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Stop focusing on the damn Norwood scale and hairloss pattern already.. Chimps go bald as well. Everything starts in the powerhouse of the cells.
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Reversing Wrinkled Skin And Hair Loss In Mice By Restoring Mitochondrial Function.
- Thread starter Squeegee 2.0
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Mitochondrial Molecular Dysfunction
Mitochondrial dysfunction arises from an inadequate number of mitochondria, an inability to provide necessary substrates to mitochondria, or a dysfunction in their electron transport and ATP-synthesis machinery. The number and functional status of mitochondria in a cell can be changed by (1) fusion of partially dysfunctional mitochondria and mixing of their undamaged components to improve overall function, (2) the generation of entirely new mitochondria (fission), and (3) the removal and complete degradation of dysfunctional mitochondria (mitophagy).33 These events are controlled by complex cellular processes that sense the deterioration of mitochondria, such as the depolarization of mitochondrial membranes or the activation of certain transcription pathways.34,35
The ability of cells to produce almost all high-energy molecules such as ATP is directly related to the ability of mitochondria to (1) convert the energy of metabolites to reduced nicotinamide adenine dinucleotide (NADH) and (2) transfer electrons from NADH to the electron transport chain and eventually to molecular oxygen while pumping protons from the mitochondrial matrix across the inner mitochondrial membrane to the intermembrane space. This process creates a transmembrane proton gradient (Δp) and an electrochemical gradient (Δψm) across the mitochondrial inner membrane.36,37 The transmembrane potential created by the proton gradient then uses ATP synthase to flow protons back across the inner mitochondrial membrane and employs the energy from this process to drive adenosine diphosphate (ADP) phosphorylation to ATP.36,38
A consequence of the electron transport process is the production of reactive oxygen species (ROS), highly reactive free radicals that are produced as a by-product of oxidative phosphorylation. The main sources of ROS and the related reactive nitrogen species (RNS) are mitochondria, and these free radicals can damage cellular lipids, proteins, and DNA.39–41 However, some mechanisms can neutralize ROS/RNS; dismutase enzymes and antioxidants can control excess amounts of ROS/RNS.42,43 In addition to creation of ROS/RNS, the electron transport process can induce uncoupling proteins, resulting in a controlled leak of protons back across the proton gradient of the inner mitochondrial membrane into the mitochondrial matrix.36,37 This leak results in reduced ATP production while it still consumes excess oxygen.43
In the presence of a controlled proton leak, excess oxygen consumption and the resulting ROS production can result in inappropriate damage to mitochondrial membrane lipids,41,42 such as the very ROS/RNS-sensitive cardiolipin, an inner mitochondrial membrane phospholipid.44 Oxidative damage to the cardiolipin and other membrane phospholipids in the inner mitochondrial membrane can result in increased proton and ion leakage back across the inner membrane into the mitochondrial matrix and partial loss of the electrochemical gradient. Cardiolipin is also an important component of the electron transport chain, providing stability for the cytochrome/enzyme complexes in the inner mitochondrial membrane.44 Once adversely damaged by ROS/RNS, oxidized cardiolipin instigates loss of electron-transport function.45
Cellular antioxidant defenses usually maintain ROS/RNS levels at concentrations that prevent excess oxidation of cellular molecules.46–48 Cellular antioxidant defenses that are endogenous are mediated by glutathione peroxidase, catalase, and superoxide dismutase, among other enzymes.48,49 Also, some dietary antioxidants with a low molecular weight can affect antioxidant status.50,51 Some of these dietary antioxidants have been used as natural preventive agents to shift the excess concentrations of oxidative molecules down to physiological levels that can be maintained by endogenous antioxidant systems.52
Mitochondrial dysfunction arises from an inadequate number of mitochondria, an inability to provide necessary substrates to mitochondria, or a dysfunction in their electron transport and ATP-synthesis machinery. The number and functional status of mitochondria in a cell can be changed by (1) fusion of partially dysfunctional mitochondria and mixing of their undamaged components to improve overall function, (2) the generation of entirely new mitochondria (fission), and (3) the removal and complete degradation of dysfunctional mitochondria (mitophagy).33 These events are controlled by complex cellular processes that sense the deterioration of mitochondria, such as the depolarization of mitochondrial membranes or the activation of certain transcription pathways.34,35
The ability of cells to produce almost all high-energy molecules such as ATP is directly related to the ability of mitochondria to (1) convert the energy of metabolites to reduced nicotinamide adenine dinucleotide (NADH) and (2) transfer electrons from NADH to the electron transport chain and eventually to molecular oxygen while pumping protons from the mitochondrial matrix across the inner mitochondrial membrane to the intermembrane space. This process creates a transmembrane proton gradient (Δp) and an electrochemical gradient (Δψm) across the mitochondrial inner membrane.36,37 The transmembrane potential created by the proton gradient then uses ATP synthase to flow protons back across the inner mitochondrial membrane and employs the energy from this process to drive adenosine diphosphate (ADP) phosphorylation to ATP.36,38
A consequence of the electron transport process is the production of reactive oxygen species (ROS), highly reactive free radicals that are produced as a by-product of oxidative phosphorylation. The main sources of ROS and the related reactive nitrogen species (RNS) are mitochondria, and these free radicals can damage cellular lipids, proteins, and DNA.39–41 However, some mechanisms can neutralize ROS/RNS; dismutase enzymes and antioxidants can control excess amounts of ROS/RNS.42,43 In addition to creation of ROS/RNS, the electron transport process can induce uncoupling proteins, resulting in a controlled leak of protons back across the proton gradient of the inner mitochondrial membrane into the mitochondrial matrix.36,37 This leak results in reduced ATP production while it still consumes excess oxygen.43
In the presence of a controlled proton leak, excess oxygen consumption and the resulting ROS production can result in inappropriate damage to mitochondrial membrane lipids,41,42 such as the very ROS/RNS-sensitive cardiolipin, an inner mitochondrial membrane phospholipid.44 Oxidative damage to the cardiolipin and other membrane phospholipids in the inner mitochondrial membrane can result in increased proton and ion leakage back across the inner membrane into the mitochondrial matrix and partial loss of the electrochemical gradient. Cardiolipin is also an important component of the electron transport chain, providing stability for the cytochrome/enzyme complexes in the inner mitochondrial membrane.44 Once adversely damaged by ROS/RNS, oxidized cardiolipin instigates loss of electron-transport function.45
Cellular antioxidant defenses usually maintain ROS/RNS levels at concentrations that prevent excess oxidation of cellular molecules.46–48 Cellular antioxidant defenses that are endogenous are mediated by glutathione peroxidase, catalase, and superoxide dismutase, among other enzymes.48,49 Also, some dietary antioxidants with a low molecular weight can affect antioxidant status.50,51 Some of these dietary antioxidants have been used as natural preventive agents to shift the excess concentrations of oxidative molecules down to physiological levels that can be maintained by endogenous antioxidant systems.52
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MitoQ is great, you need to take at least 20mg a day for results.
That study is pretty impressive:
Novel antioxidant makes old blood vessels seem young again
Older adults who take a novel antioxidant that specifically targets cellular powerhouses, or mitochondria, see age-related vascular changes reverse by the equivalent of 15 to 20 years within six weeks, according to new University of Colorado Boulder research.
https://www.sciencedaily.com/releases/2018/04/180419141523.htm
i'm a doctor, i take mitoq 10mg(2caps morning) for like 3 years already, EOD or when i remember, 80% of time after i take 2 pills 2-3hours later a receive headache and drowsiness...so 20mg will be not good for me....
and i saw all this studies.... in my case wrinkles(33-36y.o+ also after several month on minoxidil) not goes away even on mitoq+tam818+skq1....and my grandmother died of chronic heart insufficiency/copd after 2 years on mitoq+tam818+skq1. also in case of grandmother mitoq not stop septic cystitis!!! but there are articles where it miracly cured sepsis....
i also like to point! no hair regrowth and no better vision, regress of vision goes slowly on.
deuterium depleted water -4-5 years on it, great for exercises and calm but no hair regrowth/no better vision/no regress in wrinkles.....
in my case and my grandmother case i clearly saw effect after NAD+ in life extension or similar Basis... but only on physical/energy aspects, not on hair....
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We all want a simple binary answer to aging, the magic pill but it is more complicated than this...
I personally takes mitoQ 20mg + Pyrroloquinoline quinone 40mg everyday.
As males we should all take the linus Pauling protocol .. High dose of Vitamin C + L-lysine L-proline to prevents the LP(a) to stick to the arteries..
Also high dose of Vitamin K2.. Mk7 or MK4 is a must to prevents calcification and stiffness of arteries.
Cool study on K2..
Press Release 12/19/2013: MenaQ7® Vitamin K2 Supplementation May Benefit Dialysis Patients by Inhibiting Vascular Calcification
NattoPharma has announced the publication of a new study performed in collaboration with OLV Hospital, Belgium, St. Jan Hospital, Belgium and VitaK, University of Maastricht, the Netherlands, published by Nephrology Dialysis Transplantation. doi: 10.1093/ndt/gft464 .
Haemodialysis patients suffer from early and accelerated vascular calcification which is predictive for cardiovascular disease and all-cause mortality in this population. The vitamin K-dependent matrix GLA protein (MGP) is one of the most potent inhibitors of vascular calcification, and Dialysis patients have high levels of the inactive form, or undercarboxylated MGP. Thus, this patient population may benefit from Vitamin K2 as menaquinone-7 supplementation to activate MGP and prevent vascular calcification.
“Vascular calcification is a significant problem for dialysis patients. In fact, without transplant, it could be considered a terminal condition for this population. Our hope is that Vitamin K2 supplementation may slow this process and improve not only the quality, but quantity of life for these patents, ” says investigator An S. De Vriese of the Division of Nephrology and Infectious Diseases, AZ St.-Jan Hospital.
Previously vascular calcification was considered to be an entirely passive process. However it is now widely recognized that it is an actively regulated process implying death and damage of vascular smooth muscle cells (VSMCs) and transformation of these cells into osteoblast-like cells (bone producing cells). Deficiencies in calcification inhibitors – where carboxylated (active) MGP is one of the strongest, and where Vitamin K2 activates MGP – are major explanations for calcification in the vessel wall.
To determine the optimal dose of Vitamin K2 as menaquinone-7 (MK-7) for MGP activation, 200 chronic haemodialysis patients were recruited to randomly receive 360, 720 or 1080 μg of MK-7 (MenaQ7 ® ) three times weekly for 8 weeks. Vitamin K1 (phylliquone) and K2 from food sources was estimated based on a detailed questionnaire. Vitamin K1 was not associated with MGP activity. MK-7 levels in the patient groups were correlated with the reduction in the concentrations of inactive (undercarboxylated) MGP after 8 weeks. The reductions were 17, 33 and 46% in the respective K2 groups.
“This study demonstrates the benefits of vitamin K2 in the activation of MGP, a potent inhibitor of vascular calcification, ” says Hogne Vik, CEO of NattoPharma. “While dialysis patients are significantly prone to calcification, we know from population- and in vivo studies, that improving vitamin K2 status results in less arterial calcification and improved cardiovascular outcomes. A three-year interventional study with MenaQ7® actually showed an improvement in arterial elasticity in healthy postmenopausal women.”
The authors concluded that vitamin K2 supplementation may be a novel approach to prevent vascular calcifications in chronic haemodialysis patients.
It seems than nitric oxide plays a major factor in aging... Nitric Oxide controls Mitochondria biogenesis and Nitric Oxide is the cellular signal that tells stem cells to mobilize to repair damage. You can find many studies if you google Nitric Oxide and aging..
Getting enough CoQ10 in your diet not only preserves nitric oxide but can also help improve athletic performance, prevent migraines and promote heart health (18Trusted Source, 19Trusted Source, 20Trusted Source).
Vitamin K 2-MK-7 Improves Nitric Oxide-Dependent Endothelial Function in ApoE/LDLR -/- Mice
https://pubmed.ncbi.nlm.nih.gov/31421222/
Also
Study shows blood cells need nitric oxide to deliver oxygen..
https://www.medicalnewstoday.com/articles/292292
There is a cool product that just came out called Pneuma that delivers nitric oxide transdermally.
https://www.pneumanitricoxide.com/
Fun fact.. Topical Nitric Oxide is a first class local Anti androgen:
http://www.novan.com/files/8613/7398/9326/Topical_nitric_oxide_local_androgen_therapy.pdf
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inmyhead
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Should we take this stuff topically, lol? Ah, just checked. This stuff is ultra expensive, haha
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LOL I know! Still wanna try it.
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Cool link on NO and inflammation
Nitric Oxide: A Key Understanding of Inflammation
https://nutritiongenome.com/nitric-oxide-a-key-understanding-of-inflammation/
Nitric Oxide: A Key Understanding of Inflammation
https://nutritiongenome.com/nitric-oxide-a-key-understanding-of-inflammation/
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Cool Graph on NO..
inmyhead
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Perhaps anyone managed to find natural Nitric Oxide agonists?
Seems that l-arginine is precursor to NO.
Also, this article is quite interesting regarding NO agonists.
https://www.hindawi.com/journals/omcl/2016/7364138/
Seems that l-arginine is precursor to NO.
Also, this article is quite interesting regarding NO agonists.
https://www.hindawi.com/journals/omcl/2016/7364138/
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great information.
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I can only imagine what would happen if that rodent escaped with its Androgenetic Alopecia follicles in the wild. Would we start seeing bald rats in NYC?