Heales: The Healthy LIfe Extension Society

How calorie restriction influences the risk of fractures is a matter of debate. Most studies show a reduction in bone mineral density [1-3] but at the same time bone quality and strength are improved [4,5]. Another recent study showed that the reduction in BMD could be prevented by a higher intake of protein [6]. Other studies also show that calorie restriction does not negatively affect several measures of bone health [7,8]. In the new study [9] the effect of calorie restriction (~35%) on bone quality was investigated in humans. The humans had followed a calorie restricted diet for a period ranging between 3 and 20 years. The bone mineral density and the T scores were lower in the calorie restricted group. The trabecular thickness was lower in the calorie restricted group but no significant differences existed between BV/BT fraction, volume, skeletal density, surface-to-curve ratio, and erosion index. These data (surface-to-curve ratio and erosion index)show that TB microarchitecture is preserved by calorie restriction. Calorie restriction probably does not increase the rate of bone turnover as illustrated by the lack of change in serum CTX-1 and bone-specific alkaline phosphatase (BSAP). In conclusion, calorie restriction did not reduce the bone quality but longer following-up will be necessary to investigate the incidence of fractures.

[1] Villareal et al. Bone mineral density response to caloric restriction–induced weight loss or exercise-induced weight loss. Arch Int Med, 2006, 166(22): 2502-2510.

[2] Talbott et al. Energy restriction reduces bone density and biomechanical properties in aged female rats. J Nutr, 2001, 131: 2382-2387.

[3] Devlin et al. Caloric restriction leads to high marrow adiposity and low bone mass in growing mice. J Bone Miner Res, 2010, 25(9): 2078-2088.

[4] Kalu et al. Lifelong food restriction prevents senile osteopenia and hyperparathyroidism in F344 rats. Mech Aging Dev, 1984, 26: 103-112.

[5] Tatsumi et al. Life-long caloric restriction reveals biphasic and dimorphic effects on bone metabolism in rodents. Endocrinol, 2008, 149: 634-641.

[6] Sukumar et al. Areal and volumetric bone mineral density and geometry at two levels of protein intake during caloric restriction: a randomized controlled trial. J Bone Miner Res, 2010 [Epub ahead of print].

[7] Lambert et al. Dietary restriction does not adversely affect bone geometry and mechanics in rapidly growing male wister rats. Pediatr Res, 2005, 57: 227-231.

[8] Westbeek et al. Effects of aging and caloric restriction on bone structure and mechanical properties. J Gerontol A Biol Sci Med Sci, 2008, 63: 1131-1136.

[9] Villareal et al. Reduced bone mineral density is not associated with significantly reduced bone quality in men and women practicing long-term calorie restriction with adequate nutrition. Aging Cell, 2011, 10: 96-102.

Once upon a time it was thought that the lifespan extending effect of calorie restriction was due to a decrease in fat mass. In a new study, 41 inbred mice strains with varying responses to calorie restriction (from life extension to a decrease in lifespan) were tested. It was found that the strains with the least reduction in fat mass were the most likely to have their life spans extended by calorie restriction. Furthermore, none of the strains who lived longer exhibited a significant reduction in adiposity. Body weight was also positively correlated to lifespan extension by calorie restriction.

Liao et al. Fat maintenance is a predictor of the murine lifespan response to dietary restriction. Aging Cell, 2011 [Epub ahead of print].

Diallyl trisulfide, found in garlic, has been shown to extend the mean lifespan of C. elegans even when started during adulthood. It was found that the transcription factor skn-1 (mammals: Nrf-1/2/3) is involved in the mechanism of lifespan extension by diallyl trisulfide. It was also found that diallyl trisulfide extends the lifespan of daf-2 and daf-16 mutants but not of eat-2 mutants.

Powolny et al. The garlic constituent diallyl trisulfide increases the lifespan of C. elegans via skn-1 activation. Exp Gerontol, 2011 [Epub ahead of print].

Creatine has been shown to offer protection against neurodegenerative diseases such as ALS, Parkinson’s disease, and Huntington’s disease. In a new study, oral creatine supplementation increased median lifespan of C57Bl/6J mice by 9%. The supplementation also decreased ROS and a decrease in the accumulation of lipofuscin. The expression profiles also showed an upregulation of genes involved in neuronal growth, neuroprotection, and learning.

Klopstock et al. Creatine in mouse models of neurodegenerative and aging. Amino Acids, 2011 [Epub before print].

Bender et al. Creatine improves health and survival of mice. Neurobiol Aging, 2008, 29(9): 1404-1411.

Wyss M, and Schulze A. Health implications of creatine: can oral creatine supplementation protect against neurological and atherosclerotic disease? Neuroscience, 2002, 112(2): 243-260.