Signs of Depression

Patients with abnormal diastolic function (when the heart is relaxed and expanded) in the left ventricle of the heart have a substantially lower maximum capacity for exercise, as per a research studyin the January 21 issue of JAMA
A number of factors, including age, female sex, body mass index and co-existing medical conditions are known to be linked to a decrease in exercise capacity. Identifying potentially reversible mechanisms underlying the decline in maximum exercise capacity could have important implications. Some research has suggested that assessing left ventricular (one of four chambers in the heart) function could be used to predict exercise capacity, as per background information in the article.

Jasmine Grewal, M.D., of Mayo Clinic, Rochester, Minn., and his colleagues conducted a study to examine the relationship between left ventricular diastolic function and exercise capacity. The study included 2,867 patients undergoing exercise echocardiography (a noninvasive diagnostic procedure that uses ultrasound to study the structure and motions of the heart) with routine measurements of left ventricular systolic (contraction of the heart) and diastolic function. Analyses were conducted to determine the strongest correlates of exercise capacity and the age and sex interactions of these variables with exercise capacity.

The scientists observed that diastolic dysfunction (impaired relaxation) was strongly and inversely linked to exercise capacity. Compared with normal function, those with resting diastolic dysfunction had substantially lower exercise capacity. Variation of left ventricular systolic function within the normal range was not linked to exercise capacity.

Other independent correlates of exercise capacity were age, female sex, and body mass index greater than 30. Compared with those with normal diastolic function, patients with diastolic dysfunction had a progressive increase in the magnitude of reduction in exercise capacity with advancing age.

"In identifying diastolic function parameters as strong correlates of exercise capacity, we have identified potentially modifiable and preventable factors in the development of exercise intolerance. It is well known that exercise training improves diastolic function in healthy individuals ," the authors write.


Posted by: Evelyn    Source

6 Onions
1 clove of garlic
1 teaspoon of salt
1 teaspoon of blackpepper
1/2 cup of olive oil add more if you need too.
2 tablespoons of butter.


Peel the onions and rinse them in cold water. Then slice them. Peel then chop the garlic. Add the onions then the garlic. Add the olive oil. Then add the butter. Saute the onions and the garlic until they turn yellow and you smell the aroma. Add the chicken broth or water. Cover the pot. When it starts to boil add salt and pepper. Let it simmer for two hours or until done.

This is very good for the flu, coughs, or colds.




colds, coughs, flu,
Turbo Tagger

New evidence in mice bolsters the notion that a version of a gene earlier shown to protect lean people against weight gain and insulin resistance can have the opposite effect in those who eat a high-fat diet and are heavier, reveals a report in the January 7th issue of the journal Cell Metabolism, a Cell Press publication.

The findings suggest that the 12 percent of people who carry the so-called Ala12 version of the gene that serves as a master controller of fat differentiation will be more sensitive than most to the amount of fat in their diets. (That fat-moderating gene is called peroxisome proliferator-activated receptor gamma isoform 2, or Pparg2.).

The Ala12 gene variant in question is less active and less efficient in driving fat cells' formation than the more common Pro12 version, the scientists explained. As a result, individuals carrying Ala12 are generally less obese and more sensitive to insulin, but that can change if they shift to a less sensible, fat-laden meal plan.

Genetic testing for the variant might therefore be used as a diagnostic tool, said Johan Auwerx of Universit Louis Pasteur in France and the Ecole Polytechnique Fdrale de Lausanne in Switzerland. "Through dietary counseling, carriers could be informed that they really need to watch out for high fat in their diets," he said.

The findings also raise a potential caution about the long-term effects of drugs called thiazolidinediones (TZDs) now in use for the therapy of diabetes, he added. Those drugs stimulate activity of the Pparg2 receptor. The findings suggest it appears to be betterat least in some settingsto have a less active receptor.

Auwerx's team first described the Ala12 version of Pparg2 about 10 years ago when they found in a Finnish and a Japanese American population living in Hawaii that the mutation lowered the risk of diabetes. Others tried to reproduce the findings in Americans to no avail. Indeed, the Americans in the followup study, who were generally heavier than the groups Auwerx had examined earlier, showed the exact opposite pattern.

That led to the idea that effects of the gene might somehow be sensitive to initial body weight, but an animal study was needed to sort out the underlying details.

The scientists now show that mice with two copies of the Ala12 variant, when fed a balanced diet of normal mouse chow, are leaner and have improved insulin sensitivity and better plasma lipid profiles than mice with two copies of Pro12. They also live longer.

When mice with the same genetic background were instead sustained on a diet high in fat, those benefits disappeared. In fact, those Ala12 animals grew somewhat more obese than mice with the more common Pro12 variant of the gene, though not significantly so.

The result shows an important interaction between the Pparg2 gene and the environment, they report. The underlying basis for the effect seems to depend on changes in the way the Pparg2 receptor interacts with its cofactors and in its sensitivity to a fat-produced hormone known as adiponectin, which influences blood sugar control and fatty acid breakdown.

" Collectively, our results establish the diet-dependent influence of Pparg2 Pro12Ala variant on metabolic control via modulated cofactor interaction and changes in gene expression patterns in mice," the scientists concluded. "These data hence consolidate Pparg2 as an important factor at the interface between genes and the environment and may provide avenues to better, possibly Pro12Ala genotype-dependent therapy strategies for insulin resistance in type 2 diabetes and the metabolic syndrome".


Posted by: Evelyn    Source