https://scitechdaily.com/warning-popular-vitamin-supplement-causes-cancer-risk-and-brain-metastasis/
SciTechDaily
Warning: Popular Vitamin Supplement Causes Cancer Risk and Brain Metastasis
University of Missouri researchers made the discovery while using bioluminescent imaging technology to study how nicotinamide riboside supplements work inside the body. Commercial dietary supplements like nicotinamide riboside (NR), a form of vitamin B3,…
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 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/
Longevity.Technology - Latest News, Opinions, Analysis and Research
FDA says NMN cannot be sold as a dietary supplement in the US
Regulator’s decision based on NMN's investigation for use as a pharmaceutical drug – sparks immediate response from the CRN.
*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
*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
The Company of Biologists
Age reprogramming: cell rejuvenation by partial reprogramming
Summary: This Spotlight evaluates models of age reprogramming in light of recent studies that have provided molecular insights into the concept of age reprogramming.
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/
https://www.linkedin.com/events/lamortdelamort-lesavanc-esscien6999579232431411200/comments/
Linkedin
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500 million+ members | Manage your professional identity. Build and engage with your professional network. Access knowledge, insights and opportunities.
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Must read website: www.FightAging.org
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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/
MIT Technology Review
Inside the billion-dollar meeting for the mega-rich who want to live forever
Hope, hype, and self-experimentation collided at an exclusive conference for ultra-rich investors who want to extend their lives past 100. I went along for the ride.
*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/
*New Alzheimer’s genes discovered in world’s largest study*
https://longevity.technology/news/new-alzheimers-genes-discovered-in-worlds-largest-study/
Longevity.Technology - Latest News, Opinions, Analysis and Research
New Alzheimer’s genes discovered in world’s largest study
Two new genes that raise a person’s risk of developing Alzheimer’s disease have been discovered by researchers at Cardiff University.
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*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
*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
*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
Journal of the Academy of Nutrition and Dietetics
Meal Skipping and Shorter Meal Intervals Are Associated with Increased Risk of All-Cause and Cardiovascular Disease Mortality among…
Previous dietary studies and current dietary guidelines have mainly focused on dietary
intake and food patterns. Little is known about the association between eating behaviors
such as meal frequency, skipping and intervals, and mortality.
intake and food patterns. Little is known about the association between eating behaviors
such as meal frequency, skipping and intervals, and mortality.
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
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
Our genome consists of more than 3 billion nucleotides of four types: adenine (A), cytosine (C), guanine (G), and thymine (T). The individual DNA strands are wrapped around proteins called histones in the cell nucleus. Both DNA and histones can contain small chemical changes that can be used to switch individual genes on or off. The compound of these chemical changes is called the epigenome. The epigenome changes as we get older. Some of the chemical changes are misplaced, added in the wrong place, or lost. As a result, the control over gene activity also changes. Our epigenome is influenced by our diet and lifestyle, but chronic stress or certain drugs can also change it.
4. Loss of proteostasis
The DNA of our cells contains the instructions for all cellular functions. However, DNA does not carry out these functions. Instead, our DNA contains the information for the production of proteins and enzymes that take over tasks and control processes within the cell. Proteins and enzymes control all chemical reactions in the cells and also give the cell its structure. To carry out such functions, proteins must be folded precisely into a very specific structure, similar to origami. The term protein homeostasis, or proteostasis for short, describes the maintenance of the form and abundance of all proteins.
As we age, proteins get increasingly damaged due to normal cellular processes, which also influence their shape and folding. Not only can misfolded proteins no longer perform their normal work, but they also tend to clump together, which can have a toxic effect on the cell. For example, Alzheimer's disease is an age-related disease caused by misfolded proteins. Because the maintenance of proteostasis is so important the cell has several mechanisms to control the folding and quality of proteins. Our cells not only have mechanisms to repair and refuel distribute proteins there are also mechanisms to degrade such proteins and replace them with new ones. Misfolded and damaged proteins, for example, can be degraded by a recycling process known as autophagy.
Many study results suggest an important role of proteostasis in aging: misfolded proteins increase with age; several age-related diseases such as Alzheimer's are associated with misfolded proteins; improving protein quality control increases the lifespan of mice and other model organisms.
5. Deregulated nutrient-sensing
When sufficient nutrients are available, cells and tissues store energy and grow, whereas when nutrients are deficient, mechanisms for homeostasis and repair are activated. When cells are constantly exposed to excess nutrients the cellular mechanisms that recognize nutrients become less sensitive. This process also occurs during aging and causes cells to fail to respond properly to the signals that normally regulate energy production, cell growth, and other important cellular functions. Many studies have investigated the effect of food intake or the perception of food on the aging process- for example, when the overall food intake is reduced when the body is tricked to believe it has less food the insulin signaling pathway is switched off, and the lifespan increases in fruit flies. The result of many studies is that reduced food intake improves health and increases the lifespan of a wide range of animals.
Two nutrient-sensing pathways are especially the focus of aging research: The insulin/insulin growth factor (IGF) and the Target of Rapamycin (TOR) pathway together constitute a key nutrient-sensing network within the cell. Genetical or pharmacological inhibition of the insulin/TOR network extends the lifespan in a wide range of animals, making it a prime target for the development of anti-aging drugs.
6. Mitochondrial dysfunction
This cell needs the energy to sustain all its cellular functions and chemical activities. This energy production takes place in the mitochondria, by utilizing the oxygen we breathe in. however this process sometimes produces free radicals so-called reactive oxygen species, or ROS for short.
4. Loss of proteostasis
The DNA of our cells contains the instructions for all cellular functions. However, DNA does not carry out these functions. Instead, our DNA contains the information for the production of proteins and enzymes that take over tasks and control processes within the cell. Proteins and enzymes control all chemical reactions in the cells and also give the cell its structure. To carry out such functions, proteins must be folded precisely into a very specific structure, similar to origami. The term protein homeostasis, or proteostasis for short, describes the maintenance of the form and abundance of all proteins.
As we age, proteins get increasingly damaged due to normal cellular processes, which also influence their shape and folding. Not only can misfolded proteins no longer perform their normal work, but they also tend to clump together, which can have a toxic effect on the cell. For example, Alzheimer's disease is an age-related disease caused by misfolded proteins. Because the maintenance of proteostasis is so important the cell has several mechanisms to control the folding and quality of proteins. Our cells not only have mechanisms to repair and refuel distribute proteins there are also mechanisms to degrade such proteins and replace them with new ones. Misfolded and damaged proteins, for example, can be degraded by a recycling process known as autophagy.
Many study results suggest an important role of proteostasis in aging: misfolded proteins increase with age; several age-related diseases such as Alzheimer's are associated with misfolded proteins; improving protein quality control increases the lifespan of mice and other model organisms.
5. Deregulated nutrient-sensing
When sufficient nutrients are available, cells and tissues store energy and grow, whereas when nutrients are deficient, mechanisms for homeostasis and repair are activated. When cells are constantly exposed to excess nutrients the cellular mechanisms that recognize nutrients become less sensitive. This process also occurs during aging and causes cells to fail to respond properly to the signals that normally regulate energy production, cell growth, and other important cellular functions. Many studies have investigated the effect of food intake or the perception of food on the aging process- for example, when the overall food intake is reduced when the body is tricked to believe it has less food the insulin signaling pathway is switched off, and the lifespan increases in fruit flies. The result of many studies is that reduced food intake improves health and increases the lifespan of a wide range of animals.
Two nutrient-sensing pathways are especially the focus of aging research: The insulin/insulin growth factor (IGF) and the Target of Rapamycin (TOR) pathway together constitute a key nutrient-sensing network within the cell. Genetical or pharmacological inhibition of the insulin/TOR network extends the lifespan in a wide range of animals, making it a prime target for the development of anti-aging drugs.
6. Mitochondrial dysfunction
This cell needs the energy to sustain all its cellular functions and chemical activities. This energy production takes place in the mitochondria, by utilizing the oxygen we breathe in. however this process sometimes produces free radicals so-called reactive oxygen species, or ROS for short.
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