Use Of Thermobalancing Therapy In Ageing Male With Benign Prostatic Hyperplasia With A Focus On Etio

OtyMac

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Oral minoxidil restores elastin in even aged arteries. Goal: restore elastin or find elastase inhibitors.

Mice dosage: 120 mg/L






"Therefore, we have studied the effect of a 10-week chronic oral treatment with minoxidil (120 mg/L in drinking water) on the aortic structure and function in aged 24-month-old mice. Minoxidil treatment increased tropoelastin, fibulin-5, and lysyl-oxidase messenger RNA levels, reinduced a moderate expression of elastin, and lowered the levels of AGE-related molecules. This was accompanied by the formation of newly synthesized elastic fibers, which had diverse orientations in the wall. A decrease in the glycation capacity of aortic elastin was also produced by minoxidil treatment. The ascending aorta also underwent a minoxidil-induced increase in diameter and decrease in wall thickness, which partly reversed the age-associated thickening and returned the wall thickness value and strain-stress relation closer to those of younger adult animals. In conclusion, our results suggest that minoxidil presents an interesting potential for arterial remodeling in an antiaging perspective, even when treating already aged animals."
 
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pegasus2

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"The decreases found in partial
pressure of oxygen and blood flow are ~ 40 and 62%, respectively. However, it is unlikely that these decreases in partial pressure of oxygen or blood flow are the root cause of hair loss. Only a fraction of the blood flow to the skin is used for metabolic needs and the rest is for temperature regulation.Furthermore, even for metabolically very active cells, the critical partial pressure of oxygen for impairment of mitochondrial function is < 5 mmHg and about 0.1 mmHg for hypoxic cell death"

 

OtyMac

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"The decreases found in partial
pressure of oxygen and blood flow are ~ 40 and 62%, respectively. However, it is unlikely that these decreases in partial pressure of oxygen or blood flow are the root cause of hair loss. Only a fraction of the blood flow to the skin is used for metabolic needs and the rest is for temperature regulation.Furthermore, even for metabolically very active cells, the critical partial pressure of oxygen for impairment of mitochondrial function is < 5 mmHg and about 0.1 mmHg for hypoxic cell death"


This microcirculation situation is robust in many domains and not overfit to just find a model for hairloss. Microcirculation problems are evident everywhere and are likely a major driver of aging. BPH, Parkinsons, bone loss all have microcirculation problems at the core.

Look at the malocclusion study Poppyburner posted that I linked to. 100 out of 100 had hairloss BECAUSE the superior temporal artery was being blocked by some jaw alignment problem. Also, the girl with the disease that blocked the superior temporal artery had bitemporal and frontal balding and only 16 years old.

We have numerous treatments to suggest reversing some aspects of vascular aging will reverse hair loss. Microneedling, PRP injections, botox, scalp massages, LLLT, every major drug that grows any hair deals with microcirculation or reversing vascular stiffness.(estrogens, minoxidil, verapamil, sprio, IVIG, IL17 inhibitors). Any drug that inhibits NLRP3 inflammasome will also be of benefit since inflammation is either causal or strong contributor to vascular stiffness also.

PRP injections are interesting because the results last 5 years past the injection and strongly hint that something structurally outside the hair follicle was changed. Microneedling results last at least 12 months past end of treatment, again same conclusion.


Platelet degranulation allows the release of a large amount of soluble mediators, is an essential step for wound healing initiation, and stimulates clotting, and angiogenesis. The latter process is one of the most critical biological events observed during tissue repair, increasing the growth of blood vessels in the maturing wound

There are a hundred more videos like this.
 
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OtyMac

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Originally posted by Squeegee but I wanted to get this into the microcirculation thread also.


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External Counterpulsation (ECP) Therapy​


Many commented on the “remarkable” or “extreme” improvements with ECP therapy, with comments such as, “God gave man the ability to grow collateral vessels and capillaries. EECP merely harnesses this God-given ability. A surgeon can-not do this. A drug cannot do this.” And similarly, “I believe it to be a miracle.” Providers commented, “You not only improve or stop their angina, the great side effects from this treatment tremendously improve our patients quality of life. Just a few are, improve or stop having SOB, improved exercise tolerance (patient can split & stack wood with diagnosis of angina & CHF after receiving 35 treatments), lowers blood pressure (some have had meds reduced or stopped), improved kidney functions, better vision, can sleep better at nite, improve speech in a patient who, had also had a CVA, helped ED [erectile dysfunction], hair growth & one 86 y/o patient resumed driving after 1 ½ years.” Another commenter included improvement in diabetes, glaucoma, macular degeneration, and COPD. One commenter referred to the benefit as, “Lazarus like recoveries.” The expression of these personal observations and feelings is appreciated but can be influenced by many different variables, so it is difficult to sort out the possible benefits from the device. The clinical evidence does not suggest such dramatic benefit



Several mechanisms, including the promotion of collateral blood flow, improvement in endothelial function, reduction in inflammation, and the production of peripheral training effects similar to exercise, are thought to be responsible for the clinical benefits of this therapy




Many hemodynamic results can be seen in patients under EECP treatment. Some of the mechanisms accounting for both cardiac and peripheral effects are as follows.

EECP reduces cardiac demand via reduction in afterload and also helps the collateralization of myocardium through arteriogenesis and angiogenesis.38 There is also increased endothelial function and vasodilation through diastolic aug mentation of blood flow and endothelial shear stress, which may result in increased levels of prostacyclin, nitric oxide, vascular endothelial growth factor, and β fibroblast growth factor and a reduction in endothelin-1 and brain natriuretic peptide concentrations.39,40

EECP increases blood flow, not only to the heart but also throughout the body; for example, an 88% increase in infra-renal abdominal aorta, a 144% surge in internal iliac blood flow, and a significant increase in the perfusion of the brain were reported by Werner et al,41 Also, it can possibly enhance penile arterial vasodilation and improve erection by increasing nitric oxide production.11,29

EECP therapy structure includes three groups of pneumatic cuffs attached to the calves, lower and upper thighs.38 Inflation of the cuffs is triggered consecutively at the beginning of diastole resulting in a diastolic rise of blood flow, increase in venous return, cardiac output, and coronary bloodstream. At the termination of diastole, the cuff is deflated, leading to a decrease in vascular resistance, left ventricular unloading, and growing cardiac output.11
 

OtyMac

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DISCUSSION Our study revealed clear evidence of abnormal excessive growth of hair along lower limbs. This hairy change was clearly observed after treatment with spica immobilization. Probably local heat produced, affects the vascularity of the skin which leads to hair growth in an abnormal manner.

Similar to our findings(3) , Dorothea mentioned in his study, common type of circular plaster cast was applied, and over the next 7 weeks there were cast changes. Following removal of the cast a localized area of long, coarse dark hair extended almost to the knuckles on the dorsal aspect of the hand; the hair differed in both texture and pattern of growth from that over the right wrist(3) .

Because of its transient nature, aggressive investigations are definitely not indicated.

Heat and cutaneous hyperemia are acknowledged by dermatologists as definite stimulants of the hair follicle.

Although regional blood flow to a long bone is increased following a fracture, cutaneous hyperemia is definitely a transient phenomenon and may be responsible for the transient hypertrichosis

. However because this condition is transitory reaction, hormonal studies to date have not been confirmatory. A suggestion that hypertrichosis may be related to reflex sympathetic dystrophy is also not substantiated in the orthopedic literature (4-10) . Gunilla (11) explained that, mediators of paracrine and autocrine interactions trigger intracellular signals that are transmitted to the nucleus, where the activation of specific transcription factors establish and propagate proper epithelialmesenchymal interactions help in growth of hair in the skin. In conclusion, the hypertrichosis follow prolong immobilization is transient, physicians should be aware of its benign nature as it relates to cast immobilization.
 
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