SUBJ: Wise nutrition speeds recovery from surgery
SUBtitle: Taking mito-C may be brain saving
Despite an arm in a sling, I am rapidly becoming functional. There is so much news that I find worth sharing. Please just skim headlines. Go to my website where you can do a key word search for your particular concern.
Links for new readers: 1) One Day in Roc’s Life: 46 resolutions to prolong health span 2) Recent important nutrition news. 3) A contribution to this newsletter is healthier and less expensive than your multivitamin. Donation link:Nutrition Newsletter
SHORT NOTES:
- I had shoulder surgery to repair a badly ripped collar bone muscle. I took BCAAs and ate non-inflammatory diet and serious pain ended in 4 days instead of 2-3 weeks expected.
- Why taking mito-C may be brain saving: Protein aggregates are the major cause of neuronal death in many neurodegenerative disorders.
- These drugs can cause memory loss!
- Not taking rapamycin may be as dangerous as smoking. (But I do not take it as my physician is doubtflul to prescribe it.)
- why natural killer (NK) cells in the immune system lose their ability to fight cancer and how to return them to normal function.
- what makes the intestine so effective at absorbing nutrients and protecting the body from infection.
- : “Stay Healthy, Anti-Aging Tech is Coming”. Podcast.
- LPI Green Tea symposium, Aug 28, Green tea lowers blood glucose levels, improves liver, adipose lipolysis, insulin signaling, microbiota, metabolome – improves beyond a low fat diet. Liver disease affects 100 million Americans, 76% of obese adults, (Mito-C contains the active ingredient EGCG)
- Higher morning and daylight exposure levels were associated with various positive objective and subjective sleep measures in professional team sport athletes
- Our results uncovered a micronutrient-based strategy for alleviating sleep disorder symptoms, esp iron, vit B12, D, sodium.
- freezing breast cancer tumors reduced recurrence rate to 0.26%.
- How cells coordinate activity such as tissue repair.
- Global aging is rapidly accelerating, which significantly influences the health systems worldwide. Frailty emerges as the most conspicuous hallmark of aging which leads to adverse outcomes such as falls, delirium, and disability.
- Memory rebalancing requires counterbalancing to consolidate memories. Sleep is not just a time for the body to rest but also for the mind to solidify memories.
- Restoring hippocampal glucose metabolism rescues cognition across Alzheimer’s disease pathologies and could be a promising therapeutic approach to prevent or delay disease progression.
- Switching off autoimmunity: The broad success of anti-CD40L therapy is due to its pivotal function in the initiation and propagation of many of the inflammatory pathways
- “Telomere stabilization by metformin mitigates the progression of atherosclerosis.
- “Telomere dysfunction is a well-known molecular trigger of senescence and has been associated with various age-related diseases, including atherosclerosis. metformin inhibits vascular smooth muscle cell (VSMC) degeneration
- Climate science has penetrated the pentagon. It’s now cheaper to save the world than to destroy it.
- There is now a book about fatty15. My readers differ on whether it is as wonderful as I believe.
LONG NOTES:
I had shoulder surgery to repair a badly ripped collar bone muscle. I investigated how much BCAAs I should take to increase the repair rate. My surgeon said to expect 2 to 3 weeks of severe pain requiring oxycodone every 4 hrs. I followed his advice, but also took 1g BCAAs uith every dose, and ate tuna or salmon (anti-inflammatory vs red meat). Serious pain ended for me in 3 days!!! I now looked at the optimum dose. It was recently recommended that about 200 mg.kg−1.day−1 (14 g/day for a person weighing 150 lbs) over 10 days should be ingested to attenuate exercise-induced muscle damage [50]. So instead of 1g each 4 hrs, I will now take 2 g.
Science 10/30, pg 947 – Why taking mito-C may be brain saving: Protein aggregates are the major cause of neuronal death in many neurodegenerative disorders. However, in the nonaggregate form, the same proteins play important physiological roles. Benn et al. developed a strategy to target intracellular protein aggregates while sparing the monomeric form. Exploiting the clustering-dependent activation of TRIM21, the authors generated degraders combining the RING domain of TRIM21 with a target-specific nanobody. As proof of principle, they targeted tau aggregates in vitro and in vivo. In a tau-transgenic mouse model, the degraders, which were delivered through AAV vectors, reduced tau pathology, suggesting that this approach might be effective for selectively and safely removing protein aggregates.
AARP: These drugs can cause memory loss! For a long time, doctors dismissed forgetfulness, brain fog and mental confusion as normal parts of aging. But scientists now know that memory loss as you get older is by no means inevitable. In fact, routine memory, skills and knowledge may even improve with age, according to the Centers for Disease Control and Prevention.
2024 update on rapamycin– from GRG discussion-Rapamycin is a bit of an odd exception here among supplements. The primary reason to cycle it (taking it e.g. once a week instead of daily) is because that’s the only reasonable way to prevent the excessive mTORC2 inhibition which is responsible for many of the negative effects of rapamycin when taken too frequently. Dosage of 5mg/week seems common choice. Not taking rapamycin may be as dangerous as smoking. (But I do not take it as my physician is doubtflul to prescribe it.)
Rejuvenating cancer-killing cells. Researchers at Israel’s Bar-Ilan University have discovered why natural killer (NK) cells in the immune system lose their ability to fight cancer. They introduced nanoparticles that silenced the enzyme DGK alpha and the transcription factor Egr2, returning the NK cells to normal function.
The secrets of nutrient absorption. Scientists from Israel’s Weizmann Institute and Sheba Medical Center have compiled the first detailed map of the various activity areas in the human small intestine, revealing what makes it so effective at absorbing nutrients and protecting the body from infection.
Peter Diamandis: “Stay Healthy, Anti-Aging Tech is Coming”. Podcast: To put it as concisely as possible, Peter is a serial entrepreneur and investor in several fields, from commercial space flight to longevity biotech; a visionary speaker and author of several best-selling books, including Abundance, The Future is Faster Than You Think, and Life Force; creator of the world-famous XPRIZEs
LPI Green Tea symposium, Aug 28, Green tea, Up to 1,000 mg catechins dose, lowers blood glucose levels, improves liver, adipose lipolysis, insulin signaling, microbiota, metabolome – improves beyond a low fat diet. Liver disease affects 100 million Americans, 76% of obese adults, leads to liver fibrosis, cancer, cirrhosis, and death from cardiovascular disease.. Green tea is anti-inflammatory, reduces liver disease, blocks endotoxins. Have a green. Tea gummy 3x per day gives 5 cups per day. Reasonable intake for benefits is 3-5 cups/day. Contains EGCG 65%, also EGC, ECG, EC, and CAT. (Mito-C contains the active ingredient EGCG)
Higher morning and daylight exposure levels were associated with various positive objective and subjective sleep measures in professional team sport athletes, supporting the need for education on optimising light exposure to improve circadian function, sleep, and health. Healthy Sleep Pattern, Metabolic Diseases, and Risk of Stroke: The Kailuan Cohort Study. Adherence to healthy sleep pattern was associated with a lower risk of stroke, and the favorable association was partially mediated by metabolic diseases.
Our results uncovered a micronutrient-based strategy for alleviating sleep disorder symptoms. Causal Relationship Between Micronutrient and Sleep Disorder – Our results suggested that 8 genetically predicted micronutrients participated in sleep disorders, including liver iron (L-iron) and iron in sleeping too much, spleen iron (S-iron) in sleeplessness/insomnia, trouble falling or staying asleep, sleep duration (undersleepers) and nonorganic sleeping disorders, iron metabolism disorder (IMD) and vitamin B12 deficiency anaemia (VB12DA) in narcolepsy, urine sodium (uNa) in narcolepsy, sleep apnea syndrome and sleep disorder, vitamin D (VD) in sleep duration (oversleepers), 25-Hydroxyvitamin D (25(OH)D) in trouble falling or staying asleep.
Almost no re-ocurrence after freezing tumors. (TY Atid-EDI) Israel’s IceCure Medical (see here previously) presented the results of its three clinical studies using ProSense to treat breast cancer. Of the 389 patients treated, The ipsilateral breast tumor recurrence rate was 0.26%, resulting in a 99.74% recurrence-free rate.
How cells coordinate activity. Researchers from Israel’s Ben Gurion and Canada’s British Columbia universities have discovered the pathway for cells to coordinate activity such as tissue repair. 3 to 8 local cells send Calcium ion signals to “hot-spots” inside lymph nodes, which then trigger actions and send signals back.
Research Progress on Frailty in Elderly People. Global aging is rapidly accelerating, which significantly influences the health systems worldwide. Frailty emerges as the most conspicuous hallmark of aging, imposing novel global health challenges. Characterized by a multifaceted decline across physiological system, frailty diminishes an individual’s capacity to maintain equilibrium in the presence of stressors, which leads to adverse outcomes such as falls, delirium, and disability.
Science 16 Aug-pg 710-Memory rebalancing requires counterbalancing to consolidate memories. Sleep is not just a time for the body to rest but also for the mind to solidify memories. During the non-rapid eye movement (NREM) phase of sleep, neurons in the hippocampus display short bursts of firing activity called sharp-wave ripples (SWRs), which is essential for memory consolidation (1). How the brain rebalances its activity after these bursts remains unclear. On page 738 of this issue, Karaba et al. (2) report a new type of neuron activity in the rodent hippocampus that is characterized by long episodes of neuronal firing called barrage of action potentials (BARR). BARRs counteract SWRs to suppress the increased activity of neurons involved in learning during NREM sleep (2). The findings demonstrate that BARRs are crucial for memory consolidation by modulating memory reactivation and help to reconcile different theories on the role of sleep for memory formation.
23 AUG PG 826- Restoring hippocampal glucose metabolism rescues cognition across Alzheimer’s disease pathologies. Alzheimer’s disease (AD) is a neurodegenerative disorder with a complex and multifactorial etiology. In addition to the aggregation of amyloid-β (Aβ) peptide and tau protein, metabolic dysfunction is often described as both a cause and consequence of AD. The brain is energetically demanding, typically consuming ~20 to 25% of available glucose to maintain normal brain physiology. Therefore, any change in glucose availability, uptake, or use can be deleterious to healthy brain function. AD has a long presymptomatic period in which shifts in metabolism appear to be driven by glia (1–3) as well as neurons (4). On page 842 of this issue, Minhas et al. (5) demonstrate that inhibition of the kynurenine (KYN) pathway rescues astrocyte metabolism to restore synaptic activity and spatial memory in preclinical mouse models of amyloid and tau pathology. Targeting glial metabolism early in the Alzheimer’s cascade could be a promising therapeutic approach to prevent or delay disease progression.
23 AUG PG 827-Switching off autoimmunity: Discovered 30 years ago, CD40L antagonists are proving to be powerful autoimmune drugs. The ability to selectively switch off adaptive immunity presents a remarkable opportunity for therapeutic intervention in autoimmune disease. There is one molecule whose targeting will allow such unbridled control over disease, the cytokine CD40 ligand (CD40L). Transiently expressed on activated T cells, CD40L is essential for the development of antibody- and cell-mediated immune responses. For over 30 years, efforts to develop safe and effective therapeutic agents to disable the function of CD40L have been sought. Finally, that battle has been won. The broad success of anti-CD40L therapy is due to its pivotal function in the initiation and propagation of many of the inflammatory pathways that are central to the development of autoimmunity and mediation of graft rejection.
“Telomere stabilization by metformin mitigates the progression
of atherosclerosis via the AMPK-dependent p-PGC-1α pathway”. These observations show that the enhancement of telomere function by metformin is involved in specific signaling pathways during the progression of atherosclerosis. These findings suggest that telomere stabilization by metformin via the AMPK/p-PGC-1α pathway might provide a strategy for developing therapeutics against vascular diseases such as atherosclerosis.
“Telomere dysfunction is a well-known molecular trigger of senescence and has been associated with various age-related diseases, including atherosclerosis. However, the mechanisms involved have not yet been elucidated, and the extent to which telomeres contribute to
atherosclerosis is unknown. Therefore, we investigated the mechanism of
metformin-induced telomere stabilization and the ability of metformin to
inhibit vascular smooth muscle cell (VSMC) senescence caused by advanced
atherosclerosis. The present study revealed that metformin inhibited the
phenotypes of atherosclerosis and senescence in VSMCs (vascular smooth muscle cell). Metformin
increased the phosphorylation of AMPK-dependent PGC-1α and thus
increased telomerase activity and the protein level of TERT in
OA-treated VSMCs. Mechanistically, the phosphorylation of AMPK and
PGC-1α by metformin not only enhanced telomere function but also
increased the protein level of TERT, whereas TERT knockdown accelerated
the development of atherosclerosis and senescent phenotypes in
OA-treated VSMCs regardless of metformin treatment. Furthermore, the in
vivo results showed that metformin attenuated the formation of
atherosclerotic plaque markers in the aortas of HFD-fed ApoE KO mice.
Although metformin did not reduce plaque size, it inhibited the
phosphorylation of the AMPK/PGC-1α/TERT signaling cascade, which is
associated with the maintenance and progression of plaque formation, in
HFD-fed ApoE KO mice. Accordingly, metformin inhibited
atherosclerosis-associated phenotypes in vitro and in vivo. These
observations show that the enhancement of telomere function by metformin
is involved in specific signaling pathways during the progression of
atherosclerosis. These findings suggest that telomere stabilization by
metformin via the AMPK/p-PGC-1α pathway might provide a strategy for
developing therapeutics against vascular diseases such as
atherosclerosis.
Science Aug 30, pg 940 – Climate science has penetrated the pentagon. Despite Republican opposition in the House, there is a deputy undersecretary for environmental defense. Podcast: Climate capitalism-It’s now cheaper to save the world than to destroy it.
There is now a book about fatty15. My readers differ on whether it is as wonderful as I believe.