Here we are. Jose Cordeiro our advisor & Longevity “rock star” Aubrey De Grey. He is going to help Longevity InTime with data for AI simulations of clinical trials. He was happy that we said what we said, that we need to simulate existing trials to see our results and that its true that there are not so much data online even for past trials! We will meet again in Paris this Saturday

This article gives a good overview of the ongoing controversy around NMN.
*November 17, 2022*
*FDA says NMN cannot be sold as a dietary supplement in the US*
https://longevity.technology/news/fda-says-nmn-cannot-be-sold-as-a-dietary-supplement-in-the-usa/

*November 16, 2022*
*Age reprogramming: cell rejuvenation by partial reprogramming*
"Here, we highlight recent work that has provided a more nuanced understanding of age reprogramming and point to some open questions in the field that might be explored in the future."
https://journals.biologists.com/dev/article/149/22/dev200755/281768/Age-reprogramming-cell-rejuvenation-by-partial

Dear followers, our advisor Jose Cordeiro welcomes all of you online and those who are in Paris offline to his book “Death of a Death” presentation on upcoming Monday:

https://www.linkedin.com/events/lamortdelamort-lesavanc-esscien6999579232431411200/comments/

Must read website: www.FightAging.org

BTW, I just read this, MIT Technology Review quotes Jose Cordeiro 🙂 https://www.technologyreview.com/2022/11/16/1063300/billion-dollar-mega-rich-live-forever/

*November 23, 2022*
*New Alzheimer’s genes discovered in world’s largest study*
https://longevity.technology/news/new-alzheimers-genes-discovered-in-worlds-largest-study/

*November 17, 2022*
*Telomeres expand sphere of influence: emerging molecular impact of telomeres in non-telomeric functions*
https://www.cell.com/trends/genetics/fulltext/S0168-9525(22)00250-5

*August 10, 2022*
*Meal Skipping and Shorter Meal Intervals Are Associated with Increased Risk of All-Cause and Cardiovascular Disease Mortality among US Adults*
"In this large, prospective study of US adults aged 40 years or older, eating one meal per day was associated with an increased risk of all-cause and CVD mortality. Skipping breakfast was associated with increased risk of CVD mortality, whereas skipping lunch or dinner was associated with increased risk of all-cause mortality. Among participant with three meals per day, a meal interval of ≤4.5 hours in two adjacent meals was associated with higher all-cause mortality".
https://www.jandonline.org/article/S2212-2672(22)00874-7/fulltext

Why do people age?
During the first half of the 20th century, it was believed that because cultured normal cells were immortal, aging must be caused by extracellular events. but in the second half of the 20th century scientists discovered that normal cells do have a limited capacity to divide and that aging occurs intercellularly. Explanations of the aging mechanism have become unexpectedly complicated. Where gerontologists once looked for a single, all-encompassing theory that could explain aging, such as a single gene or the decline of the immune system, they are now finding that multiple processes, combining and interacting on many levels, are on the basis of the aging process. These processes take place not only at a cellular and molecular level but also on tissues and organ systems. 
Many widespread theories have been suggested, most of these if not all can, however, be classified into two categories error theories and program hypotheses. The third category “combined theories” which contains certain elements of both groups can be considered as well.
To better characterize the aging process, scientists have started to identify and categorize the cellular and molecular hallmarks of aging. Nine candidate hallmarks are generally considered to contribute to the aging process and together determine the observable characteristics of aging. A corresponding process is considered a hallmark of aging, if its deterioration causes premature aging, while its improvement ameliorates health during aging and extends lifespan.
The 9 hallmarks of aging:
1. Genomic instability
One common denominator of aging is the accumulation of genetic damage throughout life.
Apart from the red blood cells, each of our body cells contains the instructions for all the cellular processes required. This blueprint is our DNA. It consists of more than 3 billion nucleotides, which are the DNA building blocks that make up our genome. Since the genome contains the instructions for all functions in a cell, its correct operation is essential for our body to work properly. However, our genome is permanently under attack by internal and external influences. External harmful influences include UV radiation and air pollution and internally, oxygen radicals produced during our respiration can damage the genome. Scientists estimate that the DNA in every single cell of our body is damaged up to a million times a day. Fortunately for us, our DNA also contains the information for several processes that can detect and repair such damage. The problem is that these repair processes are imperfect. Although our cells can repair most DNA damage events some of these DNA damages are not properly repaired. These DNA mutations are then fixed in our genome. These mutations which can worsen all aspects of a cell’s function accumulate over time. People who have impaired repair processes of the genome often show signs of accelerated aging. The damage can also lead to the development of cancer.
On a positive note, it has been shown that caloric restriction slows down the increase in DNA damage that occurs over time, in addition, obvious health advice such as avoiding sunburn eating less fried foods, and not smoking also helps.
2. Telomere attrition
One particular type of genome instability is the shortening of our telomeres. Telomeres are the end of the chromosomes of the human genome, and they keep our chromosomes stable. Each time a cell divides, a small part of the telomeres gets lost. When the telomeres reach a critical length, the cell stops dividing. Such cells can then die or even cause inflammation, speeding up the aging process and triggering diseases. A specific enzyme called telomerase prevents telomere shortening and even restores the length of telomeres. In most adult cells, telomerase is only a little or not at all active. However, activation of telomerase to increase the lifespan is a dangerous solution, as telomerase activity is associated with many types of cancer
3. Epigenetic alterations