Calorie Restriction Diet Essay
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Discuss the relationship between calorie restriction diet and longevity
Calorie restriction (CR) diet consists of reducing the daily calorie intake by up to 40% without removing nutritional value, (Willcox et al., 2007, Katsman et al., 2010). The emphasis is based on under-nutrition and not mal-nutrition. The Okinawa diet seems to have a CR status for two main reasons, the first being that Okinawa had reduced food supplies in the first half of the 19th century and secondly the locals needed a high calorie intake to support their daily needs as vocational farmers. Together the low calorie intake coupled with high physical activity levels produced a local situation of CR estimated to be approximately 11% lower than their …show more content…
normal requirements. The local food types, dense in nutrients and low in calories are another factor leading to the mythical longevity of Okinawa centenaries, (Heilbronn & Ravussin, 2003, Willcox et al., 2007).
CR is the most potent means of extending lifespan and reducing age related disease in test animals (Vigeneau-Callahan, 2001, Heilbronn & Ravussin, 2003, Willcox et al., 2007). CR has been extensively explored on animals since the 1930s because of its ability to extend mean and maximum life span and delay or even prevent most age related disease. CR affects metabolism, hormonal balance, and the generation, detoxification and resistance to oxidisation, (Vigeneau-Callahan, 2001). Only one long-term test (>30 years) has linked CR to human longevity, reporting lower all-cause mortality in humans with a CR of 15%. CR of 50% increased risk of death. This data was consistent with previous findings in animals. It is impossible to maintain long-term energy deficit and health, which is why it is important for the nutritional value of a CR diet to be retained with specially selected foods yet still allowing the calorie intake to be reduced, (Heilbronn & Ravussin, 2003, Willcox et al., 2007). Calorie restriction in juveniles has a detrimental effect in growth and development. If the diet is poor in nutritional value as well as in calorific value then juvenile development can produce impaired fertility, impaired growth, and immune capabilities, and adverse psychological effects, (Heilbronn & Ravussin, 2003). The longer the period of CR the greater effect on longevity, however brief periods of CR of less than a year can also increase longevity, (Shanley & Kirkwood, 2000).
Longevity is an elongated lifespan that can be one of the effects resulting from calorie restriction (CR). In rodents it has been observed up to extend the lifespan up to 20-40%, (Shanley & Kirkwood, 2000). CR has successfully extended lifespan in essentially all tested animals, (Vigneau-Callahan, 2001).
The calorie restriction diet also has other effects that are part of the general physiological process that happens in the body during CR. These include an increase in gluconeogenesis and a decrease in glycolysis, the liver takes a dominant role because of the loss of fat mass, (Kubova & Guarente 2003). The liver makes keytones that result from the degradation of fat and proteins in test animals, (Kubova & Guarente 2003). The liver also needs to produce less Insulin like Growth Factor taking some of the stress off it. Gluconeogenesis is the synthesis of new glucose not from glycogen. This alternative production of glucose is necessary for use in the brain, testes, erythrocytes and kidney medulla because glucose is the only energy source these organs use, (King, 2011).
A change also occurs in hormonal balance including a reduction of lactation, reduced levels of Insulin like Growth Factors, Reduced Growth Hormone and Gonadotropins, (Kubova & Guarante, 2003). Also including infertility, not applying to male rodents with CR in late-life. Females regain function when CR returns to normal and can be fertile to a later age, however if it is present during early life in male rodents it may be irreversible, (Shanley & Kirkwood, 2000, Kubova & Guarante, 2003). These physiological changes result from the organism preserving sexual function for when there is greater nutritional resources available and to preserve their life in waiting for the famine to be over, (Shanley & Kirkwood, 2000, Kubova & Guarante, 2003). The energy diverted from maintaining sexual function and activity associated with reproduction and courting or mating behaviour is instead used in maintaining the protein structures of the body because of CR until better days. This is known as the disposable soma theory, where an organism optimizes the allocation of resources to competing physiological demands, (Shanley & Kirkwood, 2000). In this way the organism is preserving reproductive capabilities and concentrating on the overall health and longevity of the organism. Protein turnover increases, histologically the cells are maintained in newer condition by protein turnover (Shanley & Kirkwood, 2000, Vigneau-Callahan et al, 2001, Koubova & Guarente, 2003, Heilbronn & Ravussin, 2003, Willcox et al., 2007, Katsman et al., 2010). DNA repair and maintenance is increased, and the age related decline of tissue repair and wound healing is slowed, (Shanley & Kirkwood, 2000). Oxidative cellular damage is reduced as well because the CR in the organism promotes gluconeogenesis, which is a less oxidative pathway for generation of glucose than glycolysis. Aerobic energy metabolism apparently creates DNA damage and gluconeogenesis bypasses the aerobic energy metabolism pathway saving cells from DNA damage, (Heilbronn & Ravussin, 2003).
Apoptosis increases also reducing the risks of carcinoma on the major organs, (Willcox et al. 2007).
Ageing is reduction of protein turnover and a build-up of oxidativley damaged proteins, (Kubova & Guarente 2003, Heilbronn & Ravussin, 2003, Katsman et al. 2010). CR slows this process and the accumulation of potentially harmful proteins and speed up turnover, (Kubova & Guarente 2003). The age related accumulation of oxidised proteins declines with CR, (Heilbronn & Ravussin, 2003). As the body runs out of fat with CR, degradation of proteins triggers increased protein turnover.
CR also decreases insulin levels in the blood and increases insulin sensitivity, (Heilbronn & Ravussin, 2003). The pancreas doesn’t need to work as hard and reduces in size.
CR reduces cholesterol levels, (Fontana et al., 2004). Reduced Calories in the blood also reduces damage to the blood vessels. In a study by Fontana et al., (2004), they measured the thickness of the tunica intima media of subjects’ carotid arteries with one group on CR and compared it to a control group on normal diet, they discovered a reduction of thickness of the Tunica Intima Media (TIM) in middle aged humans on CR of 40%. That is the equivalent of the normal thickness of the TIM in the carotid artery of a 10-year-old human. Atherosclerosis can originate from inflammation of the artery walls, and CR reduces the incidence of inflammation (Heilbronn & Ravussin, 2003). This inflammation results from the interaction of macrophages, oxidised cholesterol and cells of the artery walls, (Fontana et al., 2004).
Blood pressure also decreases as an effect of CR, (Fontana et al., 2004). The artery walls have less pressure against them and the veins have less sugar. This reduces the amount of damage created on the artery walls. Reduced risk of arteriosclerosis results from CR.
Reduced risk of Diabetes mellitus because CR makes less sugar in the blood and less insulin. All of the cells in the body become more sensitive to insulin and insulin resistance decreases, (Heilbronn & Ravussin, 2003, Fontana et al., 2004).
Neuroendocrine response.
Neural response to CR is that the organism increases energy production from keytones forming more abundant nourishment for the brain and increase in proprioceptive function relative to the normal decline with ageing. CR also reduces the decline of dendritic spines increasing their density and maintaining memory and reducing the loss of grey matter in the central nervous system relative to ageing, (Kubova & Guarante, 2003, Katsman et al., 2010). CR is also believed to increase astrocyte activity and the uptake of glutamate into the brain, (Katsman et al., 2010). CR appears to have a protective effect on the brain, the organs, and the musculoskeletal system of the organism.
During starvation the brain can derive energy from ketone bodies for acetyl-Coenzyme A, (King, 2011). Kubova & Guarante (2003) also reckon CR has the effect on the brain of promoting the expression if genes responsible for neuroplasticity, and that this could be related to the improved psychomotor performance observed in animals relative to the decline expected with ageing. Katsman et al. (2010) found that test animals showed improved motor performance and manual dexterity in CR. In normal ageing circumstances, a build-up of nonheme iron stored in ferretin in the brain downgrades the functioning. However in CR, the nonheme Iron deposition is apparently reduced as seen in MRI scans of subjects, particularly in the parts responsible for motor functions (Kastman et al., 2010).
Glycolysis involves more oxidative reactions contributing to oxidative cell damage than gluconeogenesis, (King, 2011). The gluconeogenesis mechanism consumes skeletal muscle to derive glucose for storage as glycogen, rather than oxidizing glucose as in glycolysis, (King, 2011).
Kubova & Guarente (2003) and Heilbronn & Ravussin, (2003) claim that CR creates a reduction in body temperature in rodents and nonhuman primates because of a reduction of non-coupling proteins in the inner membrane of mitochondria that are responsible for proton leakage and the generation of heat. So the mitochondria work more efficiently in CR.
So apparenty apoptosis increases in CR reducing the expression of cancers (Willcox et al. 2007), and organs of the body downsize where as the brain does not. CR also reduces the insulin levels in the blood and the insulin receptors become more effective. So sugar is in the blood for shorter periods of time and the lower levels will create less damage to the blood vessels because the sugar is absorbed faster. Needing less insulin makes the pancreas less big, (Heilbronn & Ravussin, 2003). The increased sensitivity to insulin also creates an increase resistance to stress, decreasing stress on the whole organism.
Improves sympathetic nervous system function in animals, (Heilbronn & Ravussin, 2003).
According to Williamson et al. (2008) the dangerous effects of CR can lead to symptoms associated with anorexia and bulimia nervosa, such as preoccupation with food, reduced interest in sex, binge eating and mood swings. Furthermore subjects can become depressed and have difficulty to regain normal calorie intake. However this is a rare occurrence indeed as shown by their research and CR is proven to be safe in general, but should not be implemented in adolescent women who are more predisposed to developing eating disorders.
Conclusion
The CR diet is a powerful contributor to longevity and although very few studies have been conducted on humans, apparently similar results have been obtained as in the extensive testing on animals. Conducted in the correct conditions with a nutrient rich, low calorie diet, and avoided in juveniles CR brings a wide range of benefits, including reduction in atherosclerosis, reduction of insulin resistance, reduction of blood pressure, reduction of fat mass, reduction of oxidative stress on a cellular level, increase on protein turnover and DNA repair and maintenance. An increase in brain function relative to the expected decline with age, preserving memory and proprioceptive and motor function are also affects on the organism of CR. This shift in the metabolic function of the organism comes from the CR provoking a diversion of energy from growth and reproductive functions, advocated on a hormonal level. CR is clearly effective but should be avoided in juveniles and should not be excessive in duration or intensity. More studies should be conducted on humans, however the total lifespan is a difficult criteria to measure due to the longer lifespan of humans compared to other animal species that have been tested in the past.
(1930 words)
Refferences
Koubova J.
& Guarente L. 2003. How does calorie restriction work?
GENES & DEVELOPMENT Vol.17 pp.313–321. MIT Massachusetts USA. Cold Spring Harbor Laboratory Press .
King M. 2011. themedicalbiochemistrypage.org [Online] Available at [Accessed: 2nd, September 2011] .
Kastman E., Willette A,. Coe C., Bendlin B., Kosmatka K., McLaren D., Xu G., Canu E., Field A., Alexander A., Voytko M., Beasley M., Colman R., Weindruch R., Johnson S. 2010. A Calorie-Restricted Diet Decreases Brain Iron Accumulation and Preserves Motor Performance in Old Rhesus Monkeys Neurobiology of Disease.
Journal of Neuroscience, Vol.30(23) pp.7940 –7947.
Shanley D. & Kirkwood T. 2000. Calorie Restriction and Aging: A Life-History Analysis. Evolution, vol.54(3), pp. 740–750.
Vigneau-Callahan K., Shestopalov A., Milbury P., Matson W., Kristal B., 2001.
Calorie Restriction: Effects on Body Composition, Insulin Signaling and Ageing. Characterization of Diet-Dependent Metabolic Serotypes: Analytical and Biological Variability Issues in Rats. Journal of Nutrition, Vol.131, pp.924S–932S.
Fontana L., Meyer T., Klein S., & Holloszy J., 2004.
Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans. PNAS. Vol.101 no.17 …show more content…
pp.6659–6663.
Heilbronn L.
and Ravussin E., 2003. Calorie restriction and aging: review of the literature and implications for studies in humans. American Journal of Clinical Nutrition. Vol.78, pp.361–9.
Williamson D., Martin C., Anton S., Yourk-Crowe E., Han H., Redman L., Ravussin E., 2008. Is caloric restriction associated with development of eating disorder symptoms? Results from the Calorie trial. Health Psychology. Vol. 27 no.1 pp.32-42.
Willcox B., Willcox D., Todoriki H., Fujiyoshi A., Yano K., He Q., Curb J., & Suzuki M., 2007. Caloric Restriction, the Traditional Okinawan Diet, and Healthy
Aging
The Diet of the World’s Longest-Lived People and Its Potential Impact on Morbidity and Life Span. Annals of the New York Academy of Sciences. Vol.1114 pp.434–455.
Discuss the relationship between calorie restriction diet and longevity
Calorie restriction (CR) diet consists of reducing the daily calorie intake by up to 40% without removing nutritional value, (Willcox et al., 2007, Katsman et al., 2010). The emphasis is based on under-nutrition and not mal-nutrition. The Okinawa diet seems to have a CR status for two main reasons, the first being that Okinawa had reduced food supplies in the first half of the 19th century and secondly the locals needed a high calorie intake to support their daily needs as vocational farmers. Together the low calorie intake coupled with high physical activity levels produced a local situation of CR estimated to be approximately 11% lower than their …show more content…
normal requirements. The local food types, dense in nutrients and low in calories are another factor leading to the mythical longevity of Okinawa centenaries, (Heilbronn & Ravussin, 2003, Willcox et al., 2007).
CR is the most potent means of extending lifespan and reducing age related disease in test animals (Vigeneau-Callahan, 2001, Heilbronn & Ravussin, 2003, Willcox et al., 2007). CR has been extensively explored on animals since the 1930s because of its ability to extend mean and maximum life span and delay or even prevent most age related disease. CR affects metabolism, hormonal balance, and the generation, detoxification and resistance to oxidisation, (Vigeneau-Callahan, 2001). Only one long-term test (>30 years) has linked CR to human longevity, reporting lower all-cause mortality in humans with a CR of 15%. CR of 50% increased risk of death. This data was consistent with previous findings in animals. It is impossible to maintain long-term energy deficit and health, which is why it is important for the nutritional value of a CR diet to be retained with specially selected foods yet still allowing the calorie intake to be reduced, (Heilbronn & Ravussin, 2003, Willcox et al., 2007). Calorie restriction in juveniles has a detrimental effect in growth and development. If the diet is poor in nutritional value as well as in calorific value then juvenile development can produce impaired fertility, impaired growth, and immune capabilities, and adverse psychological effects, (Heilbronn & Ravussin, 2003). The longer the period of CR the greater effect on longevity, however brief periods of CR of less than a year can also increase longevity, (Shanley & Kirkwood, 2000).
Longevity is an elongated lifespan that can be one of the effects resulting from calorie restriction (CR). In rodents it has been observed up to extend the lifespan up to 20-40%, (Shanley & Kirkwood, 2000). CR has successfully extended lifespan in essentially all tested animals, (Vigneau-Callahan, 2001).
The calorie restriction diet also has other effects that are part of the general physiological process that happens in the body during CR. These include an increase in gluconeogenesis and a decrease in glycolysis, the liver takes a dominant role because of the loss of fat mass, (Kubova & Guarente 2003). The liver makes keytones that result from the degradation of fat and proteins in test animals, (Kubova & Guarente 2003). The liver also needs to produce less Insulin like Growth Factor taking some of the stress off it. Gluconeogenesis is the synthesis of new glucose not from glycogen. This alternative production of glucose is necessary for use in the brain, testes, erythrocytes and kidney medulla because glucose is the only energy source these organs use, (King, 2011).
A change also occurs in hormonal balance including a reduction of lactation, reduced levels of Insulin like Growth Factors, Reduced Growth Hormone and Gonadotropins, (Kubova & Guarante, 2003). Also including infertility, not applying to male rodents with CR in late-life. Females regain function when CR returns to normal and can be fertile to a later age, however if it is present during early life in male rodents it may be irreversible, (Shanley & Kirkwood, 2000, Kubova & Guarante, 2003). These physiological changes result from the organism preserving sexual function for when there is greater nutritional resources available and to preserve their life in waiting for the famine to be over, (Shanley & Kirkwood, 2000, Kubova & Guarante, 2003). The energy diverted from maintaining sexual function and activity associated with reproduction and courting or mating behaviour is instead used in maintaining the protein structures of the body because of CR until better days. This is known as the disposable soma theory, where an organism optimizes the allocation of resources to competing physiological demands, (Shanley & Kirkwood, 2000). In this way the organism is preserving reproductive capabilities and concentrating on the overall health and longevity of the organism. Protein turnover increases, histologically the cells are maintained in newer condition by protein turnover (Shanley & Kirkwood, 2000, Vigneau-Callahan et al, 2001, Koubova & Guarente, 2003, Heilbronn & Ravussin, 2003, Willcox et al., 2007, Katsman et al., 2010). DNA repair and maintenance is increased, and the age related decline of tissue repair and wound healing is slowed, (Shanley & Kirkwood, 2000). Oxidative cellular damage is reduced as well because the CR in the organism promotes gluconeogenesis, which is a less oxidative pathway for generation of glucose than glycolysis. Aerobic energy metabolism apparently creates DNA damage and gluconeogenesis bypasses the aerobic energy metabolism pathway saving cells from DNA damage, (Heilbronn & Ravussin, 2003).
Apoptosis increases also reducing the risks of carcinoma on the major organs, (Willcox et al. 2007).
Ageing is reduction of protein turnover and a build-up of oxidativley damaged proteins, (Kubova & Guarente 2003, Heilbronn & Ravussin, 2003, Katsman et al. 2010). CR slows this process and the accumulation of potentially harmful proteins and speed up turnover, (Kubova & Guarente 2003). The age related accumulation of oxidised proteins declines with CR, (Heilbronn & Ravussin, 2003). As the body runs out of fat with CR, degradation of proteins triggers increased protein turnover.
CR also decreases insulin levels in the blood and increases insulin sensitivity, (Heilbronn & Ravussin, 2003). The pancreas doesn’t need to work as hard and reduces in size.
CR reduces cholesterol levels, (Fontana et al., 2004). Reduced Calories in the blood also reduces damage to the blood vessels. In a study by Fontana et al., (2004), they measured the thickness of the tunica intima media of subjects’ carotid arteries with one group on CR and compared it to a control group on normal diet, they discovered a reduction of thickness of the Tunica Intima Media (TIM) in middle aged humans on CR of 40%. That is the equivalent of the normal thickness of the TIM in the carotid artery of a 10-year-old human. Atherosclerosis can originate from inflammation of the artery walls, and CR reduces the incidence of inflammation (Heilbronn & Ravussin, 2003). This inflammation results from the interaction of macrophages, oxidised cholesterol and cells of the artery walls, (Fontana et al., 2004).
Blood pressure also decreases as an effect of CR, (Fontana et al., 2004). The artery walls have less pressure against them and the veins have less sugar. This reduces the amount of damage created on the artery walls. Reduced risk of arteriosclerosis results from CR.
Reduced risk of Diabetes mellitus because CR makes less sugar in the blood and less insulin. All of the cells in the body become more sensitive to insulin and insulin resistance decreases, (Heilbronn & Ravussin, 2003, Fontana et al., 2004).
Neuroendocrine response.
Neural response to CR is that the organism increases energy production from keytones forming more abundant nourishment for the brain and increase in proprioceptive function relative to the normal decline with ageing. CR also reduces the decline of dendritic spines increasing their density and maintaining memory and reducing the loss of grey matter in the central nervous system relative to ageing, (Kubova & Guarante, 2003, Katsman et al., 2010). CR is also believed to increase astrocyte activity and the uptake of glutamate into the brain, (Katsman et al., 2010). CR appears to have a protective effect on the brain, the organs, and the musculoskeletal system of the organism.
During starvation the brain can derive energy from ketone bodies for acetyl-Coenzyme A, (King, 2011). Kubova & Guarante (2003) also reckon CR has the effect on the brain of promoting the expression if genes responsible for neuroplasticity, and that this could be related to the improved psychomotor performance observed in animals relative to the decline expected with ageing. Katsman et al. (2010) found that test animals showed improved motor performance and manual dexterity in CR. In normal ageing circumstances, a build-up of nonheme iron stored in ferretin in the brain downgrades the functioning. However in CR, the nonheme Iron deposition is apparently reduced as seen in MRI scans of subjects, particularly in the parts responsible for motor functions (Kastman et al., 2010).
Glycolysis involves more oxidative reactions contributing to oxidative cell damage than gluconeogenesis, (King, 2011). The gluconeogenesis mechanism consumes skeletal muscle to derive glucose for storage as glycogen, rather than oxidizing glucose as in glycolysis, (King, 2011).
Kubova & Guarente (2003) and Heilbronn & Ravussin, (2003) claim that CR creates a reduction in body temperature in rodents and nonhuman primates because of a reduction of non-coupling proteins in the inner membrane of mitochondria that are responsible for proton leakage and the generation of heat. So the mitochondria work more efficiently in CR.
So apparenty apoptosis increases in CR reducing the expression of cancers (Willcox et al. 2007), and organs of the body downsize where as the brain does not. CR also reduces the insulin levels in the blood and the insulin receptors become more effective. So sugar is in the blood for shorter periods of time and the lower levels will create less damage to the blood vessels because the sugar is absorbed faster. Needing less insulin makes the pancreas less big, (Heilbronn & Ravussin, 2003). The increased sensitivity to insulin also creates an increase resistance to stress, decreasing stress on the whole organism.
Improves sympathetic nervous system function in animals, (Heilbronn & Ravussin, 2003).
According to Williamson et al. (2008) the dangerous effects of CR can lead to symptoms associated with anorexia and bulimia nervosa, such as preoccupation with food, reduced interest in sex, binge eating and mood swings. Furthermore subjects can become depressed and have difficulty to regain normal calorie intake. However this is a rare occurrence indeed as shown by their research and CR is proven to be safe in general, but should not be implemented in adolescent women who are more predisposed to developing eating disorders.
Conclusion
The CR diet is a powerful contributor to longevity and although very few studies have been conducted on humans, apparently similar results have been obtained as in the extensive testing on animals. Conducted in the correct conditions with a nutrient rich, low calorie diet, and avoided in juveniles CR brings a wide range of benefits, including reduction in atherosclerosis, reduction of insulin resistance, reduction of blood pressure, reduction of fat mass, reduction of oxidative stress on a cellular level, increase on protein turnover and DNA repair and maintenance. An increase in brain function relative to the expected decline with age, preserving memory and proprioceptive and motor function are also affects on the organism of CR. This shift in the metabolic function of the organism comes from the CR provoking a diversion of energy from growth and reproductive functions, advocated on a hormonal level. CR is clearly effective but should be avoided in juveniles and should not be excessive in duration or intensity. More studies should be conducted on humans, however the total lifespan is a difficult criteria to measure due to the longer lifespan of humans compared to other animal species that have been tested in the past.
(1930 words)
Refferences
Koubova J.
& Guarente L. 2003. How does calorie restriction work?
GENES & DEVELOPMENT Vol.17 pp.313–321. MIT Massachusetts USA. Cold Spring Harbor Laboratory Press .
King M. 2011. themedicalbiochemistrypage.org [Online] Available at [Accessed: 2nd, September 2011] .
Kastman E., Willette A,. Coe C., Bendlin B., Kosmatka K., McLaren D., Xu G., Canu E., Field A., Alexander A., Voytko M., Beasley M., Colman R., Weindruch R., Johnson S. 2010. A Calorie-Restricted Diet Decreases Brain Iron Accumulation and Preserves Motor Performance in Old Rhesus Monkeys Neurobiology of Disease.
Journal of Neuroscience, Vol.30(23) pp.7940 –7947.
Shanley D. & Kirkwood T. 2000. Calorie Restriction and Aging: A Life-History Analysis. Evolution, vol.54(3), pp. 740–750.
Vigneau-Callahan K., Shestopalov A., Milbury P., Matson W., Kristal B., 2001.
Calorie Restriction: Effects on Body Composition, Insulin Signaling and Ageing. Characterization of Diet-Dependent Metabolic Serotypes: Analytical and Biological Variability Issues in Rats. Journal of Nutrition, Vol.131, pp.924S–932S.
Fontana L., Meyer T., Klein S., & Holloszy J., 2004.
Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans. PNAS. Vol.101 no.17 …show more content…
pp.6659–6663.
Heilbronn L.
and Ravussin E., 2003. Calorie restriction and aging: review of the literature and implications for studies in humans. American Journal of Clinical Nutrition. Vol.78, pp.361–9.
Williamson D., Martin C., Anton S., Yourk-Crowe E., Han H., Redman L., Ravussin E., 2008. Is caloric restriction associated with development of eating disorder symptoms? Results from the Calorie trial. Health Psychology. Vol. 27 no.1 pp.32-42.
Willcox B., Willcox D., Todoriki H., Fujiyoshi A., Yano K., He Q., Curb J., & Suzuki M., 2007. Caloric Restriction, the Traditional Okinawan Diet, and Healthy
Aging
The Diet of the World’s Longest-Lived People and Its Potential Impact on Morbidity and Life Span. Annals of the New York Academy of Sciences. Vol.1114 pp.434–455.