropathie Studie, patients with NIDDM and cardiac autonomic
neuropathy diagnosed by reduced heart rate variability were randomly
assigned to treatment with a daily oral dose of 800 mg alpha-lipoic acid
(ALA) (n = 39) or placebo (n = 34) for 4 months. Two out of four
parameters of heart rate variability at rest were significantly improved
in ALA compared with placebo. A trend toward a favorable effect of ALA
was noted for the remaining two indexes. In both studies, no significant
adverse events were observed. In conclusion, intravenous treatment with
alpha-lipoic acid (600 mg/day) over 3 weeks is safe and effective in
reducing symptoms of diabetic peripheral neuropathy, and oral treatment
with 800 mg/day for 4 months may improve cardiac autonomic dysfunction
in NIDDM.
PMID: 9285502, UI: 97429864

J Neural Transm 1998;105(8-9):1005-15
Cytotoxicity of advanced glycation endproducts is mediated by oxidative stress.

Loske C, Neumann A, Cunningham AM, Nichol K, Schinzel R, Riederer P,
Munch G
Physiological Chemistry I, Biocenter, Wurzburg, Federal Republic of
Germany.
Non-enzymatic glycation of proteins with reducing sugars and subsequent
transition metal catalysed oxidations leads to the formation of protein
bound "advanced glycation endproducts" (AGEs). They accumulate on
long-lived proteins and are for example structural components of the
beta-amyloid plaques in Alzheimer's disease. Since the oxidation of
glycated proteins as well as the interaction of AGEs with cell surface
receptors produces superoxide radicals, it was tested in BHK 21 hamster
fibroblast cells and SH-SY5Y human neuroblastoma cells if AGEs can exert
cytotoxic effects on cells. Cell viability was assessed with three
independent tests: MTT-assay (activity of the mitochondrial respiratory
chain), lactate dehydrogenase assay (release of cytoplasmatic enzymes,
membrane integrity) and Neutral Red assay (active uptake of a
hydrophilic dye). Two model AGEs, chicken egg albumin-AGE and BSA-AGE,
both caused significant cell death in a dose-dependent manner. The
cytotoxic effects of AGEs could be attenuated by alpha-ketoglutarate and
pyruvate, by antioxidants such as thioctic acid and N-acetylcysteine,
and by aminoguanidine, an inhibitor of nitric oxide synthase. This
suggests that reactive oxygen species as well as reactive nitrogen
species contribute to AGE mediated cytotoxicity. Since AGEs accumulate
on beta-amyloid plaques in AD over time, they may additionally
contribute to oxidative stress, cell damage, functional loss and even
neuronal cell death in the Alzheimer's disease brain.
PMID: 9869332, UI: 99084677

http://www.medscape.com/viewprogram/705

Oxidative stress, caused by enhanced free radical synthesis, may play an important role in contributing to the pathogenesis of diabetic neuropathy.[19,20,30]
Alpha-lipoic acid (ALA) is a potent lipophilic free-radical scavenger that has demonstrated effectiveness in preventing neuropathic
abnormalities in animal models of diabetes.[87-89]

In the limited clinical trials published so far, ALA administration has yielded small but significant improvements
in neuropathic pain and heart rate variability.[90,91]

87.Nagamatsu M, Nickander KK, Schmelzer JD, et al:
Lipoic acid improves nerve blood flow, reduces
oxidative stress, and improves distal nerve conduction
in experimental diabetic neuropathy. Diabetes Care
18:1160-1167, 1995.
88.Garrett NE, Malcangio M, Dewhurst M, et al:
Alpha-lipoic acid corrects neuropeptide deficits in
diabetic rats via induction of trophic support. Neurosci
Lett 222:191-194, 1997.
89.Hounsom L, Horrobin DF, Tritschler H, et al: A lipoic
acid-gamma linolenic acid conjugate is effective
against multiple indices of experimental diabetic
neuropathy. Diabetologia 41:839-843, 1998.
90.Ziegler D, Schatz H, Conrad F, et al: Effects of
treatment with the antioxidant alpha-lipoic acid on
cardiac autonomic neuropathy in NIDDM patients.
Diabetes Care 20:369-373, 1997.
91.Ziegler D, Gries FA: Alpha-lipoic acid in the treatment
of diabetic peripheral and cardiac autonomic
neuropathy. Diabetes 46(Suppl. 2):S62-S66, 1997.

http://www.medscape.com/medscape/CNO/1999/EASD/EASD-08.html
The Role of Oxidative Stress in Diabetes-Related Tissue Injury

Experimental research is focusing more and more on oxidative stress
as an important pathogenetic factor in diabetes-related tissue injury.
However, the methods to detect increased oxidative stress in
specific sites of diabetic complications, such as the eye, have yielded
conflicting results. Dr. Obrosova from the University of Michigan, Ann
Arbor, used a new quantitative method specific for malondialdehyde and
4-hydroxyalkenals (4-HA) to evaluate the level of oxidative stress in
retinae from diabetic rats.[4] This study also included measurements of
several oxidative defense systems such as reduced and oxidized
glutathione, superoxide dismutase (SOD), and others.

Early in the disease, the main unsaturated lipid aldehydes accumulating
in diabetic retinae were 4-HA. In addition, SOD was depleted. Of
significance, these changes were prevented by the antioxidant
DL-alpha-lipoic acid, presumably by free-radical scavenging and
upregulation of SOD. These data show that specific lipid peroxidation
products are early markers of oxidative stress in the diabetic retina
and point to the early involvement of specific antioxidant defense
systems as a possible new therapeutic approach.

4.Fathallah L, et al. Accumulation of 4-Hydroxyalkenals is an early
marker of oxidative stress in the diabetic retina. Program and abstracts
of the 35th Annual Meeting of the European Association for the Study of
Diabetes; September 28-October 2, 1999; Brussels, Belgium. Abstract 37.

Modulation of cellular reducing equivalent homeostasis by alpha-lipoic acid. Mechanisms and implications for diabetes and ischemic injury. (Roy S; Biochem Pharmacol, 1997 Feb 7)

The effect of alpha-lipoic acid on the neurovascular reflex arc in patients with diabetic neuropathy assessed by capillary microscopy.
(Haak ES; Microvasc Res, 1999 Jul)

Alpha-lipoic acid: antioxidant potency against lipid peroxidation of neural tissues in vitro and implications for diabetic neuropathy.
(Nickander KK; Free Radic Biol Med, 1996)

Effects of alpha-lipoic acid on neurovascular function in diabetic rats: interaction with essential fatty acids. (Cameron NE; Diabetologia, 1998 Apr)

Stimulation by alpha-lipoic acid of glucose transport activity in
skeletal muscle of lean and obese Zucker rats. (Henriksen EJ; Life Sci,
1997)

Differential effects of lipoic acid stereoisomers on glucose metabolism
in insulin-resistant skeletal muscle. (Streeper RS; Am J Physiol, 1997
Jul)

alpha-Lipoic acid: a metabolic antioxidant which regulates NF-kappa B
signal transduction and protects against oxidative injury. (Packer L;
Drug Metab Rev, 1998 May)

Diabetes-induced changes in lens antioxidant status, glucose utilization
and energy metabolism: effect of
DL-alpha-lipoic acid. (Obrosova I; Diabetologia, 1998 Dec)

Alpha-lipoic acid reduces expression of vascular cell adhesion
molecule-1 and endothelial adhesion of human monocytes after stimulation
with advanced glycation end products. (Kunt T; Clin Sci (Colch), 1999
Jan)

Advanced glycation end product-induced activation of NF-kappaB is
suppressed by alpha-lipoic acid in cultured endothelial cells. (Bierhaus
A; Diabetes, 1997 Sep)

Effects of diabetes and treatment with the antioxidant alpha-lipoic acid
on endothelial and neurogenic responses of corpus cavernosum in rats.
(Keegan A; Diabetologia, 1999 Mar)

Alpha-lipoic acid: effect on glucose uptake, sorbitol pathway, and
energy metabolism in experimental diabetic neuropathy. (Kishi Y;
Diabetes, 1999 Oct)

alpha-Lipoic acid decreases oxidative stress even in diabetic patients
with poor glycemic control and albuminuria.  (Borcea V; Free Radic Biol
Med, 1999 Jun)

Advanced glycation end product-induced activation of NF-kappaB is
suppressed by alpha-lipoic acid in cultured endothelial cells. (Bierhaus A; Diabetes, 1997 Sep)

Effects of diabetes and treatment with the antioxidant alpha-lipoic acid on endothelial and neurogenic responses of corpus cavernosum in rats.
(Keegan A; Diabetologia, 1999 Mar)

 

Editor's Note:

This article is taken from Jim Hartmann's site:  www.diabetic-talk.org


Jim helped a lot of diabetics until his death in early 2009.  This is an article which we refer to frequently and it appears that site will not continue.  If there are any objections to the use of this article, please email This e-mail address is being protected from spambots. You need JavaScript enabled to view it

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Last Updated on Wednesday, 09 June 2010 19:58
 
Painless Pricks PDF Print E-mail
Written by Alan   
Saturday, 05 June 2010 16:10

One of the common objections to testing blood glucose more frequently is a fear of pain from testing. If you are suffering pain when you test, you are doing it incorrectly.

I learned this the hard way in my first year after diagnosis. I hope it helps you.

Do not use an alcohol swab to clean the test site unless there is no other choice. Repeated use of alcohol over time for that purpose will dry out the site and may cause skin problems.

If possible wash your hands in warm soapy water, rinse well and shake them to get the circulation going. Check your lancet-holder; it should be adjustable. Mine is a Soft-clix, made by Roche and is usually painless. That brand has an excellent reputation among the diabetics I know, but any good lancet device should do the job. I get an occasional tiny sting and it lets me know if it's getting blunt sometimes, but I tested over 5000 times in the first four years after diagnosis, before I stopped counting, without any trauma. That's from a guy who was, and is, needle-phobic.

Start with the second lowest setting (1 or 1.5), hold it firmly against your skin on the side of a finger near the tip. Don't flinch when you release the button. The button releases a spring-loaded tiny needle which makes a tiny hole in your skin and instantly retracts. Using the side of your finger-tip has two advantages: there are less nerve-ends than on the pads, and it doubles the number of test-points so you can rotate through the positions.

Massage gently (milking a cow) until a drop of blood forms sufficient to put on the test strip. If this setting doesn't provide an adequate quantity, move the lancet setting up one notch for the next one. If you got a large sample and it hurt a little, go to the lower setting.

And that's all there is to it. Sometimes it helps to shake your hands a little more, or warm them up if it's cold.

The manufacturers advise changing the lancet needle every time; I change mine when I remember or if it gets a bit blunt. I have never had an infection as a result of doing that, nor have I ever heard of it happening from the people I talk to on the web. You do what you are comfortable with, subject to doctor's orders.

Cheers, Alan, T2, Australia.
Everything in Moderation - Except Laughter

Republished with kind permission of the author from the original: http://loraldiabetes.blogspot.com/2006/10/painless-pricks.html

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Is testing worthwhile? PDF Print E-mail
Written by Alan   
Friday, 04 June 2010 21:45

I have friends in the UK who are finding it increasingly difficult to get adequate test strip supplies prescribed from their NHS surgeries to use self-monitoring of their blood glucose (SMBG) in the way that enabled them to gain control of their type 2 diabetes. I am fortunate to live in Australia where the NDSS subsidises test strips. However, I am becoming concerned at several poor "studies" conducted in Australia, Canada and the UK implying that SMBG is a waste of money and time and may also cause depression.

I suspect that it is no coincidence that all of those countries subsidise test strip supplies for diagnosed diabetics. I fear a concerted push by the "bean-counters" in our various health systems to cut costs in this area; a very short-sighted view of diabetes treament in my opinion. I am convinced that systematic use of SMBG to improve and maintain dietary control of type 2, complementary to any medication or insulin treatments, will lead to much greater savings in the long term in both the cost of treating complications and the overall social and economic costs to the community.

The most recent flawed study was published in the British Medical Journal: Efficacy of self monitoring of blood glucose in patients with newly diagnosed type 2 diabetes (ESMON study): randomised controlled trial The crux of the problem in this study lies in the following section.
First, I'll give the unabridged version, then highlight some points. You can save time by scrolling down to "This is the absolutely critical part".

From the study: "After an initial assessment visit, eligible patients were randomised into intervention (self monitoring of blood glucose) or control (no monitoring) groups with a randomly generated allocation code in consecutively numbered sealed envelopes. The study diabetes nurse at each hospital site performed the treatment allocation.

Patients in the self monitoring group were all provided with a single glucose monitor (Lifescan OneTouch Ultra; Johnson and Johnson, Milpitas, CA) and instructed in its use. They were asked to monitor four fasting and four postprandial capillary blood glucose measurements each week. They were advised on appropriate responses to high or low readings. Such advice included the need for dietary review or the suggestion of exercise (such as walking) in response to high readings.

At each clinic visit, concordance with the self monitoring regimen was verified by downloading meter readings.

Patients in the no monitoring group (control) were asked not to acquire a meter or perform monitoring for the duration of the study. Patients in both groups underwent an identical structured education programme involving diabetes nurse practitioners, dieticians, podiatrists, and medical staff. All patients were reviewed by the doctor, diabetes nurse practitioner, and dietician at three monthly intervals for one year. At each visit all aspects of diabetes care were reviewed including indices of glycaemic control (HbA1c for both groups and self monitoring results for the self monitoring group).

Patients in the self monitoring group received ongoing advice and support in the appropriate interpretation of and response to their capillary glucose results. We used an identical treatment algorithm for dietary and pharmacological management of glycaemia for both groups based on HbA1c targets (figure 1). Blood concentrations of HbA1c, lipids, and electrolytes were measured at or before each clinic and results were discussed with patients in the context of the treatment targets. Measurement of HbA1c was performed in the local hospital laboratory with a diabetes control and complications trial (DCCT) aligned HbA1c assay.2 All laboratories participated in HbA1c external quality assurance, which was satisfactory for the duration of the study. All other laboratory tests were also performed in the local hospital laboratory, where staff were blinded to treatment allocation."

This is the absolutely critical part:

"They were asked to monitor four fasting and four postprandial capillary blood glucose measurements each week. They were advised on appropriate responses to high or low readings. Such advice included the need for dietary review or the suggestion of exercise (such as walking) in responseto high readings."

What were the "appropriate" responses they used? What was that advice?

Some idea of what may have been advised appears here: "Patients in both groups underwent an identical structured education programme involving diabetes nurse practitioners, dieticians, podiatrists, and medical staff."

And what do we know of the education dietary programme provided by the NHS or Diabetes UK(see P788 table 2)? Basically it is low-fat, high carb and add more metformin or insulin to counter the carbs. On the use of meds, take a look at Table 5 noting the increase in medications across the board and the higher use of multiple medications in the SMBG group.

When these meter users tested at their random four post-prandials (or, at least, the 63 of 96 who actually tested 80% of the required four FBG and four PP weekly; meaning that 50% actually tested that much, almost certainly at two hours and well after their post-prandial spike), what did they do about it if it was high? Did they reduce carbs? Possible, but most unlikely if they complied with their advice. More likely they went for a walk or the doctor upped their metformin or added a med (see Figure 1 and Figure 5). And they probably missed most of their spikes anyway, often seeing only the reactive post-spike numbers at two hours.

So they did what they were told and their numbers didn't improve. No wonder they got depressed. I would have too. What was that old definition for insanity? "To continue to do the same thing and expect a different result."

In my opinion the control group weren't as depressed because they put themselves in the hands of their doctors - no personal responsibility for their plight. But the SMBG group felt they must share the blame for their poor response; especially those who were in the 50% who didn't do all the weekly tests.

The problem was not the SMBG but the ignorance of those conducting the research on how to best train the SMBG group on how to use the test results to improve the diet to improve results. This research follows the earlier and similar BMJ report from Farmer et al, which I note is listed as the 13th reference: Impact of self monitoring of blood glucose in the management of patients with non-insulin treated diabetes: open parallel group randomised trial You will see my response to that in BMJ at the foot of that page. It is equally relevant to this load of nonsense. If you go to the ready response index you will find several other patient's and doctor's similar responses.

The only funding acknowledgement for this latest nonsense was "Funding: Northern Ireland research and development office. MC was employed as a research associate as part of the funding allocation. The blood glucose meters were supplied free of charge by Johnson and Johnson, Milpitas, CA." I am cynical enough to wonder how much of the funding effectively came from the bean-counters of the NHS.

Cheers, Alan

Everything in Moderation, Except Laughter

Republished with kind permission of the author from the original: http://loraldiabetes.blogspot.com/2008/04/is-testing-worthwhile.html

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Last Updated on Saturday, 05 June 2010 16:12
 
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