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At least 19 recordsLinked to original sources
PubMed1992

Diseases and aging: patterns of morbidity with age; relationship between aging and age-associated diseases.

Patterns of morbidity with age can be schematically represented in three situations: 1) as a progressive illness, such as Alzheimer's disease, leading to a relatively rapid functional decline. 2) as a catastrophic event, such as a stroke or hip fracture, leading to a decline in function with improvement after rehabilitation. 3) as normal aging with gradual progressive functional decline. Results from the New Mexico Aging Process Study provide some unique insights about the consequences of the effects of aging on the nutritional status of healthy elderly people. Between 1979 and 1989, anthropometric and biochemical markers as well as dietary intakes remained relatively constant in this healthy elderly population. Thus, the aging process alone may have little or no important consequences on the nutritional status of healthy elderly individuals. However, the adaptation of pancreatic and intestinal function to undernutrition and refeeding can be perturbed in these individuals.

Accidental Falls↗
PubMed1991

Age, disease, and changing sex hormone levels in middle-aged men: results of the Massachusetts Male Aging Study.

To evaluate the hypothesis that endocrine profiles change with aging independently of specific disease states, we examined the age trends of 17 major sex hormones, metabolites, and related serum proteins in 2 large groups of adult males drawn from the Massachusetts Male Aging Study, a population-based cross-sectional survey of men aged 39-70 yr conducted in 1986-89. Group 1 consisted of 415 men who were free of obesity, alcoholism, all prescription medication, prostate problems, and chronic illness (cancer, coronary heart disease, hypertension, diabetes, and ulcer). Group 2 consisted of 1294 men who reported 1 or more of the above conditions. Each age trend was satisfactorily described by a constant percent change per yr between ages 39-70 yr. Free testosterone declined by 1.2%/yr, and albumin-bound testosterone by 1.0%/yr. Sex hormone-binding globulin (SHBG), the major serum carrier of testosterone, increased by 1.2%/yr, with the net effect that total serum testosterone declined more slowly (0.4%/yr) than the free or albumin-bound pools alone. Among the major androgens and metabolites, androstane-3 alpha,17 beta-diol (androstanediol; 0.8%/yr) and androstanediol glucuronide (0.6%/yr) declined less rapidly than free testosterone, while 5 alpha-dihydrotestosterone remained essentially constant between ages 39-70 yr. Androstenedione declined at 1.3%/yr, a rate comparable to that of free testosterone, while the adrenal androgen dehydroepiandrosterone (3.1%/yr) and its sulfate (2.2%/yr) declined 2-3 times more rapidly. The levels of testosterone, SHBG, and several androgen metabolites followed a parallel course in groups 1 and 2, remaining consistently 10-15% lower in group 2 across the age range of the study. Subgroup analyses suggested that obese subjects might be responsible for much of the group difference in androgen level. Serum concentrations of estrogens and cortisol did not change significantly with age or differ between groups. Of the pituitary gonadotropins, FSH increased at 1.9%/yr, LH increased at 1.3%/yr, and PRL declined at 0.4%/yr, with no significant difference between groups 1 and 2.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed2026

Endosymbiotic theory of aging revisited: Age-related leakage of mitochondrial dsDNA/RNA stimulates cytosolic nucleic acid sensors which remodel the immune network and promote the aging process.

About 1.5-2 billion years ago, an endosymbiosis between aerobic α-proteobacteria and anaerobic archaeal cells generated mitochondria, i.e., organelles capable of producing oxidative energy. The bacterial genome was fundamentally reduced and a circular mitochondrial genome evolved containing mainly the genes coding for the subunits of the electron transport chain. Before the symbiotic event, there existed a virus-host co-evolution which involved the development of sensors for detecting dangerous viral DNA/RNA molecules. Endosymbiosis supplied eukaryotic cells not only with an oxidative powerhouse to allow the evolution of more complex multicellular organisms but it also meant that cells now housed an organelle which was able to generate reactive oxygen species (ROS) and to leak mitochondrial DNA (mtDNA) and double-stranded RNA (dsRNA) into the cytoplasm. There is now abundant evidence that during aging and age-related diseases mitochondria are prone to release both mtDNA and dsRNA. In the cytoplasm, mtDNA/dsRNA molecules activate a number of cytosolic nucleic acid sensors leading to the secretion of type-1 interferons (IFN) and many other cytokines which promote an age-related proinflammatory state. Currently, it is known that mtDNA can activate the cGAS-STING pathway, AIM2 inflammasomes, IFI16 receptors, and ZBP1 sensors and in addition mitochondrial dsRNA stimulates RIG-1/MDA5 signaling. Interestingly, there is abundant evidence that all these receptors are drivers of cellular senescence and inflammaging. For decades, there has been mounting evidence that mitochondria have a crucial role in the aging process. We will examine this question from the perspective of evolution and propose that mitochondrial evolution created an endogenic source for the leakage of dangerous mtDNA/dsRNA which subsequently stimulated cytosolic DNA/RNA sensors, an evolutionarily conserved viral defence mechanism. It seems that these two evolutionary events provided not only the basis for the inevitable process of aging but also ensuring the death of parental organisms.

Aging↗
PubMed1991

[Maturescence, a critical phase between ages 40 and 65. Health, illness, aging and social ages].

The recent emergence of a critical phase in life called maturescence, situated between the ages of 40 and 65, is a by-product of social life in industrialized societies. Because it is considered as a crossroads, this phase in life is not connected with any particular chronological age, such as reaching forty or fifty. Rather, it involves the difficulties of aging in society and the oncoming of identity conflicts, all of which must be seen in relation with the specific health-related problems that result from aging.

Adult↗
PubMed1992

Excessive testicular progesterone secretion in aged male Fischer 344 rats: a potential cause of age-related gonadotropin suppression and confounding variable in aging studies.

Previous studies have inconsistently reported elevated sex steroid levels in aging male F344 rats, which frequently develop testicular Leydig cell tumors. The aims of this study were to characterize circulating steroid levels and to determine the in vivo source and functional significance of altered steroid secretion in these animals. Progesterone (P) and to a lesser extent estradiol (E2) levels were increased, while gonadotropins and testosterone (T) were decreased, in intact 24-mo-old compared to 12-mo-old rats. P levels were inversely correlated with gonadotropins and T. All old rats demonstrated Leydig cell hyperplasia or tumors. After orchidectomy, P levels were markedly decreased. Gonadotropin levels were similar in orchidectomized 24-mo compared to 3-mo-old rats. We conclude that the testis is the source of excessive P and E2 secretion in vivo in old F344 rats. Increased P (or E2) negative feedback may contribute to the suppression of gonadotropins and reproductive function in aging male F344 rats. Finally, excessive P secretion may be a confounding pathological variable in aging studies using this rat model.

17-alpha-Hydroxyprogesterone↗
PubMed1991

Postnatal age and the metabolism of medium- and long-chain fatty acids by isolated hepatocytes from small-for-gestational-age and appropriate-for-gestational-age piglets.

Hepatocytes were isolated from full-term small-for-gestational-age (SGA) and appropriate-for-gestational-age (AGA) piglets at 6 or 48 h postpartum and incubated with 1 mmol/L [1-14C]-octanoate (8:0), -nonanoate (9:0) or -oleate (18:1). The cells oxidized [nmol 1-C/(h.10(6) cells)] 9:0 to carbon dioxide (12.5) and acid soluble products (28.9) faster than 8:0 (10.9, 20.6, respectively), and both were oxidized faster than 18:1 (3.9, 9.9) regardless of the piglet age or weight. Oleate accumulated in lipid products eightfold faster than did 8:0 and 9:0. No differences between cells from SGA and AGA piglets were detected. Recovery of 1-C in CO2 was 48% higher in incubations with cells from 48-h-old than from 6-h-old piglets. This increase was attributable to a 70% higher O2 consumption by 48-h-old cells. Theoretical O2 consumption rates were computed from the fatty acid flux data and compared with measured O2 consumption. Hepatocytes from SGA and AGA piglets were equally capable of satisfying greater than 75% of their energy needs from fatty acid oxidation. The O2 consumption attributable to 9:0 metabolism was 30% higher than observed for 8:0 and 18:1. All fatty acids apparently spared endogenous fuels to a greater degree in 6-h-old than in 48-h-old piglets.

Animals↗
PubMedDate not supplied

Interrelation between Western type cancers and non-Western type cancers as regards their risk variation in time and space. IV. Hormonal transition of Japanese women from the pro-cervical cancer age through the pro-endometrial cancer age to the pro-hypogonadism age.

Chronological trend of urinary steroid excretions in Japanese women was investigated during the period of June 1972 to August 1986 using healthy women of urban and rural origins, patients with breast cancer and patients with either cervical cancer or endometrial cancer. The excretions of 14 neutral steroids were estimated by gas liquid chromatography, and the obtained data were tentatively correlated with the epidemiological backgrounds. In the course of the chronological transition from the 1st stage (1972-1974) to the 2nd stage (1975-79), the urinary steroid pattern of Japanese women with and without cancer experienced a common change to produce specific deviations that were in agreement with the hormonal characteristics of a pill user or of an endometrial cancer patient. At the 3rd stage (1980-86), patients with either cervical cancer or endometrial cancer were distinguished from 1st stage controls by non-specific depression of all androgens, progestins and corticosteroids in urine. Throughout the whole period, both the risk for cervical cancer and the reproductive activity (birth rate) were found to decrease continuously in Japanese women. Evidence was presented to suggest that the above deterioration of the hormonal environment in Japanese women could be related to the stress of modern life rather than to defects in the diet. On the basis of the above findings, the 1st, 2nd and 3rd stages of our investigation were tentatively termed the pro-cervical cancer age, the pro-endometrial cancer age and the pro-hypogonadism age. The relation between the chronological change of urinary steroids and that of the epidemiological background was analyzed from the view point of population ecology.

Age Factors↗
PubMed1992

Age related changes in follicle stimulating hormone, luteinizing hormone, oestradiol and immunoreactive inhibin in women of reproductive age.

OBJECTIVE: In women over the age of 45 years with continuing regular menstrual cycles, follicular phase FSH levels rise without an accompanying change in LH. We determined the effect of increasing age in women with regular cycles on the serum levels of FSH, LH, immunoreactive inhibin, progesterone and oestradiol. DESIGN: Single blood samples were taken during the early follicular phase (days 4-7) and again in the midluteal phase (3-12 days before the next menses) of the menstrual cycle. PATIENTS: Regularly cycling women aged 21-49 years participated in the study (and were grouped into four groups: 20-29, 30-39, 40-44 and 45-49 years in the follicular phase and three groups: 20-29, 30-39 and 40-49 years in the luteal phase. MEASUREMENTS: Serum levels of FSH, LH, oestradiol, progesterone and immunoreactive inhibin were measured from the blood samples obtained. RESULTS: Follicular phase Mean follicular phase levels of immunoreactive inhibin were significantly lower in the 45-49 year age group (P less than 0.05) than in the younger age groups (128 U/l in the 45-49 year age group vs 239, 235 and 207 U/l in the 20-29, 30-39, 40-44 year age groups respectively), while mean FSH levels were significantly higher in the 45-49 year age group (P less than 0.05, 13.0 IU/l in the 45-49, 4.9, 5.5 and 5.2 IU/l in the 20-29, 30-39 and 40-44 year age groups respectively). Mean oestradiol levels in the 45-49 year age group were significantly lower only when compared to age group 30-39 years (P less than 0.05, 130 vs 210 pmol/l). There was no significant difference in oestradiol levels between the 45-49 year age group and the 20-29 and 40-44 year age groups. LH levels did not differ significantly across age groups. There was also a significant negative correlation between serum immunoreactive inhibin and FSH (r = -0.45, P less than 0.05) and between oestradiol and FSH (r = -0.35, P less than 0.05). There was a significant negative relationship between immunoreactive inhibin and age (r = -0.46, P less than 0.05). For every 10-year increase in age, average immunoreactive inhibin decreased by an estimated 49.3 U/l. As age increased, average FSH levels exhibited a two-phase linear increase with the change-point estimated at 42.97 (1.42) (estimate (SE)) years. Prior to 42.97 years, FSH barely changed; after 42.97 years there was a significant (P less than 0.05) increase in FSH as age increased. Oestradiol levels did not change significantly until an estimated 37.9 years of age, but then decreased significantly (P less than 0.05) with increasing age. Luteal phase Levels of FSH, LH, serum immunoreactive inhibin, oestradiol and progesterone fell slowly with increasing age. There was a significant correlation between serum immunoreactive inhibin with progesterone (r = 0.41, P less than 0.05) but there was no correlation between serum immunoreactive inhibin LH or FSH. CONCLUSION: The results are consistent with a role for serum immunoreactive inhibin, in addition to oestradiol, in the regulation of FSH during the follicular phase of the menstrual cycle as a function of increasing age. This is postulated to reflect diminished folliculogenesis as age progresses with the known decline in the numbers of primordial follicles in the ovary as the menopause approaches.

Adult↗
PubMed1990

[A comparison of growth and development of the dental arch, alveolar process, and palate in the lateral segment determined with reference to dental age and chronological age, particularly on the period of premolar eruption].

The purpose of this study is to observe and compare growth and development in the dental arch, the alveolar process, and the palate in reference to dental age, which is based on tooth emergence, and chronological age. Subjects consisted of serial dental casts taken at two-month intervals from 40 children (20 males and 20 females) with normal occlusion in permanent dentition. In terms of dental age, observations were made for a total of two years, one year before and one year after the tooth emergence of first premolar and second premolar. In terms of chronological age, observations were made for a total of two years, one year before and one year after the average age of tooth emergence of first premolars and second premolars in this sample of children. Results and Conclusions. Comparisons between growth changes in the dental arch, the alveolar process, and the palate on dental and chronological age showed some regions in which growth patterns were similar and others in which growth patterns were different. The differences between both growth patterns from two ages were classified into two groups according to the tooth which caused the difference: those produced by the tooth used as a standard for dental age and those produced by teeth other than that used as a dental-age standard. 1) Differences resulting from the influence of the tooth used as a dental-age standard In regions of the tooth used as a dental-age standard, differences occurred in growth patterns on both kinds of age in practically all measured items. In regions adjacent to that of the tooth used as a dental-age standard, the differences were observed in growth patterns of the alveolar process and the palate but not in those of the dental arch. The differences were the most pronounced in the regions of dental-age-standard teeth than in the adjacent regions. The majority of the differences caused by teeth used as standards for dental age were thought to have been the results from the influence of eruption. No growth-pattern differences were observable in regions more than two teeth away from the tooth used as a dental-age standard. 2) Differences resulting from the influences of teeth other than that used as a dental-age standard Using the emergence time of a certain tooth as a dental-age standard, the emergence times of other teeth lead to be come together in some degree.(ABSTRACT TRUNCATED AT 400 WORDS)

Alveolar Process↗
PubMed1991

Refined crystal structures of "aged" and "non-aged" organophosphoryl conjugates of gamma-chymotrypsin.

"Aged" organophosphoryl conjugates of serine hydrolases differ from the corresponding "non-aged" conjugates in their striking resistance to nucleophilic reactivation. The refined X-ray structures of "aged" and "non-aged" organophosphoryl conjugates of gamma-chymotrypsin were compared in order to understand the molecular basis for this resistance of "aged" conjugates. "Aged" and "non-aged" crystalline organophosphoryl-gamma-chymotrypsin conjugates were obtained by prolonged soaking of native gamma-chymotrypsin crystals with appropriate organophosphates. Thus, a representative "non-aged" conjugate, diethylphosphoryl-gamma-chymotrypsin, was obtained by soaking native crystals with paraoxon (diethyl-p-nitrophenyl phosphate), and a closely related "aged" conjugate, monoisopropyl-gamma-chymotrypsin, was obtained by soaking with diisopropylphosphorofluoridate. In both crystalline conjugates, the refined structures clearly reveal a high occupancy of the active site by the appropriate organophosphoryl moiety within covalent bonding distance of Ser195 O gamma. Whereas in the "non-aged" conjugate both ethyl groups can be visualized clearly, in the putative "aged" conjugate, as expected, only one isopropyl group is present. There is virtually no difference between the "aged" and "non-aged" conjugates either with respect to the conformation of the polypeptide backbone as a whole or with respect to the positioning of the side-chains within the active site. In the "aged" conjugate, however, close proximity (2.6 A) of the negatively charged phosphate oxygen atom of the dealkylated organophosphoryl group to His57 N epsilon 2 indicates the presence of a salt bridge between these two moieties. In contrast, in the "non-aged" conjugate the DEP moiety retains its two alkyl groups; thus, lacking a negative oxygen atom, it does not enter into such a charge-charge interaction and its nearest oxygen atom is 3.6 A away from His57 N epsilon 2. It is suggested that steric constraints imposed by the salt bridge in the "aged" conjugate lie at the basis of its resistance to reactivation.

Alkylation↗
PubMed1975

Prediction of adult height from height, bone age, and occurrence of menarche, at ages 4 to 16 with allowance for midparent height.

Multiple regression equations for predicting the adult height of boys and girls from height and bone age at ages 4 and upwards are presented. There is a separate equation for each half year of chronological age; and for pre- and postmenarcheal girls at ages 11 to 14. These are based on longitudinal data from 116 boys and 95 girls of the Harpenden Growth Study and the London group of the International Children's Centre longitudinal study. The bone age used is the revised version of the Tanner-Whitehouse standards, omitting the score for carpal bones (RUS age, TW 2 system). Boys aged 4 to 12 are predicted in 95% of instances to within plus or minus 7 cm of true height, and at ages 13 and 14 to within plus or minus 6 cm. Girls ages 4 to 11 are predicted to within plus or minus 6 cm; premenarcheal girls aged 12 and 13 to within plus or minus 5 and plus or minus 4 cm, respectively; and postmenarcheal girls aged 12 and 13 to within plus or minus 4 and plus or minus 3 cm, respectively. Prediction can be somewhat imporved by allowing for midparent height. One-third of the amount that midparent height differs from mean midparent height is added or subtracted. An alternative system of equations which are based on initial classification by bone age rather than chronological age is given. These have about the same accuracy as the equations based on initial classification by chronological age, but allowance for bone age retardation is less. It is not clear which system is preferable. The equations probably apply to girls complaining of tall stature and boys or girls complaining of shortness and needing reassurance as to normality. In clearly pathological children, such as those with endocrinopathies, they do not apply.

Adolescent↗
PubMed1992

Inverse relationship between age at onset of Huntington disease and paternal age suggests involvement of genetic imprinting.

It is well recognized that age at onset of Huntington disease (HD) is strongly influenced by the sex of the affected parent, and this has lead to suggestions that genetic imprinting or maternal specific factors may play a role in the expression of the disease. This study evaluated maternal and paternal ages, birth order, parental age at onset, and sex of the affected parent and grandparent in 1,764 patients in the National HD Roster by using linear-regression techniques which incorporated a weighted least-squares approach to accommodate the correlation among siblings. It was found that paternal age is negatively associated with age at onset of HD, particularly among subjects who inherit the mutant gene from grandfathers. Apparent associations between age at onset and birth order and between age at onset and maternal age were not significant after adjustment for paternal age. The paternal age effect is strongest among juvenile-onset cases and individuals with anticipation of greater than or equal to 10 years, although it is detectable across the entire age-at-onset distribution. The tendency for older fathers, including those not transmitting the HD gene, to have affected offspring with early-onset disease may be consistent with a gene imprinting mechanism involving DNA methylation. Because paternal age in unaffected fathers is also a significant determinant of age at onset, methylation in this context might involve HD modifier genes or the normal HD allele.

Adolescent↗
PubMed1978

Down syndrome, paternal age, maternal age and birth order.

Recent cytogenetic evidence has shown that trisomy 21 can arise, perphaps even in substantial proportion, from paternal nondisjunction. The statistical association between Down syndrome incidence and maternal age, paternal age and birth order has been studied in a sample of over 4000 cases. The size of this sample made it possible to control for the effect of maternal age by single years of age during the search for a paternal age effect and vice versa, and the importance of such stringent control is emphasized. The maternal age association was confirmed with an extremely high degree of statistical significance while no independent effect of paternal age was found; indeed, the rates at paternal ages over 45 years appear to be nearly constant. After adjusting for the effects of parental age, a significant inverse association of birth order with incidence was noted. It also appears that the incidence among very young mothers may be high: for maternal ages 15 years and less the rates seem to be equivalent to those found at 30 or 35 years. In order to help answer the question of whether the maternal age association is the result of increasing rates of nondisjunction or of some other mechanism (for example, an age related defect in a spontaneous abortion screening mechanism), the proportion of cases due to maternal and paternal nondisjunction at different parental ages must be determined.

Adolescent↗
PubMed1992

Differential effects of swimming and running on microsomal metabolism in middle-aged and aged Fischer 344 rats.

Cytochrome P-450 (P-450) content as well as p-nitroanisole (pNA) O-demethylase and UDP-glucuronyltransferase (UDPGT) activities were determined in livers of middle-aged (MA; 12 or 18 months) and aged (24-26 months) rats exercised by either treadmill running or swimming. In addition, aniline hydroxylase activity was measured in MA runners and aged swimmers and compared to respective sham and non-handled controls. Treadmill exercise consisted of running aged and MA rats on a motorized treadmill for 16 and 20 m/min respectively, 60 min/day and 4 times per week, for 8 weeks. Sham rats were placed on the treadmill twice per week for 5 min at 8 m/min. No differences were found in any parameter comparing sham rats to non-handled controls. Running did not affect body weight or hepatic microsomal protein during the 8-week study. A 33-35% decline in microsomal P-450 content in treadmill exercised MA and aged rats was found. PNA O-demethylase activity was decreased 30% in MA and 45% in aged runners and aniline metabolism was inhibited 21% in MA rats. UDPGT activity was not affected by running in MA or aged rats. Swimming exercise was accomplished by placing the rats in a tank of water (32-33 degrees C) filled to a depth of 2 ft. Swim time was 60 min twice daily, 5 times per week. The aged and MA rats were trained for 6 months and 1 year, respectively. Two control groups, non-swimming sedentary (dry control) and 1 min swim/day sham (wet control), were utilized. MA and aged wet controls and swimmers weighted 8% and 15% less respectively, than MA and aged sedentary rats. Microsomal protein was significantly increased in MA swimmers compared to sedentary (20%) and wet control (35%) but no change was found with swimming in the aged rats. The results of the enzymatic studies were variable in the MA rats. Increases in P-450 content were found in wet controls (16%) and swimmers (27%) of the MA group, but only the swimming change was significant. No significant change was determined for pNA metabolism between swimmers and wet (22%) or dry (17%) controls. Aged swimmers and wet controls were more consistent, with no change in any of the parameters except aniline metabolism which was significantly increased in wet controls (25%) and swimmers (28%) as compared to dry controls. No significant change in UDPGT activity was measured in either age group of swimmers.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1992

Age and gender effects on ondansetron pharmacokinetics: evaluation of healthy aged volunteers.

Modest differences in the clearance of the 5HT3 antagonist, ondansetron, among different age groups were detected in two groups of healthy elderly volunteers, one group aged 61 to 74 years ("elderly") and the other 75 to 82 ("aged") years, in addition to young healthy subjects. Both a single 0.15 mg/kg intravenous dose and a single 8 mg oral dose were administered according to a randomized crossover design with a minimum 3-day washout period between treatments. Mean plasma clearance decreased (young, 0.349 L/hr/kg; elderly, 0.279 L/hr/kg; aged, 0.214 L/hr/kg; p less than 0.05) with increasing age. Volume of distribution at steady state was unaffected by age (young, 1.81 L/kg; elderly, 1.94 L/kg; aged, 1.71 L/kg), resulting in increases in mean plasma half-life (young, 3.4 hours; elderly, 4.5 hours; aged, 5.4 hours) and mean absolute bioavailability (young, 57%; elderly, 61%; aged, 69%) with increasing age. Female subjects cleared ondansetron more slowly than males (p less than 0.05), resulting in higher absolute bioavailability. Ondansetron was well tolerated by all age groups with no increase in the number of adverse events observed in older volunteers.

Administration, Oral↗
PubMed2026

Sex-specific aging clocks from a large-scale human phenome reveal distinct aging transitions and circulating signatures.

Aging is a primary risk factor for chronic diseases, yet its progression varies among individuals and between sexes. Here, under the X-Age Project, we profiled the clinical aging phenome of the Multicentric Chinese Aging Study (mCAS) through a cross-sectional analysis of 172 clinical measures from more than 100,000 participants aged 18-98 years across three centers. These profiles enabled sex-specific clinical aging clocks that revealed divergent aging trajectories between women and men during midlife that converged in later life. Phenome-wide analyses revealed age-related accumulation of metabolic factors, including low-density lipoprotein, triglycerides, glucose and uric acid, and tumor markers, such as carcinoembryonic antigen and human epithelial protein 4. These age-accumulating factors induced senescence-related phenotypes in human endothelial cells. Furthermore, a high-fat diet mouse model with dietary reversal supported the modifiability of metabolic burden-induced aging. Together, this work establishes metabolic and tumor marker accumulation as actionable drivers of human aging, paving the way for personalized, sex-stratified geroprotective interventions.

Humans↗