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The Thymus, Immune System, and Aging
Published in Nate F. Cardarelli, The Thymus in Health and Senescence, 2019
As Walford notes in his justly famed opus, “Maximum Life Span”, one can extend lifespan through diet, changing environmental temperature (with fish) and conquering infectious diseases, but maximum lifespan remains unchanged due to the presence of a biological clock in each body.254 Watson and Yunis describe aging as a genetically programmed decline in functional effectiveness of the organism.255 The schedules for development and thymic involution are set by a clocking mechanism which they locate in the thymus. Underfeeding, of course, retards thymus growth and thus also retards the onset of involution. Jackson and Watson view the thymus as “translating nutritional causes into immunological effects”.256 In general, the nutrition-thymus interactions fit well into the concept of a thymic clock controlling the rate of aging.
Healthy and Successful Aging
Published in Joseph P. Hou, The Healing Power of Ginseng, 2019
If we can live healthily, it has been said that the maximum life span of the human species is about 140 years. How would you feel if you could live happily and healthily for over 100 years? Would you call it an extra gift from God? Gerontologists are sometimes asked if they really think it is a good idea for people to live this long. Obviously, the increased population of seniors would raise many socioeconomic problems with regard to their health and well-being, as well as nursing care, welfare, and disability costs. However, these problems would not be so unmanageable if the aged seniors were kept healthy. If people lived longer but were isolated, sick, disabled, and miserable, it would not be ideal.14
Kinetics and Metabolism
Published in Lars Friberg, Tord Kjellström, Carl-Gustaf Elinder, Gunnar F. Nordberg, Cadmium and Health: A Toxicological and Epidemiological Appraisal, 2019
Gunnar F. Nordberg, Tord Kjellström, Monica Nordberg
Many studies on urinary cadmium after low level long-term exposure (Section II) have shown an increase with age similar to that of body burden. In areas with daily cadmium intakes via food of 10 to 20 μg Cd per day, nonsmoking adults excrete 0.5 to 1 μg/day (Chapter 5). This constitutes about 0.005 to 0.01%/day of a body burden of 10 mg (Table 5). In addition, cadmium excretion in feces contributes about the same amount to total excretion (Section V.B.4). This implies a whole body half-time for humans of about 10 to 20 years, which is about 12 to 25% of the maximum life span, similar to the findings for other species (Table 7).
The annoying flaws of gerontological research
Published in Drug Metabolism Reviews, 2022
Magomed Khaidakov, Valeria Troshina, Dmitry Menglet, Yusef Yusef, Alexander Plotkin
Similar reasoning applies to oxidative stress. The still popular oxidative stress theory of aging that has been around for more than 60 years (Harman 1956) seems to be largely discredited at least regarding mammals (Pérez et al. 2009). The exaggeration of function of any major antioxidant enzyme does not increase the lifespan of mice, although in some cases it does noticeably reduce oxidative damage (Pérez et al. 2009). Epidemiological studies on the effects of dietary antioxidants in humans have not revealed positive effects on morbidity (except, perhaps, possible attenuation of cognitive decline) and mortality (Kamel et al. 2006). Various dietary antioxidants did not show consistent lifespan-extending effects in mice, whereas in C. elegans most tested antioxidants produced an extension of either median or maximum lifespan (Sadowska-Bartosz and Bartos 2014). Existence of several confounding factors such as poor absorption, enzymatic modification of absorbed antioxidants, difficulties with delivery to cells and to relevant organelles within the cells still animates the field, but for now the high relevance of oxidative stress to mammalian aging seems to be doubtful.
First dose in neonates: pharmacokinetic bridging study from juvenile mice to neonates for drugs metabolized by CYP3A
Published in Xenobiotica, 2020
Pan-Pan Ye, Yi Zheng, Bin Du, Xi-Ting Liu, Bo-Hao Tang, Min Kan, Yue Zhou, Guo-Xiang Hao, Xin Huang, Le-Qun Su, Wen-Qi Wang, Feng Yu, Wei Zhao
Simple allometry with a correction factor for maximum lifespan potential (MLP) in years for CL: CLn is the predicted CL in neonates; WTn is the bodyweight in neonates. Brain and body weights are given in kilograms. MLP is an estimate of the maximum amount of time, calculated by the equation described by Sacher (1959), that a given species could survive. It has been used as a correction factor of inter-species scaling for the prediction bias from animals to humans (Mahmood & Balian, 1996). In this method, the individual CL estimated by Bayesian inference in juvenile mice was multiplied by its MLP value and plotted on a log-log scale as a function of body weight. The coefficient and exponent (a and b in the equation) were estimated from the allometric equation. The MLP value of the human body is 818,000 h, which is about 93.4 yr. The relationship between brain weight and PNA of mice at 1, 5, and 11 days (120, 248, and 314 mg, respectively) was mapped. The brain weight of mice at 1–12 days was obtained by incorporating mouse PNA into the equation. The MLP of each mouse was calculated according to its brain weight and bodyweight, and the average MLP of all juvenile mice was calculated.
Is anti-ageing drug discovery becoming a reality?
Published in Expert Opinion on Drug Discovery, 2020
Life extension in experiments with wild type animal models. Theoretically, based on the meaning of the term, the geroprotector should prolong the life of the model beyond the intact species’ maximum lifespan, protecting it from one or more mechanism of aging. However, in practice, at best, we are talking about increasing the lifespan by tens of percent. Therefore, it is more accurate to talk about gerosuppressors, and not geroprotectors.Improvement of molecular, cellular, and physiological biomarkers to a younger state or slow down the progression of age-related changes in human.Most potential geroprotectors are preventive only when applied at relatively high concentrations. The lifespan-extending dose should be several orders of magnitude less than the toxic dose.Minimal side effects at the therapeutic dosage at chronical application.The potential benefit of taking the geroprotector may come after a long period of time. Potential geroprotectors should initially improve some parameters of health-related quality of life: physical, mental, emotional, or social functioning of the person. This can serve as the basis for their chronical use.