Get Fat or Thin by growing Gut Bacteria

It's not just calories - calories in and calories out. It is the form of the calories and the digestive culture we build. This research will change the way we think of 'healthy' bacteria, and gives strength to the raw food movement.

The Gut Response To What We Eat : NPR

A high-fat, high-sugar diet can quickly and dramatically change the population of microbes living in the digestive tract, according to a new study of human gut bugs transplanted into mice.

Trillions of microbes live inside the human gut, and one of their functions is to process parts of foods that we can't digest on our own. Recent studies have suggested that certain populations of microbes may be associated with obesity.

"The energetic and nutrient value of food may not be an absolute term, but one that is modified in part by the microbes that live in our gut — who's there in this community, how they operate, and how they operate in relationship to what we are eating," says Jeffrey Gordon of Washington University School of Medicine in St. Louis, Mo.

He and other scientists are eager to start doing experiments to see what happens if the gut populations are modified by changes in diet, antibiotics, or dietary supplements. To make such experiments possible, Gordon has been working with colleagues to take gut microbes from human feces and transplant them into the intestinal tracts of previously germ-free mice.

How Inflammation causes Fatigue

We have known anecdotally that inflammation causes fatigue, but now one of the underlying mechanisms has been explained in this article in Science Daily. More on how this relates to diet coming.

How Inflammatory Disease Causes Fatigue

ScienceDaily (Feb. 28, 2009) — New animal research in the February 18 issue of The Journal of Neuroscience may indicate how certain diseases make people feel so tired and listless. Although the brain is usually isolated from the immune system, the study suggests that certain behavioral changes suffered by those with chronic inflammatory diseases are caused by the infiltration of immune cells into the brain. The findings suggest possible new treatment avenues to improve patients' quality of life.

Does your BP Medication Cause Diabetes or Prevent it?

The "take home" in a nutshell:

Their findings showed that the lowest risk for new-onset diabetes occurred with

AII receptor antagonists (OR=0.57; 95% CI, 0.46-0.72),
which were better but not significantly better than ACE inhibitors (OR=0.67; 95% CI, 0.56-0.80)

followed by calcium channel blockers (OR=0.75; 95% CI, 0.62-0.90) and

placebo (OR=0.77; 95% CI, 0.63-0.94).

The risk was highest with diuretics and beta-blockers (OR=0.90; 95% CI, 0.75-1.09),
according to Elliott.



Endocrine Today

Hypertension treatment with angiotensin II receptor antagonists and ACE inhibitors is least likely to lead to diabetes; however, diuretics or beta-blockers increase a patient’s chance of developing diabetes, according to a report published in The Lancet.

“We should monitor our patients for the development of diabetes, and we should remain cognizant that different medicines have different propensities. But we should use all the medicines necessary to get and keep blood pressure under control,” said William J. Elliott, MD, PhD, professor of preventive medicine, internal medicine and pharmacology at Rush Medical College of Rush University Medical Center, Chicago.

Several long-term clinical trials have shown that patients on antihypertension medications are more likely to have reduced glucose tolerance and precipitated new-onset diabetes than those without hypertension. This is often attributed to increased weight, recent weight gain or stronger family history of diabetes among those with hypertension.

Elliott and colleagues analyzed data to assess the relationship between long-term treatment with classes of antihypertensive drugs and incident diabetes.
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Evaluating a relationship

The researchers conducted a network meta-analysis of long-term, randomized clinical trials from 1966 to 2006 among 143,153 participants who did not have diabetes at randomization. They identified 22 clinical trials of each class of antihypertensive drugs. They assessed the chance that a person would develop diabetes during one to about five years of observation.

Their findings showed that the lowest risk for new-onset diabetes occurred with AII receptor antagonists (OR=0.57; 95% CI, 0.46-0.72), which were better but not significantly better than ACE inhibitors (OR=0.67; 95% CI, 0.56-0.80) followed by calcium channel blockers (OR=0.75; 95% CI, 0.62-0.90) and placebo (OR=0.77; 95% CI, 0.63-0.94). The risk was highest with diuretics and beta-blockers (OR=0.90; 95% CI, 0.75-1.09), according to Elliott. Compared with placebo, diuretics or beta-blockers slightly but significantly increased the risk for developing diabetes. AII receptor antagonists or ACE inhibitors significantly decreased the risk. These findings suggest that the differences between antihypertensive drugs and the risk for new-onset diabetes are real and significant.

“Don’t throw out the blood pressure medicines because you are worried about the risk for getting diabetes; instead, monitor patients,” Elliott advised. “It is certainly important when you find out a patient has diabetes because it changes their blood pressure target and their cholesterol target, and they probably ought to always be on aspirin after that.”

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