3 Comments

Excellent proposals and recommendations. The analysis of the lives of healthy centenarians gives us some clues to achieve a healthy old age, such as the following:---

1) Stay physically active and take care of your circadian rhythms..---

2) Take care of social relationships, express love to loved ones and have a helpful attitude.---

3) Promote attitudes of commitment, responsibility, honesty and perseverance throughout life.---

4) Set realistic short/medium term objectives and strive to achieve them.

5) Establish order and certain habits in daily life, so that daily demands do not overwhelm us.--

6) Keep your mind active, even exploring new areas of knowledge and learning (painting, writing, etc.). Try to solve problems that are progressively more difficult.

7) Practice gratitude, being aware of all the good in life.--

8) Enjoy, learning to identify and exploit positive daily experiences.--

9) Develop skills that allow us to accept negative and stressful events ---as part of life. .----

10) Practice meditation.---

https://www.iflscience.com/the-8-psychological-traits-associated-with-living-past-100-71700 (2023).--

https://www.vogue.com/article/10-expert-tips-on-how-to-live-a-longer-healthier-life (2024).--

141 BENEFITS OF MEDITATION.--

https://eocinstitute.org/meditation/10-key-brain-regions-upgraded-with-meditation-2/ (2023).--

Aging is largely defined as a gradual and progressive time-dependent decline in cellular and organ functions of living organisms, leading to increased susceptibility to chronic diseases, including cancer and death. Senescent cells are involved in a series of biological functions, from embryogenesis to aging. An excessive accumulation of senescent cells is associated with a decrease in regenerative capacity and chronic inflammation and mitochondrial dysfunction, characterized by a reduced oxidative capacity and the consequent increase in oxidative damage, contributes decisively and significantly to diseases and biological aging. .

Studies are investigating foods and substances that promote longevity. These include some phytonutrients such as epigallocatechin gallate, resveratrol, fisetin, berberine, apigenin, quercetin and curcumin and minerals such as magnesium and selenium also present in foods. Some of them also have senolytic effects, which promote the apoptosis of defective cells that accumulate over the years (senescent cells) and alter normal metabolism. Nicotinamide increases levels of sirtuins, called the “longevity proteins.”

These natural compounds protect mitochondrial function, reducing inflammation, chronic diseases and cancer.

https://www.mdpi.com/1422-0067/23/24/16219 (2022).---

https://onlinelibrary.wiley.com/doi/full/10.1002/fft2.129 (2022).---

https://www.sciencedirect.com/science/article/abs/pii/S092422442200108X (2022).----

https://www.mdpi.com/2073-4409/12/6/915 (2023).---

https://www.sciencedirect.com/science/article/pii/S1568163723001022 (2023).----

https://www.mdpi.com/1424-8247/15/12/1528 (2022).---

https://www.mdpi.com/1424-8247/16/2/196 (2023).---

https://www.tandfonline.com/doi/full/10.1080/10942912.2023.2236329 (2023).---

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10929829/ (2024).—

https://www.ingentaconnect.com/content/ben/ctmc/2024/00000024/00000002/art00005 (2024).--

https://academic.oup.com/edrv/advance-article/doi/10.1210/endrev/bnae010/7631421?login=false (2024).--

All of the aforementioned people will contribute to the regulation of oxidative stress, as well as the release of free radicals, inflammation, immune response, insulin resistance, lipid metabolism and the intestinal microbiota. There is strong evidence supporting the role of the microbiome in the development and progression of diseases, and this microbiome is modified (dysbiosis) by diet; Therefore, the consumption of phytochemical products helps maintain and restore health. In this link different phytochemicals with benefits in various diseases.

https://www.mdpi.com/2223-7747/13/4/523 (2024).-

Expand full comment

Pentadecanoic acid (C15:0), an odd-chain saturated fatty acid, has growing evidence of being essential in supporting cardiometabolic and liver health. People with low circulating concentrations of C15:0 have an increased risk of having or developing type 2 diabetes, heart disease, nonalcoholic fatty liver disease, and nonalcoholic steatohepatitis, as well as specific types of cancer. C15:0 is present in 1 to 3% of dairy fat, and as a primarily exogenous molecule, circulating C15:0 concentrations reflect dietary intake of C15:0. Epidemiological, in vivo, and in vitro studies support the idea that 100 to 300 mg of C15:0 per day are required to effectively achieve and maintain active circulating C15:0 concentrations of 10 to 30 µM.

C15:0 and rapamycin, a leading candidate for an intervention to improve longevity and health, share numerous clinically relevant activities, including anti-inflammatory, anticancer, antifibrotic, antimicrobial, and mTOR inhibitory activities. Furthermore, as an AMPK activator, C15:0 also showed multiple similarities with metformin, especially at specific doses. Studies consistently show that people with higher circulating concentrations of C15:0 have a lower risk of conditions associated with aging. C15:0 is an essential nutrient that supports healthy aging and longevity in humans, with cell-based activities that are as good as, or better than, leading prescription therapies for improving longevity. Given the decline in C15:0 levels throughout the population, there is a need to evaluate the possible effects of C15:0 nutritional deficiencies on our life expectancy and longevity.

https://www.mdpi.com/2072-6643/15/21/4607 (2023).--

Three recognized types of cell death have been established: apoptosis, necrosis and autophagy. Ferroptosis involves lipid peroxidation of fragile polyunsaturated fatty acids in cell membranes, which combines with abnormal intracellular iron to induce massive production of reactive oxygen species, resulting in disabled mitochondria and cell death. Ferroptosis has been linked to many aging-related diseases in humans, including type 2 diabetes, cardiovascular disease, NAFLD, and neurodegenerative diseases.

Ferroptosis requires two instigators: fragile polyunsaturated fatty acids in cell membranes that are susceptible to lipid peroxidation and excess intracellular iron. As Dr. Mercola has reported, lipid peroxidation from PUFAs is a major contributor to numerous diseases related to aging, including metabolic syndrome, NAFLD, cardiovascular disease, and neurodegenerative diseases. Furthermore, dysregulated iron metabolism and direct tissue damage caused by iron overload are increasingly recognized as drivers of type 2 diabetes, NAFLD, cardiovascular disease, and neurodegenerative diseases. When lipid peroxidation is combined with iron overload, the result is ferroptosis, which has wide-ranging effects that contribute to the onset and progression of metabolic and related diseases (Figure 1).

Although the decrease in cow's milk fat intake in the diet may explain the decrease in circulating C15:0 concentrations in Western countries, so can changes in habits related to fish in the diet. As seen in Table 1, C15:0 content varies greatly by fish species, with mullet and catfish having a C15:0 content similar to milk fat. As such, changes in the type or amount of fish consumed may influence a person's circulating C15:0 concentrations.

Expand full comment

C15:0 is a recently discovered essential fatty acid that plays a critical role in physically strengthening cell membranes and protecting cells against lipid peroxidation. As part of a cell stability hypothesis, it is proposed that adequate concentrations of C15:0 in cell membranes are required to prevent ferroptosis, a recently discovered method of cell death that involves lipid peroxidation of cell membrane fatty acids and intracellular iron, which has also been linked to type 2 diabetes, cardiovascular disease, and NAFLD.

Based on numerous studies provided in this review, a definition of C15:0 nutritional deficiency (circulating C15:0 ≤ 0.2% of total fatty acids) is offered. A description of the pathophysiology behind this C15:0 nutritional deficiency syndrome (cell fragility syndrome) is provided, explaining how low C15:0 can accelerate the progression of diseases associated with aging, including overload syndrome. of dysmetabolic iron, type 2 diabetes, cardiovascular disease and NAFLD.

In addition to correcting nutritional deficiencies, there is evidence that optimal concentrations of circulating C15:0 (>0.4% to 0.64% total fatty acids) may support cardiovascular health and long-term longevity. Continued studies, including clinical trials, will help to further test the cellular stability hypothesis and the proposed definition of C15:0 nutritional deficiencies. Given the global decreases in dietary C15:0 intake, further studies are needed to better understand the depth and breadth of the cellular fragility syndrome driven by C15:0 deficiency in different human populations and how this syndrome may be contributing to the increase in diseases associated with aging, especially among younger people.

https://www.mdpi.com/2218-1989/14/7/355 (2024).--

Expand full comment