U.S. Study: Insulin Possible New Treatment For Alzheimer's Disease

WASHINGTON, Feb. 2 (Xinhua) -- A Northwestern University-led research team reports that insulin, by shielding memory-forming synapses from harm, may slow or prevent the damage and memory loss caused by toxic proteins in Alzheimer's disease.

The findings, which provide additional new evidence that Alzheimer's could be due to a novel third form of diabetes, was published Monday in the online edition of the Proceedings of the National Academy of Sciences.

In a study of neurons taken from the hippocampus, one of the brain's crucial memory centers, the scientists treated cells with insulin and the insulin-sensitizing drug rosiglitazone, which has been used to treat type 2 diabetes. (Isolated hippocampal cells are used by scientists to study memory chemistry; the cells are susceptible to damage caused by ADDLs, toxic proteins that build up in persons with Alzheimer's disease.)

The researchers discovered that damage to neurons exposed to ADDLs was blocked by insulin, which kept ADDLs from attaching to the cells. They also found that protection by low levels of insulin was enhanced by rosiglitazone.

ADDLs, short for "amyloid beta-derived diffusible ligands," are known to attack memory-forming synapses. After ADDL binding, synapses lose their capacity to respond to incoming information, resulting in memory loss.

The protective mechanism of insulin works through a series of steps by ultimately reducing the actual number of ADDL binding sites, which in turn results in a marked reduction of ADDL attachment to synapses, the researchers report.

"Therapeutics designed to increase insulin sensitivity in the brain could provide new avenues for treating Alzheimer's disease," said senior author William L. Klein, a researcher in North western's Cognitive Neurology and Alzheimer's Disease Center." Sensitivity to insulin can decline with aging, which presents a novel risk factor for Alzheimer's disease. Our results demonstrate that bolstering insulin signaling can protect neurons from harm."

Bisphenol A May Linger in Body

By Daniel J. DeNoon
Study Shows More Than Expected Amounts of BPA May Accumulate in Americans' Bodies

Jan. 28, 2009 -- The plastics chemical bisphenol A (BPA) doesn't leave the body as easily as previously thought, a new study suggests.

BPA is everywhere: in PVC pipe, in polycarbonate drink containers, in the plastic that lines food and soft-drink cans, and even in dental sealants. It's also in our bodies. Virtually everyone has detectable levels of BPA in his or her body.

Although Canada last October banned BPA from plastic baby bottles, the U.S. FDA still considers it safe. The U.S. National Toxicology Program, however, notes "concerns" over BPA safety. Not taking any chances, several baby-bottle makers have stopped using BPA in their products.

Based on limited evidence, most researchers have assumed that most of our BPA exposure comes from food, and that the body gets rid of each BPA dose within 24 hours.

Now there's evidence that BPA might be in our water as well as in our food, and that it lingers in our fat tissues. If confirmed -- and the current findings are very preliminary -- it could mean BPA is a bigger problem than thought.

University of Rochester researcher Richard Stahlhut, MD, MPH, analyzed data on 1,469 U.S. adults from the CDC's huge 2003-2004 NHANES study. That study gave fasting people one-time BPA tests, and also collected extensive dietary data.

Stahlhut compared people's BPA levels to how long it had been since their last meal. Since virtually all BPA is supposed to come from food, and BPA is supposed to have a short half-life, he expected that average BPA levels would dwindle in people who fasted longer than that.

"After 10 to 15 hours of fasting, there shouldn't be anybody with any detectable levels of BPA," Stahlhut tells WebMD. "But it just hangs there like the London fog. You do see a subtle downward trend, but what you don't see is it falling off the map. And by 24 hours it's still there."

What's going on? The people in the NHANES study really fasted -- CDC researchers made sure of that. But they were allowed to drink water, black coffee, and diet soda.

The BPA could have come from the diet soda or other things the CDC researchers couldn't control, points out University of Miami medical toxicologist John Cienki, MD. Cienki, who was not involved in the Stahlhut or NHANES studies, says he worries about BPA. But he warns that there are too many unknowns in the NHANES data to draw any definite conclusions.

"I think we are using data here that was not designed to be used this way," Cienki cautions. "Yes, we would anticipate a greater BPA excretion if people were fasting -- if they had not continued to ingest BPA. But this study did not control for consumption of or exposure to BPA."

Stahlhut fully agrees. However, he notes that the BPA could have come from another source: tap water. Surprisingly few BPA tests have been done on tap water. And those tests did not look for chlorinated BPA, which would be the form of BPA leached from PVC pipes into municipal tap water.

Or maybe, Stahlhut says, not all the BPA was being ingested. Maybe a lot of it really lingers in fat tissues, as some studies suggest. And far from being a stored harmlessly, BPA may be a bad actor in human fat.

A 2008 study in the Journal of the American Medical Association showed that people with higher urinary BPA levels have more medical disorders. Another intriguing study from 2008 showed that BPA -- at normal levels of exposure -- disrupts a hormone involved in insulin sensitivity and diabetes. And a 2007 study showed that obese people are much more likely to suffer insulin resistance if they have high fat levels of organic pollutants.

"Imagine if what we think is caused by obesity is actually caused by persistent organics in the fat of obese people," Stahlhut says. "If they don't have the organics, they don't have the diabetes. That would be huge."

But first things first. Stahlhut agrees with Cienki that his study is not grounds for any kind of regulatory action. He calls for rigidly controlled experiments to find out what happens to people after long-term exposure to BPA. He also urges studies measuring BPA in human fat tissues. And he thinks it's urgent to search for new, potentially important sources of BPA exposure.

Stahlhut and colleagues report their findings in the Jan. 28 online issue of Environmental Health Perspectives.

source: webmd.com

Vitamin B1 May Reverse Kidney Disease in Diabetes Patients

Researchers at the University of Warwick have discovered high doses of thiamine (vitamin B1) can reverse the onset of early diabetic kidney disease.

Kidney disease, or diabetic nephropathy, develops progressively in patients with type 2 diabetes. Early development of kidney disease is assessed by a high excretion rate of the protein albumin from the body in the urine, known as microalbuminuria.

The researchers have discovered taking high oral doses of thiamine can dramatically decrease the excretion of albumin and reverse early stage kidney disease in type 2 diabetes patients.

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It was shown that 300 mg of thiamine taken orally each day for three months reduced the rate of albumin excretion in type 2 diabetes patients.

The albumin excretion rate was decreased by 41% from the value at the start of the study. The results also showed 35% of patients with microalbuminuria saw a return to normal urinary albumin excretion after being treated with thiamine.

Forty patients with type 2 diabetes aged between 35 and 65 years old took part in the trial. They were randomly assigned a placebo or 3 x 100mg tablets of thiamine a day for three months.

The Warwick research group has already conclusively proven that type 2 diabetes patients have a thiamine deficiency. In an earlier study led by Professor Paul Thornalley at Warwick Medical School, the research team showed that thiamine deficiency could be key to a range of vascular problems for diabetes patients.
Source: elements4health.com