The results of these experiments strongly suggest that the Japanese diets of and are healthier for mice than that of But do the outcomes apply to human beings as well?
- German Airborne Divisions: Blitzkrieg 1940-41.
- Land Use Policy and Practice on Karst Terrains: Living on Limestone.
- Detection of Malingering during Head Injury Litigation.
- Controlling protein intake may be key to longevity, studies show?
- Yoga Sutras of Patanjali.
For our first experiment, we assembled a group of moderately obese subjects aged 20 to 70 and divided them into two groups, then had those two groups adhere to distinct diets for 28 days three meals a day. The first group ate meals consistent with a typical Japanese diet of today, while the second group adhered to the diet. By the end of the experiment, the average body mass index and weight of the group members had declined significantly, along with waist circumference.
Hemoglobin A1C used to diagnose and monitor diabetes and pre-diabetes declined as well. Next, we performed a similar dietary experiment on non-obese subjects aged 20 to In this case, we also had the subjects engage in an hour or more of moderately intense exercise three days a week for the duration of the experiment. Pre- and post-experiment measurements showed reduced stress and increased fitness among the group. In short, our research to date supports the hypothesis that, when it comes to health and longevity, the Japanese diet is superior to the typical Japanese diet of today.
I believe that it strengths of the former can be boiled down to the following attributes. Variety : The daily menu featured a relatively large number of small dishes typically at least three, in addition to soup and rice. Cooking methods : The top three modes of preparation were simmered, steamed, and raw, followed by boiled and grilled. Frying and sauteeing were somewhat less common. Cooking at high heat, as when frying in oil, can cause nutrients to break down. Ingredients : The diet was rich in soy products, seafood, tubers, green and yellow vegetables including pickles , fruit, seaweed, mushrooms, and green tea.
Eggs, dairy products, and meat were consumed as well, but in moderation. Seasoning : The skillful use of fermented seasonings soy sauce, miso, vinegar, mirin , and sake along with dashi broth helped impart a satisfying flavor to foods without the heavy use of salt and sugar. The segment of the population that is pushing the average Japanese lifespan to record levels is the and-up age group, which was still largely adhering to the diet in middle age—the time when adults become vulnerable to lifestyle diseases. In fact, the incidence of diabetes and other lifestyle diseases among the Japanese has been rising year by year, raising concerns that life expectancy in Japan is approaching its peak.
On the other hand, if we can make a timely course correction and recapture the health benefits of the Japanese diet, the day may come when almost anyone can reasonably expect to live to In practice, this generally means one main dish frequently fish or another protein and two side dishes often vegetables , in addition to rice and soup. Japanese food longevity health. Food scientists in Japan have homed in on the nutritional keys to health and longevity, and their conclusions may bode ill for the younger generation.
Japanese Versus American First, we conducted experiments on lab rats to compare the health impact of a typical Japanese diet of the late s with an American diet of roughly the same period. The differences between aging and longevity became clearer with the mathematical descriptions by W.
Hamilton [ 1 ] and later by B. Charlesworth [ 10 ]. However, these genes were not the type that Medawar had suggested, i. His model showed that the force of natural selection on mortality was highest before the start of the reproduction phase and declined thereafter Figure 1. Because the force of mortality was highest prior to reproduction, evolution would have worked to select genes that were necessary for combating mortality in early life, i. Mortality life span , therefore, must be related to genes selected for survival to reproduction age. Hamilton provided the first mathematically implicit evidence that life span longevity had evolved and was directly related to genes that optimized survival to the age of reproduction.
Importantly, his model was specific to longevity and did not include variables of age-related functional loss. Populations of Drosophila selected in the laboratory for their timing of reproduction showed that late-life reproducers do indeed live significantly longer than flies having their highest rate of reproduction early in the life span Figure 2.
Genetic studies in yeast, C. Data used are from life-tables of the United States between and Adapted from [ 2 ]. Mathematical models and empirical experimentation have unequivocally established that longevity evolved from genes selected for their impact on survival to the age of reproduction. Because these investigations did not include measures of age-related degeneration, conclusions as to the genetic basis of aging cannot be made. Nonetheless, hundreds if not thousands of publications exist describing research that either directly or indirectly implicate specific genes as being involved in age-related degeneration.
Not one gene has been identified that causes osteoarthritis, presbyopia, sarcopenia, or any other of the hundreds of age-related degenerative and chronic disorders observed in the aged population. The reason for this is simple-these genes do not exist. Aging arose serendipitously in evolutionary history as a result of a trade-off between the germ line and somatic cells in the distribution of resources.
This trade-off has been developed into a formal theory by Thomas Kirkwood and is known as the Disposable Soma Theory of Aging [ 15 ]. The foundation of this theory lies directly in a basic principle of natural selection, i. Organisms that use the finite resources most efficiently will be the ones to successfully survive to reproduction age.
The Disposable Soma Theory posits that the most efficient use of resources in multicellular organisms is to give highest priority to the cells that are responsible for the continuation of the species, i. Supporting cells, those of the soma, would only need enough resources to accomplish their primary task of supporting the germ line.
That is, the soma could be disposed of once reproduction had occurred.
But, where and how were those resources being spent? The Disposable Soma Theory predicts that that the distribution of resources by the early metazoans was preferentially diverted to repair mechanisms of the DNA in the germ line. This suggestion is consistent with the observation that the energetic cost for maintaining DNA fidelity is rather high. If, because of finite resources, an organism had to make an evolutionary choice between accuracy in the DNA of the germ cell or repair of a somatic cell, the germ cell would be chosen so as to provide the best chance of survival for the next generation.
A quick lesson in cell biology
The immortality of the germ line has come at the cost of somatic mortality. A substantial literature exists describing that the primary mechanism associated with the random nature of aging is entropy, a property of the Second Law of Thermodynamics see reviews [ 5 , 6 , 7 ]. Briefly, biological systems defend themselves against the unceasing disorder of entropy by continuously restoring the free energy lost to chemical reactions that maintain molecular fidelity structure, function. At its very basic level, survival to reproduction age simply reflects the selection of genes that maintain free energy states conducive to life.
However, there is no reproductive advantage for an individual to sustain molecular fidelity after the age of reproduction. Genes would not have been selected for the purpose of maintaining the high cost of combating entropy throughout the life span. The age-related decline in physiological function reflects a gradual loss in the ability to defend against the Second Law of Thermodynamics, i. Importantly, the age-related loss in the ability to defend against entropy manifests purely as random events with respect to the physiological systems affected. The random nature of aging suggests that chance plays a significant part in determining the physiological system or systems that experience declining function in the older population.
The role of chance as a factor in the aging process has been reviewed in detail [ 3 ]. Chance precludes genetic determinism and introduces an element of uncertainty that cannot be controlled easily in population-based research, the type of research commonly used as the basis for establishing nutritional recommendations. The CDRI recognizes the problem of random variation in the aging population when stating that research investigating dietary recommendations for the older population is confounded by increased error random variation in the data [ 4 ].
Moreover, the error becomes greater with advancing age, suggesting that nutritional recommendations based on the current scientific rationale, i. Chance also raises the possibility that every sample population will be unique and that no sample population can be relied upon to provide meaningful predictive results for the entire aged population. Take for example the results from studies investigating the value of nutritional antioxidants as modulators of aging. Nutritional antioxidants prevent damage to the cell in vitro and the accumulation of cellular damage has found wide acceptance as a proximal cause of organism aging.
The epidemiological data suggest that the rate of aging and age-related disease may decrease in populations consuming foods high in antioxidants [ 16 , 17 ]. Consistent with the epidemiological data, small sample size cross-sectional supplementation investigations tend to find positive outcomes between experimental supplemented and control non-supplemented. However, several large randomized clinical trials have failed to demonstrate the benefit of antioxidant supplements in the aging population see review [ 18 ]. That is, the small cross-sectional studies have not been reliable indicators of the usefulness of antioxidant nutrition in the general older population.
The dominant role of chance in the aging process but not longevity leads to the inevitable conclusion that the fundamental process of biological aging cannot be modulated through interventions during old age. The nutrition researcher may find this statement difficult to accept given the overwhelming successes that nutrition interventions had on infant and childhood health.
The reason that nutrition interventions improved the health of infants and children was that nutrients had targets to interact with, i. Since aging did not arise through selective evolution, nutrients may or may not alter expression of genes in the older population. Recommendations for the older population arrived at by using genetic determinism will be unreliable—without genetic determinism, it is a matter of chance.
12222- Longevity & Aging: Nutritional and Metabolic Mechanisms
If modulating aging by nutritional intervention during old age will not produce the desired results, how then will nutrition intervention be effective in improving the health of the older population? We suggest that the research approach should focus on possible variation in function among individuals in younger age groups that may predispose them to differential rates of functional decline during advancing age. We must focus our attention on the time in the life span in which genetic determinism has the greatest influence on random aging outcomes, i.
Only after gaining a clear understanding of how chance and randomness shape the genetic pathways in younger populations that, in turn, affect the outcomes in the older population, should nutrition recommendations be considered. Refocusing nutrition and aging research to be consistent with the current understanding of the cause of aging may not be as difficult as it first may appear. While a personal genomic approach will ultimately be required in humans, several investigative models exist that may prove useful. The Fetal Origins Hypothesis a. These investigations suggest that undernutrition in utero leads to higher incidences of adult-onset obesity, hypertension, cardiovascular disease, and type II diabetes [ 20 ].
Although the current focus of research linking the developmental environment with aging remains on age-related disease, it would not be surprising to find that the rate of aging and the trajectory in the age-related loss of soma maintenance, independent of overt disease, may also have fetal origins. The age-related alterations to the vascular system and the development of certain types of cancer have been used extensively as models of the aging phenotype. A substantial literature exists describing how dietary habits during childhood may induce dysfunction of various systems during aging.
Some recent publications provide additional examples of specific research areas that should be given consideration [ 3 , 5 , 6 ] in this regard. Knowing the difference between aging and longevity will determine, in part, the scientific approach to research questions aimed at evaluating the impact that nutrition may have on the aging population. If the primary purpose of the research is to determine the factors involved with longevity, then focusing on altering the expression of specific genes by specific nutrients will be appropriate.
If, however, the aim of the research is to evaluate how nutritional interventions can modulate the aging process and improve the health of the older population, then the genetic determinism model will be inappropriate. Research designs that focus on chance events in young populations that lead to altered states of aging will be the more powerful. Effective nutritional recommendations for the aged population will most likely be ones that focus on dietary changes in the younger populations. The author wishes to acknowledge Jon Ramsey for his critical review of the manuscript, and Jennifer Ruhe for her technical assistance.
National Center for Biotechnology Information , U. Journal List Nutrients v. Published online Feb Roger B. Author information Article notes Copyright and License information Disclaimer. Abstract Life expectancies after the age of 70 and the number of individuals living with age-related chronic conditions that affect daily activities continue to increase. Keywords: chance and aging, evolution of longevity, genetic determinism, nutrition recommendations.
Looking for other ways to read this?
Introduction Life expectancies after the age of 70 and especially after the age of 85 have yet to reach a plateau. Imprecise Terminology: Aging vs. Figure 1. Open in a separate window. Figure 2. The Disposable Nature of the Soma and the Cause of Aging Aging arose serendipitously in evolutionary history as a result of a trade-off between the germ line and somatic cells in the distribution of resources. Acknowledgements The author wishes to acknowledge Jon Ramsey for his critical review of the manuscript, and Jennifer Ruhe for her technical assistance.
References 1. Hamilton W. The moulding of senescence by natural selection.
Nutrition for Health and Longevity
Rose M. Evolution of ageing since Darwin. Finch C. Chance, Development, and Aging.
Related Nutrition, Longevity and Ageing
Copyright 2019 - All Right Reserved