Monday, October 18, 2010

Exercise just makes you eat more

So the weight loss from doing exercise is small. Abstract from Am J Clin Nutr. below

Nonprescribed physical activity energy expenditure is maintained with structured exercise and implicates a compensatory increase in energy intake

By James E Turner et al.


Background: Exercise interventions elicit only modest weight loss, which might reflect a compensatory reduction in nonprescribed physical activity energy expenditure (PAEE).

Objective: The objective was to investigate whether there is a reduction in nonprescribed PAEE as a result of participation in a 6-mo structured exercise intervention in middle-aged men.

Design: Sedentary male participants [age: 54 6 5 y; body mass index (in kg/m2): 28 6 3] were randomly assigned to a 6-mo progressive exercise (EX) or control (CON) group. Energy expenditure during structured exercise (prescribed PAEE) and nonprescribed PAEE were determined with the use of synchronized accelerometry and heart rate before the intervention, during the intervention (2, 9, and 18 wk), and within a 2-wk period of detraining after the intervention.

Results: Structured prescribed exercise increased total PAEE and had no detrimental effect on nonprescribed PAEE. Indeed, there was a trend for greater nonprescribed PAEE in the EX group (P = 0.09). Weight loss in the EX group (21.8 6 2.2 kg compared with +0.2 6 2.2 kg in the CON group, P , 0.02) reflected only ’40% of the 300–373 kcal/kg body mass potential energy deficit from prescribed exercise. Serum leptin concentration decreased by 24% in the EX group (compared with 3% in the CON group, P , 0.03), and we estimate that this was accompanied by a compensatory increase in energy intake of ’100 kcal/d.

Conclusions: The adoption of regular structured exercise in previously sedentary, middle-aged, and overweight men does not result in a negative compensatory reduction in nonprescribed physical activity. The less-than-predicted weight loss is likely to reflect a compensatory increase in energy intake in response to a perceived state of relative energy insufficiency.


Vitamin A pill 'could save the sight of millions as they get older'

A drug based on vitamin A could prevent millions from going blind as they get older, doctors believe. The treatment was able to stop the most common cause of blindness in old age during trials.

Researchers behind the drug, fenretinide, found it halted the advance of age-related macular degeneration, for which there is currently no cure. They targeted the most prevalent form of the condition, known as ‘dry’ AMD, which is caused by the deterioration and death of cells in the macula – the part of the retina used to see straight ahead.

The disease robs sufferers of their sight by creating a blackspot in the centre of their vision. It can make it impossible to carry out everyday tasks such as reading, driving and watching television. While the less common ‘wet’ form can be treated, nothing can be done to help the bulk of patients.

The U.S. research studied fenretinide, which is derived from vitamin A, the vitamin found in carrots, and which was originally designed to tackle arthritis. Almost 250 men and women with dry AMD took a fenretinide pill a day or a placebo.

In the highest dose, the drug halted visual deterioration after a year. This suggests that while it was unable to do anything to stop cells that were already damaged from dying, it protected healthy cells. Although the research is still preliminary, it offers promise of a treatment for the disease.

It affects millions across the world and 300,000 Britons. The number of UK sufferers could more than treble to one million within 25 years as the population ages.

Dr Jason Slakter, of New York University School of Medicine, said: ‘There are currently no effective treatments for dry AMD and the need for finding one is grave. ‘Our study wasn’t designed to give a final answer. ‘It was designed to see if there was a biological effect and if the drug was working in the way we’d expect and to find out if it was well tolerated by patents. ‘I think we answered all of these points favourably. The bottom line is that I am excited about doing more studies.’

Further, larger trials are planned for the end of next year. If the drug lives up to its initial promise, it could be in widespread use for dry AMD by 2015. The treatment works because in normal circumstances the eye needs vitamin A to help it see. The retina naturally uses the vitamin and is helped to do so by a compound called retinol binding protein, or RBP.

However in some patients, the vitamin can produce poisons that kill the delicate cells, leading to loss of vision. Fenretinide acts as a decoy, attaching itself to the RBP and stopping vitamin A from causing harm, the American Academy of Ophthalmology’s annual conference heard.

Wet AMD, in which tiny blood vessels bleed into the retina, is less common, but progresses more rapidly, with central vision being lost within months of diagnosis.

Caught early enough, wet AMD can be stopped in its tracks by a technique called photodynamic therapy, which uses a light-activated dye to destroy abnormal blood vessels. Drug treatments are also available.

Fenretinide also halved the odds of the patients, who already had dry AMD, going on to develop wet AMD.

A spokesman for the research team said: ‘Years of use of fenretinide to treat cancers, rheumatoid arthritis have shown it to be safe and well-tolerated.’


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