Pre-Diabetes Community (original) (raw)

03 January 2010 @ 11:36 am

"The Diabetes Prevention Program (DPP) was a randomized clinical trial involving 3,234 volunteers at high risk for diabetes. All participants had impaired glucose tolerance (IGT), defined as having a fasting plasma glucose level of 95-125 mg/dL. (5.3-6.9 mmol/L) and attaining a 2-hour glucose of 140-198mg/dL. (7.8-11.0 mmol/L) during a 75-g oral glucose tolerance test. The study discussed here evaluated a subgroup of participants who also had impaired fasting glucose (IFG), defined by the American Diabetes Association as a baseline fasting glucose of >100mg/dL. and <126mg/dL.( 5.6 mmol/L and < 7.0 mmol/L).

Regression from this combined IFG/IGT state to normal glucose regulation (NGR) (fasting glucose < 100mg/dL.(5.6 mmol/L) and 2-hour glucose < 140mg/dL. (7.8 mmol/L) was the primary outcome measure, and regression to isolated IFG or isolated IGT was the secondary outcome measure. In addition, the study sought to identify predictors for regression to NGR, isolated IFG, or isolated IGT within each treatment group (intensive lifestyle modification or metformin vs placebo) using Cox regression analyses.

At the first annual examination, 16.5% of the 2,528 study participants had had regression to NGR. Of those who still had combined IFG/IGT, another 8% had regression to NGR at year 2, and among the remaining volunteers who still had IFG/IGT, another 4.4% had regression by year 3. Thus, a total of 600 (23.7%) participants had regression to NGR within 3 years. Lower baseline fasting and lower 2-hour glucose predicted regression to NGR, as did younger age and a greater insulin secretion to the oral glucose load. The intensive lifestyle intervention group was twice as likely to have regression as the placebo group (hazard ratio 2.05; 95% confidence interval 1.66-2.53), but the trend toward greater regression in the metformin group was not statistically significant (hazard ratio 1.25; 95% confidence interval 0.99-1.58). Greater weight loss also had a significant and independent effect on regression to NGR (hazard ratio 1.34; 95% confidence interval 1.21-1.49).

No one would argue that preventing progression to diabetes is a worthwhile pursuit. However, even in subdiabetic states of IFG and IGT, the microvascular and macrovascular complications generally associated with diabetes are more common than in patients with NGR. As the investigators of the current study point out, "True diabetes prevention likely resides in the restoration of NGR rather than in the maintenance of a high-risk state, such as pre-diabetes." Therefore, it is encouraging to note that nearly one quarter of the study participants achieved NGR within the 3-year study window. Over half of those patients did so in the first year, so for the most part, those who succeed in having NGR restored will do so relatively quickly.

One important finding was that if NGR is to be regained, it will likely occur through healthy eating and exercise and that this effect is probably independent of weight loss. However, it is important to remember that the DPP was a clinical trial of healthy volunteers who received a structured intervention. Whether these findings can translate to clinical practice needs further study.

In addition, as noted by the study authors, some factors associated with restoration of NGR are not modifiable. In particular, younger age and greater insulin secretion, which is likely also age related, are not reversible, as much as we might like them to be. Still, it was older DPP participants who had the greatest success achieving intensive lifestyle goals and subsequently the greatest reduction in diabetes incidence. If younger patients can more easily attain NGR, then perhaps a less structured intervention (more like what they would receive in clinical practice) will be equally effective."

[From an article in diabetesincontrol.com reviewing a study published in Diabetes Care - 2009; 32(9):1583-8 (ISSN: 1935-5548)]

04 August 2008 @ 12:11 pm

Hi, I just learned that even though my fasting and two hour glucose levels are normal (just barely), 92 and 141, my insulin level is high, 22 and 120. My doctor is pushing metformin because meta-analysis of all related studies shows metformin to be significantly better than just diet and exercise (even assuming you are strict about it). Any ideas and experiences that would help me decide?

02 August 2008 @ 08:37 am

The long-term effect of lifestyle interventions to prevent diabetes in the China Da Qing Diabetes Prevention Study: a 20-year follow-up study. Prof Guangwei Li MD, Dr Ping Zhang PhD, Jinping Wang MD et al.

The Lancet, 24 May 2008, Volume 371, Issue 9626, Pg 1783-1789

Intensive lifestyle interventions can reduce the incidence of type 2 diabetes in people with impaired glucose tolerance, but how long these benefits extend beyond the period of active intervention, and whether such interventions reduce the risk of cardiovascular disease (CVD) and mortality, is unclear. The researchers from China, the USA and Switzerland aimed to assess whether intensive lifestyle interventions have a long-term effect on the risk of diabetes, diabetes-related macrovascular and microvascular complications, and mortality. In 1986, 577 adults with impaired glucose tolerance from 33 clinics in China were randomly assigned to either the control group or to one of three lifestyle intervention groups (diet, exercise, or diet plus exercise). Active intervention took place over 6 years until 1992. In 2006, study participants were followed-up to assess the long-term effect of the interventions.

Compared with control participants, those in the combined lifestyle intervention groups had a 51% lower incidence of diabetes (hazard rate ratio or "HRR" = 0.49) during the active intervention period and a 43% lower incidence (HRR = 0.57) over the 20 year period, controlled for age and clustering by clinic. The average annual incidence of diabetes was 7% for intervention participants versus 11% in control participants, with 20-year cumulative incidence of 80% in the intervention groups and 93% in the control group. Participants in the intervention group spent an average of 3.6 fewer years with diabetes than those in the control group. There was no significant difference between the intervention and control groups in the rate of first CVD events (HRR = 0.98), CVD mortality (HRR = 0.83), and all-cause mortality (HRR = 0.96), but our study had limited statistical power to detect differences for these outcomes.

Conclusion: "Group-based lifestyle interventions over 6 years can prevent or delay diabetes for up to 14 years after the active intervention. However, whether lifestyle intervention also leads to reduced CVD and mortality remains unclear."

The consensus statement was released July 23, 2008 by the American Association of Clinical Endocrinologists (AACE). Publication of the final document is planned for later this year.

You can read the consensus statement at https://www.aace.com/files/prediabetesconsensus.pdf

Questions? Feel free to ask!

In prior entries, I've indicated how my own fasting glucose results (avg 96mg/dl which is considered 'normal') were not helpful in discovering my prediabetic state. It wasn't until I performed a 2 hour glucose tolerance test (GTT) that I learned my glucose levels (180mg/dl) were well into the prediabetic state known as "Impaired Glucose Tolerance (IGT)". For reference, a full blown Type 2 diagnosis is determined when the 2 hour GTT reaches 200mg/dl.

Here's the result of a study that confirms my own experience:

Normal Fasting Plasma Glucose and Risk of Type 2 Diabetes Diagnosis Gregory A. Nichols, PhD, Teresa A. Hillier, MD, MS, Jonathan B. Brown, PhD, MPP Center for Health Research, Kaiser Permanente Northwest, Portland, Oregon.

PURPOSE: The study compares the risk of incident diabetes associated with fasting plasma glucose levels in the normal range, controlling for other risk factors.

METHODS: We identified 46,578 members of Kaiser Permanente Northwest who had fasting plasma glucose levels less than 100 mg/dL between January 1, 1997, and December 31, 2000, and who did not previously have diabetes or impaired fasting glucose. After assigning subjects to 1 of 4 categories (<85, 85-89, 90-94, or 95-99 mg/dL), we followed them until they developed diabetes, died, or left the health plan, or until April 30, 2007. We used Cox regression analysis to estimate the risk of incident diabetes, adjusted for age, sex, body mass index, blood pressure, lipids, smoking, cardiovascular disease, and hypertension.

RESULTS: Subjects developed diabetes at a rate of less than 1% per year during a mean follow-up of 81.0 months. Each milligram per deciliter of fasting plasma glucose increased diabetes risk by 6% (hazard ratio [HR] 1.06, 95% confidence interval [CI], 1.05-1.07, P < .0001) after controlling for other risk factors. Compared with those with fasting plasma glucose levels less than 85 mg/dL, subjects with glucose levels of 95 to 99 mg/dL were 2.33 times more likely to develop diabetes (HR 2.33; 95% CI, 1.95-2.79; P < .0001). Subjects in the 90 to 94 mg/dL group were 49% more likely to progress to diabetes (HR 1.49; 95% CI, 1.23-1.79; P <.0001). All other risk factors except sex were significantly associated with a diabetes diagnosis.

CONCLUSIONS: The strong independent association between the level of normal fasting plasma glucose and the incidence of diabetes after controlling for other risk factors suggests that diabetes risk increases as fasting plasma glucose levels increase, even within the currently accepted normal range.

Full text PDF at: http://download.journals.elsevierhealth.com/pdfs/journals/0002-9343/PIIS0002934308002313.pdf

Essentially, the ADA is finally admitting that:

[1] not only is there a prediabetic stage between normal glucose tolerance and type 2 diabetes,

[2] but if detected early, progression to type 2 could be delayed/stopped if the right interventions are put in place.

Before this consensus statement, the ADA dragged its collective feet about the subject of prediabetes, never really committing themselves.

Because of the ADA's non-commitment, many insurance companies didn't recognize prediabetes as a treatable condition and wouldn't pay for testing, education and medication unless one's blood sugar control had deteriorated enough to be diagnosed with Type 2 diabetes.

Hopefully, this new statement will get insurance companies to pay for earlier interventions and save folks from a lot of grief. :)

While they still don't get it quite right, at least they're on the right track:

The most efficient sequence of testing is an FPG1 first (currently recommended as the preferred test to detect diabetes) followed by the 2-h OGTT2 on a subsequent day to demonstrate the presence of combined IFG/IGT.

The part they got wrong is depending on FPG results to trigger the OGTT.

There are many people, myself included, with normal FPG results that are well within impaired glucose tolerance (IGT) and sometimes Type 2 range when an OGTT is performed.

However, the fact that the ADA is actually recommending the OGTT at all is nothing short of a miracle.

The entire article can be read at: http://care.diabetesjournals.org/cgi/content/full/30/3/753

1 = fasting plasma glucose
2 = oral glucose tolerance test

07 December 2006 @ 05:50 am

Taste test may identify best drugs for depression
Press release issued 6 December 2006

New research has shown that it might be possible to use taste as an indicator as to whether someone is depressed, and as a way of determining which is the most suitable drug to treat their depression.

Research from the University of Bristol has shown that our ability to recognise certain tastes can be improved by administering drugs usually given for depression.

The researchers gave healthy volunteers antidepressant drugs that increase levels of the neurotransmitters serotonin and noradrenaline. They report today in the Journal of Neuroscience that these tests resulted in the volunteers being able to detect different tastes (salt, sugar, sour, and bitter) at lower concentrations, thus enhancing their ability to taste.

Dr Lucy Donaldson, senior author on the paper, said: "When we increased serotonin levels we found that people could recognise sweet and bitter taste at much lower concentrations than when their serotonin levels were normal. With increased noradrenaline levels the same people could recognise bitter and sour tastes at lower concentrations. Salt taste doesn't seem to be affected at all by altering either of these neurotransmitters."

She added: "Because we have found that different tastes change in response to changes in the two different neurotransmitters, we hope that using a taste test in depressed people will tell us which neurotransmitter is affected in their illness."

Dr Jan Melichar, the lead psychiatrist on the paper, added: "This is very exciting. Until now we have had no easy way of deciding which is the best medication for depression. As a result, we get it right about 60-80% of the time. It then takes up to four weeks to see if the drug is working, or if we need to change it. However, with a taste test, we may be able to get it right first time."

Taste is often thought to be determined genetically and, until now, people assumed it was fixed throughout life. But these studies show that the ability to recognise different tastes can be altered by the neurotransmitters serotonin and noradrenaline and by people's mood.

In the study, three drugs were given to the volunteers: SSRI (serotonin specific reuptake inhibitor) to raise serotonin levels; NARI (noradrenaline reuptake inhibitor) to raise noradrenaline levels (another neurotransmitter important in depression, and also found in taste buds); and an inactive placebo.

The volunteers were first tested for their ability to recognise certain tastes. The drug was then administered and two hours afterwards they were asked to take the same test again.

The volunteers were also assessed for anxiety levels, their overall level of anxiety being related to their ability to taste; the more anxious a person was, the less sensitive to bitter and salt taste they were.

These results give an important insight into how neurotransmitters affect the taste system. It seems that tasting bitter things can be changed by changes in both serotonin and noradrenaline levels, that sweet taste is affected by only serotonin levels, and that sour taste is affected by noradrenaline.

These findings may also explain why anxious and depressed individuals have diminished appetite. The results also show that taste is related to anxiety levels, even in generally well people.

Heath TP, Melichar JK, Nutt DJ, Donaldson LF.
Human Taste Thresholds Are Modulated by Serotonin and Noradrenaline
J. Neurosci. 2006 26: 12664-12671

30 October 2006 @ 12:17 pm

Hi there!

Best to introduce myself, my name is Mary, I love in London and about a month ago, my GP alluded to the fact I am pre-diabetic.

Diabetes runs in my family, specifically most of the women on my mother's side of the family has Type II Diabetes, my (passed on) great-grandmother had it (during a time not much could be done, and so was blinded and had both legs amputated at the thigh) my grand-mother and great-aunts have it also, as far as I'm aware my mother and her sisters have fought it off by being careful with sugar all their lives. Unfortunately, all the women in my family have a tendancy to gain weight easily - which never helps.

I was basically diagnosed when I went for my yearly check up and to get a renewed prescription of the pill. I was weighed and blood pressure checked. My blood pressure was prefectly normal, but my weight (of 81.5 kgs -179.3lbs, at the time - I'm 4'11.5" tall) seriously worried my doctor who knew of my families history, asking whether I felt sudden bursts of energy and feeling tired for most of the day when I shouldn't be and if I had cravings for sugar (which was most of the time), among other questions. Basically telling me if I stayed at the weight I was, or kept gaining weight, and didn't cut back on sugar and monitored my energy levels by the time I was 30 (I'm 23) I would have Type II Diabetes. She told me that she could only give me a 3 months supply of the pill until I could proove I could lose the weight on my own and cut back on sugar, as the side effects of being on a contraceptive increase for those who are overweight, as well as being harmful for those with diabetes.

Naturally this scared the living daylights out of me.

To combat this, I have tried to cut out added sugars in my diet, trying to eat 5 small meals a day to stave off both hunger and energy spikes, keeping my body feulled for longer and trying to get to the gym 4 times a week, keeping my heart rate at 155bpm for at least 30 mins (if my heart rate goes over about 160bpm, I then enter anaerobic excercise, instead of aerobic, which is what I want). I'm trying to approach this with a more scientific mind, treating my body as a machine that needs proper maintenance.

So far I've lost about 4kgs (8.8 lbs) in the last 6 weeks and hope to lose a further 5kgs (11 lbs) in the next 8 weeks to try and get to the weight I was a year ago, as well as prove I can do it to my doctor and to stave off her threat of looking into "medical options" of getting my weight down and getting me out of the pre-diabetic stage. My ultimate goal is to get to 50kgs (110 lbs) within the next 18 months and steer clear of diabetes for good.

Just glad there's a community targeting pre-diabetics, any information I can get in combating this would be excellent.

25 October 2006 @ 10:45 am

Metformin Use Increases Vitamin B12 Deficiency

Results indicate an increased risk of vitamin B12 deficiency associated with current dose and duration of metformin.

A nested case-control study identified risk factors for vitamin B12 deficiency in patients with diabetes treated with metformin.

"Identification of risk factors for metformin-related vitamin B12 deficiency has major potential implications regarding the management of diabetes mellitus," write Rose Zhao-Wei Ting, MBBS, from Prince of Wales Hospital. "First, there is likely to be an improved yield of detecting vitamin B12 deficiency if high-risk individuals can be identified. Second, subjects identified as having substantial risk for metformin-related vitamin B12 deficiency might benefit from empirical screening or primary prevention with other means such as calcium supplementation."

The source population for this nested case-control study was a database that consisted of subjects who had levels of both serum vitamin B12 and hemoglobin A1c and were checked in a central laboratory. The investigators identified 155 cases of diabetes mellitus and vitamin B12 deficiency secondary to metformin treatment, as well as 310 controls who did not have vitamin B12 deficiency while taking metformin.

After adjustment for confounders, there were clinically important and statistically significant associations of vitamin B12 deficiency with dose and duration of metformin use. Each 1-g/day increment in metformin dose conferred an odds ratio of 2.88 (95% confidence interval [CI], 2.15 - 3.87) of developing vitamin B12 deficiency (P < .001).

"Our results indicate an increased risk of vitamin B12 deficiency associated with current dose and duration of metformin use despite adjustment for many potential confounders," the authors write. "The risk factors identified have implications for planning screening or prevention strategies in metformin-treated patients."

"We believe our findings should reinforce the heightened vigilance about vitamin B12 deficiency," the authors conclude. "Enough concerns exist to call attention to the value of vitamin B12 screening, particularly among at-risk patients receiving metformin. Our data underscore the need for monitoring subjects undergoing high-dose and/or prolonged-course metformin therapy."

Arch Intern Med. 2006;166:1975-1979.

Here's a review of what vitamin B12 is, why it's important, and what foods have it: http://dietary-supplements.info.nih.gov/factsheets/vitaminb12.asp