Lyme Disease Support Group

http://flash.lymenet.org/ubb/ultimatebb.php/topic/1/96492

Pinelady

Frequent Contributor (1K+ posts)

Member # 18524

posted 07-07-2010 10:25 AM

------------------------------

Meaning have you been able to reduce or change

meds/possibly go from shots to orals/ etc. after treatment?

Or has treatment made it worse??? More meds nessasary?

Posts: 4329 | From Kentucky | Registered: Dec 2008 *****************

nspiker

LymeNet Contributor

Member # 22824

posted 07-07-2010 10:35 AM

Pinelady,

I don't have diabetes, but I did improve my blood sugar and blood pressure. I have an IV nurse from the Philippines that recommended bitter melon.

She took it and has gone off all medications. She recommended it to someone who has type 1 diabetes, and they were able to completely get off injections, and now is only on orals.

http://www.vitacost.com/Charantea-Bitter-Melon?csrc=GPF- 858101001064

--------------------

Posts: 186 | From san diego | Registered: Oct 2009 **********

LightAtTheEnd

LymeNet Contributor

Member # 24065

posted 07-07-2010 11:55 AM

I don't have diabetes, but I was close until I averted it with a low carb, high protein diet. The same diet is good for Lyme and for prevention of yeast (candida), and for weight loss if desired.

A diet based on protein and fat that gets its limited carbs mainly from non-starchy vegetables benefits you by regulating your blood sugar so it doesn't go up too fast or too high, and by reducing the systemic inflammation in your body, which is at the root of many diseases and can be involved with Lyme symptoms.

People with Lyme have various different problems with disregulated hormones and metabolism, and with gaining or losing weight when they don't want to, digestion/absorption problems, and have different reactions to various drugs, etc.

I don't think Lyme treatment would automatically help with diabetes, but I suspect that living a generally healthier lifestyle with less refined carbs, more sleep, etc. would be good for it.

Of course if you have diabetes, you might already be doing all those healthy things.

Posts: 445 | From Inside the tunnel | Jan 2010

//////////

Keebler

Honored Contributor (10K+ posts)

Member # 12673

posted 07-07-2010 12:08 PM

-

I've been on the fence for years. Lyme can be a cause of diabetes (as can other infections that stress the endocrine system).

However, certain herbs really help me. Bitter Melon is good; Gymnema Sylvestre, too.

======================

This book is specific to lyme and other chronic stealth infections.

The author discusses the endocrine connection and effects of STRESS on a person with such infections.

Adrenal support is one key to helping keep cortisol down (and that helps with blood glucose stability).

For adrenal support, other books and articles offer more detail. This is more of a place to begin looking at connections.

You can read customer reviews and look inside the book at this link to its page at Amazon.

http://tinyurl.com/6xse7l

THE POTBELLY SYNDROME: HOW COMMON GERMS CAUSE OBESITY, DIABETES, and HEART DISEASE - 2005

by Russell Farris and Per Marin, MD, PhD

==============

www.ncbi.nlm.nih.gov/sites/entrez

PubMed Search:

Gymnema Sylvestre – 138 abstracts

=======================

From a fabulous book, "The One Earth Herbal Sourcebook" (Tillotson, et.al.):

http://tinyurl.com/5z2klz

GYMNEMA (Gymnema sylvestre). . . is bitter in taste, and cooling in action. It improves blood sugar control in diabetics, numbs the taste of sweet completely (for about 20 minutes), and decreases appetite (for about 90 minutes).

. . . Should not be used by people with low blood sugars (hypoglycemia). . . .

. . .Gymnema actually means "sugar destroyer." It grows in the wild forests of central India, all the way to Western Ghats and up to the Himalayas.

Research indicates that gymnema stimulates insulin secretion or release of insulin from the pancreas. Japanese studies have shown that it improves glucose tolerance in animal models of diabetes, and other studies show that the effects can last for up to two months after discontinuation.

This herb is a good long-term tonic for Type I and II diabetics. Results are best seen after long-term administration, over six months to a year. I prefer to use it in combination with several other herbs for blood sugar control, because it affects only a few aspects of the imbalance.

In case you’re curious, sugar tastes like sand for twenty minutes after you chew on a little gymnema. . . .

- Full chapter at link above. And you can also search the book for “Diabetes” for a gold mine of more information.

=====================

http://www.vrp.com/ArticlesSearch.aspx?k=Gymnema

Search results for Gymnema: 6 articles

(Other beneficial supplements are also included in most of the articles).

===================

http://www.itmonline.org - ITM

Search: Gymnema - 2 articles, one on interaction with drugs

Search: Diabetes

– Eight pages of links, the top three focus on “Treatment of Diabetes with Chinese Herbs . . . “

======================

This is the formula my ND suggests:

http://www.acuatlanta.net/gymnema-capsules-p-18480.html? osCsid=753b4cc3d371e8f224053b6ccded731e

Ayush Herbs - Bio Gymnema

You can read the Ingredients here, too.

http://www.msnbc.msn.com/id/35099601/ns/health-diabetes/

Avoid extremes in diabetes control, study warns

Driving blood sugar down too low can be as risky as leaving it too high

Jan. 27, 2010

LONDON - Moderation appears to be the best approach to controlling blood sugar in a form of diabetes that affects many adults, researchers said Wednesday, since lowering it too far can be as risky as letting it stay too high. . . .

- full article

-

Posts: 15026 | From Tranquil Tree House in my dreams | Registered: Jul 2007

*******************

Pinelady

Frequent Contributor (1K+ posts)

Member # 18524

posted 07-07-2010 12:39 PM

This is just one infection that is suspect to high incidence of diabetes.

Gosh I wish we had Millions to work through all that needs done.

http://www.jbc.org/content/280/25/24085.full

For many years, the association between human T. cruzi infection and diabetes has received little formal evaluation.

Anecdotally, there is a general belief that the incidence of diabetes is greater in the chagasic population.

In recent years, there have been several reports suggesting that diabetes is indeed more common in the setting of increased T. cruzi infection (6, 7).

One study demonstrated a significant reduction in insulin among chronically infected individuals (8).

Interestingly, our previous studies indicated that when mice with chemically induced diabetes are infected with T. cruzi, they have a higher parasitemia and mortality (9).

The same observation is seen when diabetic db/db mice are infected (9, 10). The underlying reasons for these phenomena are unknown.

By Kristina Fiore, Staff Writer, MedPage Today

Published: June 30, 2010

Reviewed by

Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and

Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner Earn CME/CE credit

Action Points

■Explain that a novel DPP-4 inhibitor -- linagliptin -- appears to improve glycemic control alone, as an add-on, and in combination with a thiazolidinedione.

■Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.

ORLANDO -- A novel dipeptidyl peptidase 4 (DPP-4) inhibitor -- linagliptin -- appears to improve glycemic control as monotherapy, as an add-on, and in combination with other oral diabetes medications, researchers reported here.

In four phase-III trials, linagliptin significantly improved glycated hemoglobin (HbA1c) alone, as an add-on to metformin or metformin plus a sulfonylurea, and in combination with pioglitazone (Actos), according to four posters presented at the American Diabetes Association (ADA) meeting here.

However, hypoglycemia appeared to be a concern in both the metformin-plus-sulfonylurea and the pioglitazone groups.

"Linagliptin is a very viable alternative for the treatment of diabetes," Giora Davidai, MD, director of medical affairs for Boehringer Ingelheim, told MedPage Today in an interview.

He added that linagliptin appears to have a primarily non-renal route of excretion, which may bode well for the large numbers of diabetes patients who do have renal problems.

"Only 5% is cleared by the kidney," he said. "All the rest is cleared by other means."

Researchers presented the results of four 24-week, randomized, double-blind, placebo-controlled trials of linagliptin during an ADA poster session.

In the linagliptin-as-monotherapy trial, 503 patients were randomized to 5 mg daily of the drug or placebo.

At the end of the study, those on the drug had a 0.69% greater reduction in HbA1c from baseline compared with those on placebo (P<0.0001), and more patients on linagliptin achieved an HbA1c reduction of 0.5% or greater (47.1% versus 19%).

There were also greater reductions in fasting plasma glucose (-23.3 mg/dL) and postprandial glucose (-58.4 mg/dL) for linagliptin compared with placebo (P<0.0001), as well as improved insulin secretion (P<0.05).

Adverse events were the same in both groups, and hypoglycemia was rare.

In another trial, 601 patients were randomized to linagliptin or placebo as an add-on to metformin.

Again, the researchers found a significantly greater reduction in HbA1c in the active drug group compared with placebo (-0.64%, P<0.0001), and those in the linagliptin group were more likely to reach an HbA1c of 7% (OR 4.4, P=0.0001).

Patients on the drug combo had significantly better improvements in fasting plasma glucose and postprandial glucose as well. Adverse events were comparable and hypoglycemia was rare.

In a third trial, 1,058 patients were randomized to either linagliptin as an add-on to both metformin and a sulfonylurea, or a placebo add-on.

The researchers found a significantly greater reduction in HbA1c among those in the drug group compared with the placebo group (-0.62%, P<0.0001), and they also had a greater likelihood of achieving an HbA1c of 7% (OR 5.5, P<0.0001).

The linagliptin patients also had better fasting plasma glucose and improvements in beta-cell function (P<0.005), but the trial didn't assess postprandial glucose.

Still, the researchers cautioned that there was significantly more hypoglycemia in the drug group (22.7% versus 14.8%), warning that "when linagliptin is added on to preexisting sulfonylurea therapy, hypoglycemia may occur."

More hypoglycemic events were also seen when patients took linagliptin in combination with pioglitazone, compared with a placebo in combination with the thiazolidinedione.

Among 389 patients, there were three episodes of hypoglycemia (1.2%) in the drug group, compared with none in the placebo plus pioglitazone group.

"So far it appears very safe ... but we will continue monitoring safety very carefully," Davidai said.

Those in the linagliptin combination group had greater improvements in HbA1c (-0.51%, P<0.001) and were twice as likely to achieve an HbA1c target of 7% (OR 2.1, P<0.0051).

Davidai said the researchers "still have a lot of work to do," including assessing weight loss or gain, but the company plans to file a new drug application "in the near future."

A number of the researchers presenting posters were employees of Boehringer Ingelheim.

Davidai is an employee of Boehringer Ingelheim.

Primary source: American Diabetes Association

Source reference:

Del Prato S, et al "Linagliptin monotherapy improves glycemic control and measures of beta-cell function in type 2 diabetes" ADA 2010; Abstract 695-P.

Additional source: American Diabetes Association

Source reference:

Taskinen MR, et al "Efficacy and safety of linagliptin in type 2 diabetes patients inadequately controlled on metformin monotherapy" ADA 2010; Abstract 579-P.

Additional source: American Diabetes Association

Source reference:

Owens DR, et al "Linagliptin improves glycemic control in type 2 diabetes patients inadequately controlled by metformin and sulfonylurea without weight gain and low risk of hypoglycemia" ADA 2010; Abstract 548-P.

Gromis R, et al "Efficacy and safety of initial combination therapy with linagliptin and pioglitazone in patients with inadequately controlled type 2 diabetes" ADA 2010; Abstract 551-P.

http://tinyurl.com/2ddxf2l

*****************************************

Mortality Lower with Metformin

By Kristina Fiore, Staff Writer, MedPage Today

Published: June 30, 2010

Reviewed by

Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston and

Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner

Action Points

■Explain that patients with type 2 diabetes taking metformin appeared to have a 24% lower risk of death from any cause than patients who weren't taking it.

■Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.

ORLANDO -- Metformin use may reduce mortality among patients with type 2 diabetes who are at risk for cardiovascular events, researchers say.

A large, multicenter trial found a 24% reduced risk of all-cause mortality among patients on the drug, compared with those not taking it, according to Ronan Roussel, MD, PhD, of Groupe Hospitalier Bichat-Claude Bernard in Paris, and colleagues.

They presented their findings during a late-breaking session at the American Diabetes Association (ADA) meeting here.

"In secondary prevention patients, the use of metformin was associated with a significant reduction in all-cause mortality after two years of follow-up," Roussel said.

Previous studies, including the United Kingdom Prospective Diabetes Study (UKPDS) have suggested that metformin may carry a decreased risk of overall mortality.

To explore the relationship, Roussel and colleagues assessed data from the Reduction of Atherosclerosis for Continued Health (REACH) registry, which enrolled more than 67,000 patients from 5,473 sites in 44 countries.

Its purpose was to investigate risk factors for cardiovascular events in patients at risk of atherothrombotic disease and to assess the use of risk management strategies.

In this analysis, the Roussel and colleagues assessed the 19,699 patients over age 45 who had diabetes as well as documented cardiovascular disease or other atherothrombotic risk factors.

Only 40% of the patients were treated with metformin at baseline, and they tended to be younger, [u]heavier, and had better renal function.[/u]

To take into account any of these potential confounding factors, the researchers used a propensity score, which included controlling for factors such as use of more cardioprotective drugs in patients on metformin.

Over a two-year period, there were a total of 1,270 fatalities.

The researchers found that patients on metformin had a significant 33% reduction in the risk of death compared with those not on the drug (95% CI 0.59 to 0.75, P<0.001).

After adjustment with the propensity score, there was still a significant 24% reduction in death (95% CI 0.65 to 0.89, P<0.001).

In additional analyses, Roussel said the protective effect may be more applicable to women, patients between 40 and 80, those with a history of heart failure, and concomitant use of insulin, but not all of these interactions were significant.

Roussel concluded that the mortality finding "is consistent with the results of the UKPDS, with a Cochrane systematic review of trials of metformin as monotherapy, and with two other observational studies focusing on diabetic patients with congestive heart failure."

He added that the data have broad applicability and should be explored in further trials.

David M. Kendall, MD, of the University of Minnesota and the ADA's chief scientific & medical officer, moderated the session at which Roussel presented his findings.

"Certainly while the world is not looking for more reasons to use metformin," Kendall said, "this adds to the strength of the evidence that suggests a mortality benefit."

The REACH Registry is sponsored by sanofi-aventis, Bristol-Myers Squibb, and the Waksman Foundation in Tokyo, Japan.

Roussel said he has received research grants, honoraria, or consulting fees from sanofi-aventis, MSD Chibret, Servier, Roche, Eli Lilly, Novo Nordisk, Medtronic, and Lifescan.

Primary source: American Diabetes Association

Source reference:

Roussel R, et al "Metformin use and mortality among diabetic patients with established atherothrombosis" ADA 2010.

http://tinyurl.com/2fml3cn

************************************

Top Choice for Breast CA Is Aromatase Inhibitor

By Crystal Phend, Senior Staff Writer, MedPage Today

Published: July 15, 2010

Reviewed by

Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and

Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner

Aromatase inhibitor therapy should be considered for all postmenopausal women with hormone receptor-positive breast cancers, the American Society of Clinical Oncology re-emphasized.

An update to their guidelines on adjuvant endocrine therapy again supported the aromatase inhibitors, saying they provide better disease-free survival than tamoxifen (Nolvadex) in this patient population.

But what strategy to use them in -- upfront as monotherapy or sequential after two to three years of tamoxifen -- remains unresolved, according to the update committee led by Harold J. Burstein, MD, PhD, of the Dana-Farber Cancer Institute in Boston.

ASCO has recommended an aromatase inhibitor for these patients since 2004 but provided no guidance on the optimal duration until now.

Action Points

■Note that the guidelines update recommended consideration of aromatase inhibitors at some point for all postmenopausal women with hormone receptor-positive breast cancer, though not for more than five years.

The update, published online in the Journal of Clinical Oncology, recommends no more than five years' duration for aromatase inhibitors.

If sequential therapy is the strategy used, the available evidence supports an aromatase inhibitor after two or three years of tamoxifen for a total of five years of adjuvant endocrine therapy.

If patients discontinue initial aromatase inhibitor use before the full five years, tamoxifen can be considered for the remainder of the five years.

If an extended strategy of up to 10 years of total endocrine therapy is used, the order should be five years of tamoxifen followed by three to five years of an aromatase inhibitor, according to the guidelines update.

The aromatase inhibitors appear to be interchangeable such that patients who can't tolerate one may be advised to consider not only tamoxifen but another aromatase inhibitor, Burstein's group wrote, noting this was their clinical opinion without randomized trial evidence.

The choice of when and whether to use an aromatase inhibitor for an individual patient may depend on the distinct adverse effect profiles of tamoxifen and aromatase inhibitors and patient preferences, the update writers acknowledged.

Aromatase inhibitors aren't less toxic or better tolerated than tamoxifen; rather, "both drug classes have distinct adverse event profiles that are relevant to individualizing therapy for patients," according to the update.

The newer class appears to increase serious cardiac disease incidence, though by less than 1% compared with tamoxifen, as well as high cholesterol, hypertension, bone mineral density loss, fracture, uterine cancer, benign endometrial pathology, hysterectomy, and vaginal discharge.

Tamoxifen, on the other hand, raises venous thromboembolic event risk by 1% to 2% compared with the aromatase inhibitors and is associated with more hot flashes.

The advantage in reducing risk of recurrence with the aromatase inhibitors in absolute terms is modest, "typically amounting to less than 5% through multiple years of follow-up," and without any difference in overall survival, Burstein's group wrote in the guidelines.

For the systematic review, they reviewed 12 prospective, randomized trials of adjuvant aromatase inhibitor or tamoxifen use in different strategies -- initial, sequential, or extended therapy after five years of treatment with adjuvant tamoxifen.

The evidence didn't support using any markers to determine who would benefit most from which strategy, the researchers noted.

They specifically recommended against use of CYP2D6 genotype to select adjuvant endocrine therapy.

The only important factor is menopausal status.

Women who are pre- or perimenopausal at the time of breast cancer diagnosis should only get tamoxifen, the guideline update cautioned.

Burstein disclosed that he had no finanical conflicts of interest.

Co-authors reported consultant or advisory roles with Pfizer and Novartis; honoraria from Novartis, Astra Zeneca, and Pfizer; and research funding from Novartis and Pfizer.

Primary source: Journal of Clinical Oncology

Source reference:

Burstein HJ, et al "American Society of Clinical Oncology clinical practice guideline: Update on adjuvant endocrine therapy for women with hormone receptor–positive breast cancer" J Clin Oncol 2010; DOI: 10.1200/JCO.2009.26.3756.

http://tinyur

Post edited by: Bettyg, at: 07/17/2010 10:01 PM

By Charles Bankhead, Staff Writer, MedPage Today

Published: July 29, 2010

Reviewed by

Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and

Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner

Action Points

■Note that in this study fracture risk in postmenopausal women was associated with use of thiazolidinedione diabetes drugs.

■Note also that fracture in men was associated with concurrent use of a thiazolidinedione and a loop diuretic but not with the individual drugs.

■Note that the findings are based on a retrospective review of a large database, not a prospective clinical trial.

Patients with type 2 diabetes may face an increased fracture risk when treated with thiazolidinedione (TZD) drugs, data from a large observational study suggest.

Use of rosiglitazone (Avandia) or pioglitazone (Actos) was 70% more common among postmenopausal women with diabetes and a history of fractures, compared with a matched control group without fractures.

Among diabetic men with a history of fractures, concurrent use of a TZD and a loop diuretic was more than three times as common as in similar men with no history of fractures.

Fracture risk was associated with TZD dose, but the risk was similar for rosiglitazone and pioglitazone, suggesting a class effect, William Herman, MD, of the University of Michigan in Ann Arbor, and co-authors wrote in an article published online in the Journal of Clinical Endocrinology and Metabolism.

Laboratory studies have suggested that TZD activation of peroxisome proliferator-activated receptor-gamma may reduce bone formation.

Use of TZDs previously has been associated with a risk of fracture in postmenopausal women, but the studies were limited to patients with newly diagnosed type 2 diabetes, [u]excluding patients taking other diabetes drugs and corticosteroids. [/u]

The studies also did not take into account racial/ethnic influences in case-control matching, according to the article's background information.

In an effort to define the risks more precisely, Herman and colleagues examined data from the Translating Research into Action for Diabetes (TRIAD) observational study.

The study had a geographically, racially, and ethnically diverse population, and investigators accumulated detailed patient information from multiple sources.

The authors identified

786 fracture cases involving 54 women younger than 50 years,

457 women 50 years or older, and

275 men.

The cases were matched by age, sex, race/ethnicity, and body mass index with 2,657 patients with diabetes but no history of fracture.

Troglitazone, the first marketed TZD, was withdrawn from the market in 2000, two years before the beginning of TRIAD's administrative data.

After the first prescription for rosiglitazone was filled, the number of patients with prescriptions increased from 500 at one year to 1,400 at four years.

Patients with prescriptions for pioglitazone increased from 500 to 1,300 during years one through four.

Follow-up averaged 1.9 years and ranged from less than a week to almost five years.

Among women 50 and older, TZD use was significantly more common in patients with fractures compared with controls (P<0.05).

Fracture doubled the likelihood of treatment with glucocorticoids and was associated with a 50% increase in the use of loop diuretics.

The patients also were 50% more likely to have limited mobility.

Use of higher doses of TZDs was 40% more common in women with a history of fracture.

The analysis showed no association between fracture and TZD use in women younger than 50.

Among men, fracture more than tripled the odds of concurrent use of a TZD and a loop diuretic (OR 3.46). However, neither drug by itself had a significant association with fracture.

Fracture also increased the likelihood of exposure to glucocorticoids by 80% and insulin by 60%, and doubled the odds for limited mobility and lower-extremity amputation.

The authors noted several limitations to their study, including the use of pharmacy data to determine medication use -- which may have resulted in some noncovered medication purchases not being detected -- and the small number of women in the study under age 50.

Additionally, administrative data were used to determine occurrence of fractures; x-ray data were not inspected.

The study was funded by the Centers for Disease Control and Prevention and the National institute of Diabetes and Digestive and Kidney Diseases.

The authors reported that they had no relevant disclosures.

Primary source:

Journal of Clinical Endocrinology and Metabolism

Source reference:

Bilik D, et al "Thiazolidinediones and fractures: Evidence from Translating Research into Action for Diabetes (TRIAD)" J Clin Endicrinol Metab 2010; DOI:10.1210/jc.2009-2638.

© 2004-2010 MedPage Today, LLC. All Rights Reserved.

http://tinyurl.com/25mtkdf

By Todd Neale, Staff Writer, MedPage Today

Published: August 06, 2010

Reviewed by

Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston and

Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner

Designing public health interventions to prevent diabetes may be an effective way of reducing the burden of dementia in the absence of a cure for cognitive impairment, researchers found.

Diabetes was one of four potentially modifiable factors that, if eliminated or improved, would reduce rates of dementia in the general population, Karen Ritchie, PhD, of the French National Institute of Health and Medical Research (INSERM) in Montpellier, and colleagues reported online in BMJ.

The percentage of dementia cases that hypothetically would be avoided if diabetes were eliminated was 4.9%.

Action Points

■Explain to interested patients that a study of older patients in France found that elimination of diabetes as a risk factor for dementia had the greatest likelihood of being a significant public health measure.

■Note that other risk factors such as ApoE4-epsilon 4 allele, depression, intellectual exposure, and decreased fruit and vegetable consumption were not considered as amenable to a big public health intervention as diabetes prevention.

The proportion of cases that would be eliminated with a higher score on a measure of intellectual exposure, elimination of depression, and increased fruit and vegetable consumption was 18.1%, 10.3% and 6.5%, respectively.

Even though the attributable fraction was greater for those three factors than for diabetes, it would be easier to design interventions to prevent diabetes, "which is a well-established risk factor for dementia, is unlikely to be simply a dementia prodrome, is highly prevalent, and is treatable," according to the researchers.

"The high prevalence of this disorder in the elderly population means that intervention is likely to have a high impact and be cost-effective, even though the relative risk is modest."

Developing public health interventions to increase intellectual exposure, ease depression, and increase fruit and vegetable consumption would be more difficult, they noted.

"Although causal relations cannot be concluded with certainty, the study suggests priorities that may inform public health programs," the researchers concluded.

To explore the influence of various potentially modifiable risk factors identified from the literature, Ritchie and her colleagues turned to the Esprit Study, a cohort study of people older than 65 living in Montpellier, France.

All were free of mild cognitive impairment and dementia at baseline.

The current analysis included 1,433 participants (mean age 72.5).

Through a median follow-up of 7.31 years, there were 31 incident cases of dementia and 374 cases of mild cognitive impairment.

The following variables were associated with a greater risk of being diagnosed with dementia or mild cognitive impairment:

•Crystallized intelligence (according to scores on the Neale adult reading test, which serves a proxy measure of lifelong cognitive activity or intellectual exposure):

HR 1.72 (95% 1.41 to 2.09)

•Depression: HR 1.39 (95% CI 1.13 to 1.71)

•Fruit and vegetable consumption less than twice per day: HR 1.26 (95% CI 1.02 to 1.56)

•Diabetes: HR 1.85 (95% CI 1.34 to 2.56)

Treatment of depression and diabetes were analyzed as variables related to the population attributable risk of dementia and mild cognitive impairment as well, but were not found to be significant contributors.

"The underlying assumption was that although treatment may have eliminated symptoms and reduced risk through decreasing length of exposure, the person has nevertheless been exposed to all the underlying negative biological effects associated with the disease state that may be linked to the etiology of dementia, such as inflammation, increased permeability of the blood-brain barrier, damage to white matter, and raised cortisol concentrations," the researchers said.

"In this context, the corollary of our population attributable fraction analyses in terms of public health interventions is that these disorders should not so much be treated as prevented from occurring at all."

Presence of the epsilon-4 allele of the apolipoprotein E gene was also associated with an increased risk of dementia or mild cognitive impairment (HR 1.47, 95% CI 1.16 to 1.86).

"Genetic modification is clearly not a feasible goal for public health intervention, but as it constitutes one of the most significant risk factors for dementia, we have taken it as a benchmark for the comparison of other exposures," the researchers noted.

They acknowledged some limitations of the study, including the use of many assumptions about the levels of exposure, the treatment of dimensional variables as binary variables, and the grouping of mild cognitive impairment with dementia.

The Esprit Study was funded by an unconditional grant from Novartis and from the National Research Agency. Funding from Novartis was used to purchase equipment and pay for secretarial assistance. The National Research Agency funding provided salaries for the interviewers and the costs of clinical and biological examinations.

Ritchie and her co-authors reported having technical support from Novartis for the study.

Primary source: BMJ

Source reference:

Ritchie K, et al "Designing prevention programs to reduce incidence of dementia: prospective cohort study of modifiable risk factors" BMJ 2010; DOI: 10.1136/bmj.c3885.

http://tinyurl.com/2edwov6

© 2004-2010 MedPage Today, LLC. All Rights Reserved.

By Charles Bankhead, Staff Writer, MedPage Today

Published: August 17, 2010

Reviewed by

Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and

Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner

Three-fourths of patients with type 2 diabetes were able to stop taking medications six months after undergoing bariatric surgery -- and almost 85% no longer needed drug treatment at two years -- cutting their healthcare costs, according to a review of health insurance records.

The analysis of insurance claims data for more than 2,200 adults with type 2 diabetes who underwent bariatric surgery found that --

despite the $30,000 median price tag for the procedure and hospitalization --

the surgery also saved money in the long run, Martin A. Makary, MD, of Johns Hopkins, and co-authors reported.

While annual healthcare costs increased by 9.7% in the first year after bariatric surgery, costs decreased by 34% in the second year, and dropped by 70.5% in the third year, compared with preoperative expenditures, the team wrote in the August issue of the Archives of Surgery.

Action Points

■Explain to interested patients that a review of insurance claims showed that a majority of patients with type 2 diabetes no longer required medications two years after undergoing bariatric surgery.

■Further note that, compared with preoperative expenditures, annual healthcare costs dropped by more than 70% three years after patients had bariatric surgery.

"Health insurers, private and public, should pay for bariatric surgery for appropriate candidates, recognizing a potential annualized cost savings in addition to the benefit to health," Makary and co-authors commented.

"Coverage of bariatric surgery should be available to all obese patients who meet criteria, regardless of their degree of coverage provided the patient possess the appropriate degree of personal health responsibility and access to a physician in the event of a surgical complication," they added.

Bariatric surgery results in long-term weight loss, improved lifestyle, and decreased mortality among obese patients -- factors that have contributed to a 200% increase in the number of procedures over the past five years, the authors noted.

However, limited data have accumulated regarding the effects of surgery on diabetes and diabetes-related healthcare costs.

To examine the impact of bariatric surgery on diabetes, Makary and co-authors analyzed claims data from Blue Cross/Blue Shield health plans covering 15.9 million people in seven states.

They identified 2,235 adults with type 2 diabetes who had bariatric surgery from January 2002 through December 2005.

The authors used administrative claims data to assess use of diabetes medications at specified intervals before and after surgery. They also determined median healthcare costs per year.

Prior to surgery, 1,918 (85.8%) of the patients were taking at least one diabetes medication, and the number of medications per patient averaged 4.4.

Within six months of surgery, 1,669 of 2,235 (74.7%) patients did not require diabetes medications.

The proportion increased to 80.6% (1,489 of 1,847) at one year and to 84.5% (906 of 1,072) at two years.

Roux-en-Y gastric bypass surgery accounted for 84.2% of the bariatric procedures. The median cost for all procedures (including hospitalization) was $29,959.

The patients' total healthcare expenditures averaged $6,376 per year in the one to two years prior to surgery.

In the first year after surgery, expenditures increased by 9.7% ($616) then decreased by 34.2% ($2,179) in the second year, and by 70.5% ($4,498) in the third postoperative year.

The findings are consistent with data reported the past two years at the American Society of Metabolic and Bariatric Surgery meeting.

Multiple studies documented high rates of diabetes resolution following surgery, and investigators in one study employed statistical modeling to estimate that bariatric surgery paid for itself in four years, two years in patients with diabetes.

The study was supported by the Agency for Healthcare Research and Quality and by the Blue Cross/Blue Shield Obesity Care Collaborative.

The authors reported that they had no relevant disclosures.

Primary source: Archives of Surgery

Source reference:

Makary MA, et al "Medication utilization and annual health care costs in patients with type 2 diabetes mellitus before and after bariatric surgery" Arch Surg 2010; 145: 726-731.

© 2004-2010 MedPage Today, LLC. All Rights Reserved.

http://tinyurl.com/2cca9ts

http://tinyurl.com/35nxtfr

By: John Gever | August 24, 2010

Could nerve surgery cure type 2 diabetes?

A group at Allegheny General Hospital in Pittsburgh thinks so. But the rest of the world seems pretty skeptical so far.

The possibility was suggested in a press release from the hospital a couple weeks ago, describing work by Peter Jannetta, MD, and colleagues reported in the the journal Surgical Neurology International.

According to the report, seven of 10 patients with type 2 diabetes showed improved glycemic control -- including one who went off diabetes meds entirely -- following surgery for vascular compression of cranial nerves.

Jannetta has published extensively on the relationships between vascular compression and various nervous system abnormalities such as hemifacial spasm.

He says he has performed more than 6,000 surgeries to relocate cranial arteries whose pulsation pressed on nerve fibers.

In the past, he has claimed to successfully treat hypertension with such procedures focusing on vessels in the left lateral medulla.

In the new report, Jannetta and colleagues argued that it would be "reasonable to assume that there should be a right lateral medullary syndrome" and noted that the right vagus nerve, among others, serves the pancreas.

They found 10 diabetic patients with right-sided vascular compression in the medulla, according to MRI data, and offered them surgery.

The results appeared spectactular, but we at MedPage Today, and nearly every other reputable news outlet, chose not to report on it because of gaping holes in the journal report.

Like, the authors didn't say how many patients they screened to find the 10 included in the study.

They gave almost no baseline clinical or demographic information on the 10 patients.

No glucose or insulin tolerance tests were performed.

Nor did Jannetta and colleagues offer any specific rationale for how compressed medullary nerves might cause or aggravate loss of insulin sensitivity in tissues throughout the body.

The best they could offer was data from diabetic animal models showing that medullary neurotransmitter levels are altered.

The data did not show that messing around with medullary neurotransmitters or nerve function could induce diabetes.

Perhaps that's why the report appeared in an obscure neurosurgery journal.

The whole thing is reminiscent of the vascular theory of multiple sclerosis, which also came out of nowhere and made little sense in the context of what was already known about the disease.

In that case, however, the MS community immediately glommed on to the new theory and essentially forced funding agencies to divert millions of dollars into studying the possibility that it might not be completely off-base.

(Efforts to replicate the initial findings have failed thus far.)

I'm not sure why this hasn't happened with Jannetta's theory. Perhaps it's just too kooky even for desperate patients to believe.

Or perhaps they simply haven't heard about it because the media have largely taken a pass on covering it, in which case we can expect to be accused of suppressing the discovery of the century.

3 Comments

August 25, 2010

Mr. Gever, the author, makes some valid points about this.

Not too long ago, I recall reading about how cutting the vagus nerve near the stomach helped with weight loss.

I believe studies with larger patients are pending.

Regarding the vascular theory and MS, I've also read that none of the current studies to date that have failed to replicate the Italian's doctor's results have used the same or similar methodologies to duplicate his results.

So, I wouldn't discount it yet. Research is to be encouraged: even the crazy ideas can sometimes work out.

Recall the Australian doctor, who thought he was crazy because he had discovered that H. Pylori caused stomach ulcers. He later went on to win a Nobel prize.

-- Posted by Jorge Quiñónez

------------------------------------------------------------ --------------------

August 25, 2010

I have known Jannetta's work since my Neurology residency in the mid 70's when he was developing his Trigeminal Neuralgia decompression surgery.

to his credit he had Neurology see most of his preops and did not operate on a lot of atypical face pain and somatic patients.

Note all of the Neurology Residents at that time became expert in the diagnosis and treatment of Trigeminal Neuralgia.

I do not think Dr. J has anything to gain by any new discoveries. Time will tell.

-- Posted by marvin rachelefsky

------------------------------------------------------------ --------------------

August 24, 2010

I agree that this could be the discovery of the century

- Posted by juan m. gonzalez bernal

Post edited by: Bettyg, at: 08/26/2010 01:32 AM

Women who don't breast-feed their babies are at an increased risk for type 2 diabetes, researchers found.

Women who had never breast-fed were almost twice as likely to develop the disease as women who had never had children (OR 1.93, 95% CI 1.14 to... full story

http://www.medpagetoday.com/OBGYN/Pregnancy/tb/21910

By Crystal Phend, Senior Staff Writer, MedPage Today

Published: August 27, 2010

Reviewed by

Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston and

Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner

Insulin resistance and type 2 diabetes may contribute to the development of one type of brain plaque linked to Alzheimer's disease, according to an autopsy study.

An analysis of autopsy samples from 135 Japanese men and women found that high insulin and glucose levels appeared to accelerate the formation of neuritic plaques, especially among those carrying a high-risk gene for Alzheimer's, Kensuke Sasaki, MD, PhD, of Kyushu University in Fukuoka City, Japan, and colleagues, reported.

Action Points

■Explain to interested patients that a Japanese autopsy study found an association between hyperglycemia and insulin resistance documented during the decade before death and neuritic plaques -- one pathologic finding of Alzheimer's disease -- at autopsy.

■Note that the study was small and there was no association between the diabetes-related factors and neurofibrillary tangles connected to amyloid deposits, a different pathologic finding in Alzheimer's.

The association of neuritic plaques with higher levels of two-hour post-load plasma glucose, fasting insulin, and insulin resistance measured in the decade before death was found to be independent of other risk factors like age, blood pressure, smoking, and cerebrovascular disease, Sasaki and co-authors wrote in the Aug. 25 issue of Neurology.

Thus, "adequate control of diabetes might contribute to a strategy for the prevention of Alzheimer's disease," they concluded.

Although these findings strengthen evidence for a causal link with dementia, an accompanying editorial by José A. Luchsinger, MD, MPH, of Columbia University Medical Center and School of Public Health in New York City, cautioned that alternative explanations must be considered.

For example, Luchsinger noted, the relatively small sample size selected from a much larger pool of participants who did not have an autopsy may have led to selection bias or to chance findings.

Reverse causality was also a possibility since brain pathology and metabolic changes may precede dementia diagnosis by decades and diabetes and insulin resistance could result from or correlate with Alzheimer's, he added.

On the assumption that the association may be causal, though, several randomized trials are already testing insulin sensitizers in older adults or those with mild cognitive impairment to see if the strategy has an effect on cognition.

"This is urgent considering that over half the U.S. population in the age group most at risk for cognitive impairment has prediabetes or type 2 diabetes, preceded or accompanied by insulin resistance and hyperinsulinemia," Luchsinger concluded in the editorial.

The researchers analyzed autopsy results from 74 men and 64 women (average age 67) who died between 1998 and 2003 after participating in the long-term prospective Hisayama Study, which looked at cerebro-cardiovascular diseases among almost 3,400 residents of the Japanese town.

During this period 290 Hisayama residents died and 214 were autopsied (73.8%).

A total of 2,520 participants had received oral glucose tolerance tests in 1988 and were free of signs of dementia at that time. During the ensuing decades, 15.6% developed Alzheimer's-type dementia.

However, among the 135 participants autopsied, 65% actually had neuritic plaques characteristic of Alzheimer's disease.

Presence of these plaques was associated with significantly higher levels of the following after adjustment for age, sex, and a full set of potential confounders:

•Two-hour post-load plasma glucose in a 75-g oral glucose tolerance test (odds ratio 1.71, P=0.03)

•Fasting insulin (OR 2.03, P=0.02)

•Insulin resistance measured by the homeostasis model of assessment (HOMA-IR, OR 2.11, P=0.01)

These endocrine factors also appeared to combine with genetic risk to accelerate formation of neuritic plaques.

Those with low glucose levels on the glucose tolerance test who didn't carry the apolipoprotein E-4 gene (APOE-4) allele associated with Alzheimer's disease were least likely to show neuritic plaques in their brain on autopsy whereas hyperglycemia alone was associated with 1.5-fold risk and the APOE carriers had 19.7-fold risk.

The greatest likelihood of neuritic plaques was seen in those with both hyperglycemia and the APOE allele (38.0-fold compared with neither).

The pattern was similar for fasting insulin and insulin resistance, although the interactions with the APOE genotype weren't statistically significant.

Neurofibrillary tangles -- another type of brain pathology seen with Alzheimer's disease considered to be due to beta-amyloid plaque deposition -- correlated neither with any insulin or glucose measures nor with the presence of neuritic plaques.

"The diabetes-related factors may act upstream of the cascade, and might trigger the Alzheimer's disease pathogenesis," Sasaki's group suggested in the paper.

The authors cited several limitations to their study:

First, the crude, semiquantitative evaluations of neuritic plaques could have affected the statistical analyses, and "the medical history of diabetes, such as disease duration, glucose control, and complications, were not considered in this study," they wrote.

The study was supported by a grants from the Ministry of Health, Labour and Welfare of Japan and the Ministry of Education, Culture, Sports, Science and Technology of Japan.

Matsuzaki reported having no conflicts of interest to disclose.

Co-authors reported having received research support from

the Ministry of Health, Labor and Welfare of Japan;

having served on scientific advisory boards for Eli Lilly, GlaxoSmithKline, Pfizer, Mitsubishi Tanabe Pharma, Ono Pharmaceutical, Astellas Pharma, Asahi Kasei, Shionogi, and Otsuka Pharmaceutical;

having served on the editorial boards of multiple journals;

having received speaker honoraria from Eli Lilly, GlaxoSmithKline, Pfizer, Asahi Kasei, Janssen, Tsumura, Ajinomoto, Mitsubishi Tanabe Pharma, Meiji Techno, Kyowa Hakko Kirin Pharma, Dainippon Sumitomo Pharma, Organon International (Schering-Plough), Otsuka Pharmaceutical, and Astellas Pharma;

and having received research support from Eli Lilly, GlaxoSmithKline, Pfizer, Asahi Kasei, Janssen, Tsumura, Ajinomoto, Mitsubishi Tanabe Pharma, Meiji Techno, Kyowa Hakko Kirin Pharma, Dainippon Sumitomo Pharma, Organon International (Schering-Plough), Otsuka Pharmaceutical, and the Ministry of Education, Culture, Sports, Science and Technology of Japan.

Primary source: Neurology

Source reference:

Matsuzaki T, et al "Insulin resistance is associated with the pathology of Alzheimer disease: The Hisayama Study" Neurology 2010; 75: 764–770.

Additional source: Neurology

Source reference:

Luchsinger JA "Insulin resistance, type 2 diabetes, and AD: Cerebrovascular disease or neurodegeneration?" Neurology 2010; 75: 758–759.

http://tinyurl.com/25n5q6j

By Charles Bankhead, Staff Writer, MedPage Today

Published: September 03, 2010

Reviewed by

Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston and

Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner

Action Points

■Explain to interested patients that two studies -- one in nondiabetic humans and the other in mice -- suggest that metformin has antitumor effects.

■Note that the mechanisms of this potential effect remain to be elucidated.

Nondiabetic patients with precancerous rectal lesions had significant histologic improvement after one month of treatment with metformin, data from a small randomized clinical trial showed.

The average number of rectal aberrant crypt foci decreased by more than 40% in patients in the metformin group but did not change in controls who received no treatment, according to a report in the September issue of Cancer Prevention Research.

In normal rectal tissue metformin was associated with a significant decrease in the proliferating cell nuclear antigen index, but the apoptotic index did not change, Atsushi Nakajima, MD, PhD, of Yokohama City University in Japan, and co-authors wrote.

The drug was not associated with any significant changes in metabolic parameters related to insulin or lipids.

"The present study clearly shows that metformin suppressed the formation of human colorectal aberrant crypt foci [ACF]," Nakajima and colleagues wrote.

"Furthermore, metformin ... did not decrease blood glucose or affect insulin resistance, plasma cholesterol, or plasma triglyceride levels of nondiabetic ACF patients, indicating that the ACF suppression effect was direct rather than due to the attenuation of insulin resistance or hyperlipidemia."

A preclinical study reported in the same issue of the journal showed as much as a 72% reduction in lung cancer burden in tumor-prone mice treated with metformin.

The two studies add to a growing volume of evidence that the diabetes drug might have anticancer activity, participants in a media teleconference indicated.

However, a better understanding of the underlying mechanisms will be required to take full advantage of any anticancer potential.

"We still don't know the exact mechanisms by which metformin is accomplishing this protective effect," said Jeffrey A. Engelman, MD, PhD, of Massachusetts General Hospital in Boston, and co-author of a commentary that accompanied the lung cancer study.

"This could be just a glimpse at the power of manipulating these pathways to have a much more profound effect on chemoprevention," he added. "Hopefully, when we know more about how metformin accomplishes the chemoprevention, we will be able to leverage that information to develop even more potent therapeutics to accomplish this."

Interest in metformin's chemopreventive potential has come from recognition that the drug stimulates AMP-activated protein kinase, which can inhibit the mammalian target of rapamycin (mTOR) pathway. Activation of the mTOR pathway has been implicated in several types of tumorigenesis.

Nakajima and colleagues previously showed a chemopreventive effect of metformin in two different rodent models of colorectal carcinogenesis.

Both models involved nondiabetic animals, suggesting metformin has chemopreventive potential in nondiabetic humans.

Clinical trials of colorectal cancer chemoprevention usually have endpoints of adenomatous polyps or cancer, either of which may require years to manifest.

Aberrant crypt foci arise in the earliest stages of colorectal carcinogenesis and might represent a suitable surrogate endpoint for colorectal cancer chemoprevention studies, the researchers theorized.

So on the basis of preceding clinical and preclinical findings, Nakajima and colleagues performed a prospective randomized clinical trial to evaluate the safety and efficacy of metformin for chemoprevention of aberrant crypt foci in nondiabetic patients.

Eligible patients with colonoscopy-proven aberrant crypt foci were randomized to metformin or observation and followed for one month.

Each participant underwent colonoscopy at baseline and after one month. The primary endpoint was the change in the mean number of aberrant crypt foci from baseline to one month.

The study involved 26 patients, 23 of whom were evaluable for the primary endpoint (nine in the metformin group, 14 in the observation group).

In the metformin group, the mean number of aberrant crypt foci declined from 8.78 at baseline to 5.11 at one month (P=0.007) but did not change in the control group (7.23 versus 7.56).

In the preclinical study, investigators at the National Cancer Institute evaluated metformin's potential to prevent lung cancer in mice exposed to a tobacco carcinogen.

A total of 45 mice received three weekly injections of the carcinogen. All animals consumed a tumorigenic diet. A week after the final injection, the mice were randomized to a control group or to 1 or 5 mg/mL of metformin dissolved in drinking water.

Two additional groups of mice were exposed to the carcinogen and then randomized to daily intraperitoneal injections of saline or metformin for 13 weeks.

The primary endpoint was tumor burden, derived from the sum of individual lung tumor volumes in each animal.

Oral metformin did not affect tumor incidence or pathology, but tumor multiplicity declined by about 30% with either metformin dose compared with the control group.

Tumor burden declined by 39% in the 1 mg/mL metformin group (P=0.042) and by 53% in the 5 mg/mL group (P=0.003) compared with the control group.

Intraperitoneal administration of metformin reduced tumor number by 66% (P<0.0001), tumor volume by 50% (P<0.0001), and tumor burden by 72% (P=0.0002) compared with the control animals. Levels of the drug were higher in mice treated by the intraperitoneal route.

Studies aimed at elucidating the potential mechanisms of metformin's observed anticancer activity led investigators to the liver.

"The animals were fed the same high-fat, tumorigenic diet, but the control animals had fatty liver, whereas the animals treated with metformin had more normal-appearing livers," Phillip A. Dennis, MD, PhD, senior investigator in the lung cancer study, said during the teleconference.

"We saw small but statistically significant decreases in hormones produced in the liver and pancreas, specifically IGF-1 and insulin."

Although preliminary, the findings related to potential mechanisms strengthen the case for hypotheses supporting an indirect effect of metformin.

"The debate has always been whether metformin is working just by lowering whole-body insulin and IGF-1 levels or might it be working directly on the site of the tumor and the tissue that is potentially developing the tumor," said Lewis C. Cantley, PhD, of Beth Israel Deaconess Medical Center in Boston, and co-author of the commentary.

"Dr. Dennis' study looked at this very carefully and argues that lowering insulin and IGF-1 is the protective event."

Hosono and coauthors reported that they had no relevant disclosures.

Dennis and co-authors reported that they had no relevant disclosures.

Engelman and Cantley disclosed relationships with Agios.

Primary source: Cancer Prevention Research

Source reference:

Hosono K, et al "Metformin suppresses colorectal aberrant crypt foci in a short-term clinical trial" Cancer Prev Res 2010; 3: 1077-1083.

Additional source: Cancer Prevention Research

Source reference:

Memmott RM, et al "Metformin prevents tobacco carcinogene-induced lung tumorigenesis" Cancer Prev Res 2010; 3: 1066-1076.

Additional source: Cancer Prevention Research

Source reference:

Engleman JA, Cantley LC "Chemoprevention meets glucose control" Cancer Prev Res 2010; 3: 1049-1052.

http://tinyurl.com/2bhoshj

© 2004-2010 MedPage Today, LLC. All Rights Reserved.

By Peggy Peck, Executive Editor, MedPage Today

Published: September 13, 2010

Serious hypersensitivity reactions combined with gastrointestinal side effects have forced drugmaker Roche to order a halt to its clinical development program for the novel glucagon-like peptide-1 (GLP-1) analogue taspoglutide.

Roche said Friday that it had ordered investigators to stop giving the drug to patients enrolled in extensions of its phase III clinical trial program of the diabetes drug.

Despite a number of reports that touted the drug's efficacy, Roche has been wrestling with the unexpectedly high rate of adverse events associated with taspoglutide since early this year.

In interviews Friday with Bloomberg and Reuters news services, Roche officials confirmed the decision to shut down the clinical trial program.

But the company said it was considering a reformulation of the drug rather than simply abandoning what had been a promising agent.

http://tinyurl.com/39ysjxz

© 2004-2010 MedPage Today, LLC. All Rights Reserved.