Bald scalp in men with androgenetic alopecia retains hair fo

[squeegee]

Effects of interleukins, colony-stimulating factor and tumour necrosis factor on human hair follicle growth in vitro: a possible role for interleukin-1 and tumour necrosis factor-alpha in alopecia areata.
Philpott MP, Sanders DA, Bowen J, Kealey T.
Source

Department of Clinical Biochemistry, University of Cambridge, Addenbrookes Hospital, London, U.K.
Abstract

The immune system may be involved in the regulation of normal hair follicle growth as well as in the pathogenesis of some hair diseases. Immunomodulatory cytokines not only act as mediators of immunity and inflammation but also regulate cell proliferation and differentiation and, as such, may play an important part in regulating hair growth. We have investigated the effects of a number of interleukins (IL), colony stimulating factors and tumour necrosis factors (TNF) on hair follicle growth in vitro. Dose-response studies showed that IL-1 alpha, IL-1 beta and TNF-alpha were potent inhibitors of hair follicle growth. The histology of hair follicles maintained with inhibitory doses of IL-1 alpha, IL-1 beta and TNF-alpha showed similar changes in hair follicle morphology, resulting in the formation of dystrophic anagen hair follicles. These changes in histology were characterized by the condensation and distortion of the dermal papilla, marked vacuolation of the hair follicle matrix, abnormal keratinization of the follicle bulb and inner root sheath, disruption of follicular melanocytes and the presence of melanin granules within the dermal papilla. Moreover, these changes in hair follicle morphology are similar to those reported in alopecia areata and suggest that IL-1 alpha, IL-1 beta and TNF-alpha may play an important part in the pathophysiology of inflammatory hair disease.

 

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Dkk-1: Upsetting the Balance in Rheumatoid Arthritis

http://www.rndsystems.com/cb_detail_obj ... _DKK1.aspx

 

[optimus prime]

squeegee, squeegee, squeegee.

You are on so many things how do you know if it works?

Also, when are you going to bring back the hotdog avatar?

 

[squeegee]

squeegee, squeegee, squeegee.

You are on so many things how do you know if it works?

Also, when are you going to bring back the hotdog avatar?

Because all this crap is to kill inflammation at every levels without being unsafe.. BTW.. the dog is back in business! unk: Thanks for the reminder..again Optimus! I don't believe in the old saying of being sensitive to DHT. There is big time inflammation..this is why DHT is acting this way.

http://en.wikipedia.org/wiki/Endothelial_dysfunction
Endothelial dysfunction is a systemic pathological state of the endothelium (the inner lining of our blood vessels) and can be broadly defined as an imbalance between vasodilating and vasoconstricting substances produced by (or acting on) the endothelium.[1] Normal functions of endothelial cells include mediation of coagulation, platelet adhesion, immune function, control of volume and electrolyte content of the intravascular and extravascular spaces. Endothelial dysfunction can result from and/or contribute to several disease processes, as occurs in septic shock, hypertension, hypercholesterolaemia, diabetes as well from environmental factors, such as from smoking tobacco products and exposure to air pollution.

Endothelial dysfunction is thought to be a key event in the development of atherosclerosis and predates clinically obvious vascular pathology by many years. This is because endothelial dysfunction is associated with reduced anticoagulant properties as well as increased adhesion molecule expression, chemokine and other cytokine release, and reactive oxygen species production from the endothelium, all of which play important roles in the development of atherosclerosis. In fact, endothelial dysfunction has been shown to be of prognostic significance in predicting vascular events including stroke and heart attacks. Because of this, endothelial function testing may have great potential prognostic value for the detection of cardiovascular disease, but currently the available tests are too difficult, expensive, and/or variable for routine clinical use.

A key and quantifiable feature of endothelial dysfunction is the inability of arteries and arterioles to dilate fully in response to an appropriate stimulus that stimulates release of vasodilators from the endothelium like nitric oxide (NO). Endothelial dyfunction is commonly associated with decreased NO bioavailability, which is due to impaired NO production by the endothelium and/or increased inactivation of NO by reactive oxygen species.This can be tested by a variety of methods including iontophoresis of acetylcholine, direct administration of various vasoactive agents to segments of blood vessels, localised heating of the skin and temporary arterial occlusion by inflating a blood pressure cuff to high pressures. Testing can also take place in the coronary arteries themselves but this is invasive and not normally conducted unless there is a clinical reason for intracoronary catheterisation. Of all the current tests employed in the research setting, flow-mediated dilation is the most widely used non-invasive test for assessing endothelial function. This technique measures endothelial function by inducing reactive hyperemic via temporary arterial occlusion and measuring the resultant relative increase in blood vessel diameter via ultrasound. As people with endothelial dysfunction have low NO bioavailability, their blood vessels have a decreased capacity to dilate in response to certain stimuli, compared to those with normal endothelial function.

Because NO has anti-inflammatory and anti-proliferative effects and therefore helps inhibit atherosclerosis, it is easy to see how endothelial dysfunction may contribute to future adverse cardiovascular events. Unfortunately the variability in such tests (e.g. due to time of day, food, menstrual cycle, temperature, etc.) means that no technique has yet been identified that would allow endothelial testing to attain routine clinical significance, although there are some tests under clinical evaluation such as measuring of arterial stiffness.

As more research is conducted to improve testing methodologies for endothelial dysfunction, however, several non-invasive tests have been created by various medical-research companies.[2]

Endothelial function can be improved significantly by exercise and improved diet. A study published in 2005 has determined that a positive relationship exists between the consumption of trans fat (commonly found in hydrogenated products such as margarine) and the development of endothelial dysfunction.[3] Other factors have been identified as improving endothelial function and include cessation of smoking, loss of weight and treatment of hypertension and hypercholesterolemia amongst other things. Some studies have found antioxidant and arginine supplementation to restore impaired endothelial dysfunction.

Endothelial dysfunction has been observed in a 2001 study of women where it was found that this disorder is present in approximately half of women with chest pain, in the absence of overt blockages in large coronary arteries. This endothelial dysfunction cannot be predicted by typical risk factors for atherosclerosis (e.g., obesity, cholesterol, smoking) and hormones.[4]

 

[squeegee]

Benfotiamine
http://www.lef.org/magazine/mag2007/jan ... ine_02.htm

Two recent studies from Italy validate benfotiamine’s ability to support healthy endothelial function, even in the presence of high blood glucose levels. Independent Italian research teams showed that, in addition to preserving mature endothelial cells lining blood vessels, benfotiamine also protects endothelial progenitor cells, or cells that develop into endothelial cells. These progenitor cells are crucial to the repair and maintenance of healthy endothelial tissue.23,24 While hyperglycemia, or high blood sugar, interferes with the normal development of progenitor cells, the Italian scientists noted that normal development of these cells can be restored by the administration of benfotiamine.23 Similarly, benfotiamine inhibited human epithelial progenitor cell death, which is caused by high glucose levels.24

 

[optimus prime]

Vitamin c + L-Lysine/L-Proline keep an healthy profile of Lipoprotein A.

They are others factors that can cause the problem

Elevated LDL cholesterol as explained
Low HDL cholesterol
Elevated Tryglycerides
Oxidized LDL
Hypertension
Elevated C-Protein
Elevated Lipoprotein A
Omega 3-6 imbalance
Elevated Glucose
Excess insulin
Elevated Homocycteine
Elevated Fibrinogen....................

This is why hairloss is a pain in the arse to cure. But one of the biggest factor is inflammation.

My dad is a NW6 and has type 2 diabetes, which I imagine would cause elevated levels of Glucose and excess insulin.

There are so many factors I don't know where to start.

BTW.. the dog is back in business! Thanks for the reminder..again Optimus!

Nice. Best avatar on the site.

 

[squeegee]

Vitamin c + L-Lysine/L-Proline keep an healthy profile of Lipoprotein A.

They are others factors that can cause the problem

Elevated LDL cholesterol as explained
Low HDL cholesterol
Elevated Tryglycerides
Oxidized LDL
Hypertension
Elevated C-Protein
Elevated Lipoprotein A
Omega 3-6 imbalance
Elevated Glucose
Excess insulin
Elevated Homocycteine
Elevated Fibrinogen....................

This is why hairloss is a pain in the arse to cure. But one of the biggest factor is inflammation.

My dad is a NW6 and has type 2 diabetes, which I imagine would cause elevated levels of Glucose and excess insulin.

There are so many factors I don't know where to start.

BTW.. the dog is back in business! Thanks for the reminder..again Optimus!

Nice. Best avatar on the site.

Like your trooper too!!

 

[squeegee]

Protein Glycation
A Firm Link to Endothelial Cell Dysfunction

http://circres.ahajournals.org/cgi/cont ... a;95/3/233

 

[DarkDays]

One of the things I have been looking at is potassium and how it relates to cardiovascular health. The biggest reason is because of the product TRX2 and why they thought of using potassium(it is a common substance so it is a weird choice). Reading more into the literature of potassium I have seen that potassium kinda relates to anything that happens in the body and that we, as human beings in modern society, are mostly deficient in this mineral. The biggest reason is that sodium tends to make the body excrete more potassium so the ratio between the two increases and you need a healthy ratio to keep cellular communication at optimum level.
Now, the problem is, we are in a society where sodium is rather excessive(it is used to store food and keep it tasty) and sugar, coffee, and other factors make the body lose potassium faster. Even healthy athletes lose a lot of potassium due to exercise, as potassium loss is high during heavy exercise(gets secreted with sweat. A common death among athletes are those who sweat, drink a lot of water and then get their electrolytes out of balance). Also, potassium tends to get lost during cooking, so unless you are eating 10 bananas a day(vomit), and not drinking coffee or eating sugar, you will probably have potassium levels in the lower range compared to sodium.

To even make this more interesting, estrogen and progesterone have different effect on potassium in the body(as well as potassium channels). To make this even more convoluted, spironlactone, if taken internally, is a potassium sparing diuretic. This means that people on spironolactone are actually retaining more potassium than normally(and which is why you must be careful when taking spironolactone internally).

Now, if Biolabs are doing real research with their TRX2 formula and promise to release the studies Q3 or Q4 as promised, and it shows efficiacy despite being a natural supplement, I think we are in for a change regarding what actually causes hairloss or at least how it is addressed, but I guess we will have to wait and see. If the research shows nothing than we can probably throw out several theories, at least several of them being natural approaches.

Personally I started to take potassium religiously 3 weeks ago and although I am not sure about hair loss(diffuse thinning is my problem), it has reduced my blood pressure drastically and reduced overall water retention(a common problem when sodium exceeds potassium).

Again, just ideas and nothing concrete(at least not until those studies ever come from Biolabs).

 

[DarkDays]

Found this paper:

Potassium softens vascular endothelium and increases nitric oxide release

http://www.pnas.org/content/106/8/2829.abstract

 

[squeegee]

Endothelial cell dysfunction, a broad term that implies reduced production of nitric oxide (NO) and an imbalance in the relative contribution of endothelium relaxing and contracting factors and oxidants, is emerging as a key component in the pathophysiology of diverse cardiovascular abnormalities associated with atherosclerosis, hypertension, diabetes, renal failure, and aging.13,14 In addition to its vasodilatory effect, NO also protects against vascular injury, inflammation, and leukocyte adhesion. When endothelial cells undergo inflammatory activation, the increased expression of selectins, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1 may promote the adherence of monocytes.15–17 Adherent monocytes transmigrate into the arterial wall, passing between the endothelial cells. Endothelial cells, rather than providing protection against thrombosis, then become prothrombotic and may produce tissue factor.

 

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Inflammation and Atherosclerosis
Oxidized Lipoproteins and Inflammation
For almost a century, many have regarded lipids as the sine qua non of atherosclerosis. Over the last few decades, a plausible model linking lipids and inflammation to atherogenesis has emerged....

http://circ.ahajournals.org/cgi/content/full/105/9/1135

 

[squeegee]

Hyaluronic Acid in Scalp Tissue and Hair Follicles

Structurally the scalp is identical to the skin tissue located throughout the body except it also contains about 100,000 hair follicles that give rise to hair. Actually the hair and the hair follicle are a derivative of skin tissue. There are two distinctive skin layers, one, the epidermis (outer layer) which gives rise to the protective shield of the body and the other, the dermal layer (deep layer) which makes up the bulk of the skin and is where the hair follicle is located. This dermal layer is composed of connective tissue and the connective tissue, with its gelatinous fluid like characteristics provides support, nourishes and hydrates the deep layers of the scalp. The result is healthy lustrous hair and a moisturized scalp. Again, all of this is made possible because of the presence of HA in the scalp.

http://www.hyalogic.com/main/about_hyaluronic_acid

idontwanttobebalding.. I took HA topical for a while just to try it.. You hair turn really dark and looks healthy..I bought it for cheap on purebulk.. There is a shampoo on the market claiming that HA is fighting DHT...don't remember the brand...I stopped it because I hate topical.. such a pain in the arse and HA has to be in a fridge all the time or it turns in water..

 

[squeegee]

Hyaluronic Acid in Scalp Tissue and Hair Follicles

Structurally the scalp is identical to the skin tissue located throughout the body except it also contains about 100,000 hair follicles that give rise to hair. Actually the hair and the hair follicle are a derivative of skin tissue. There are two distinctive skin layers, one, the epidermis (outer layer) which gives rise to the protective shield of the body and the other, the dermal layer (deep layer) which makes up the bulk of the skin and is where the hair follicle is located. This dermal layer is composed of connective tissue and the connective tissue, with its gelatinous fluid like characteristics provides support, nourishes and hydrates the deep layers of the scalp. The result is healthy lustrous hair and a moisturized scalp. Again, all of this is made possible because of the presence of HA in the scalp.

http://www.hyalogic.com/main/about_hyaluronic_acid

idontwanttobebalding.. I took HA topical for a while just to try it.. You hair turn really dark and looks healthy..I bought it for cheap on purebulk.. There is a shampoo on the market claiming that HA is fighting DHT...don't remember the brand...I stopped it because I hate topical.. such a pain in the arse and HA has to be in a fridge all the time or it turns in water..

Thanks squeegee.....now, by any chance did you get a sun burn on your head while using the product? See, I think there needs to be some wounding (like a sun burn) to the skin, then the application.....been reading about products that generate new follicles during the healing process of a wound....a sun burn is the most common skin "injury" I can think of....a light burn may be the safest way to test this theory.

nope no sunburn... Sounds like a plan..go get a tan in a booth but stay few more minutes!!

 

[squeegee]

Found this paper:

Potassium softens vascular endothelium and increases nitric oxide release

http://www.pnas.org/content/106/8/2829.abstract

5-Methyltetrahydrofolate and tetrahydrobiopterin is 2 things we hav to look up.

 

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Interaction of 5-methyltetrahydrofolate and tetrahydrobiopterin on endothelial function.
Hyndman ME, Verma S, Rosenfeld RJ, Anderson TJ, Parsons HG.
Source

Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada T2N 4N1.
Abstract

The present study was designed to investigate the interaction between 5-methyltetrahydrofolate and tetrahydrobiopterin in modulating endothelial function. Tetrahydrobiopterin is a critical cofactor for nitric oxide synthase and maintains this enzyme as a nitric oxide- versus superoxide-producing enzyme. The structure of 5-methyltetrahydrofolate is similar to tetrahydrobiopterin and both agents have been shown to improve endothelium-dependent vasodilatation. We hypothesized that 5-methyltetrahydrofolate interacts with nitric oxide synthase in a fashion analogous, yet independent, of tetrahydrobiopterin to improve endothelial function. We demonstrate that 5-methyltetrahydrofolate binds the active site of nitric oxide synthase and mimics the orientation of tetrahydrobiopterin. Furthermore, 5-methyltetrahydrofolate attenuates superoxide production (induced by inhibition of tetrahydrobiopterin synthesis) and improves endothelial function in aortae isolated from tetrahydrobiopterin-deficient rats. We suggest that 5-methyltetrahydrofolate directly interacts with nitric oxide synthase to promote nitric oxide (vs. superoxide) production and improve endothelial function. 5-Methyltetrahydrofolate may represent an important strategy for intervention aimed at improving tetrahydrobiopterin bioavailability.

 

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5-Methyltetrahydrofolate and tetrahydrobiopterin can modulate electrotonically mediated endothelium-dependent vascular relaxation.
Griffith TM, Chaytor AT, Bakker LM, Edwards DH.
Source

Department of Diagnostic Radiology, Wales Heart Research Institute, Cardiff University, Heath Park, Cardiff CF14 4XN, United Kingdom. griffith@cardiff.ac.uk
Erratum in

Proc Natl Acad Sci U S A. 2005 Aug 30;102(35):12644.

Abstract

We have investigated the ability of 5-methyltetrahydrofolate (5-MTHF) and tetrahydrobiopterin (BH(4)) to modulate nitric oxide (NO)-independent vascular relaxations that are mediated by the sequential spread of endothelial hyperpolarization through the wall of the rabbit iliac artery by means of myoendothelial and homocellular smooth muscle gap junctions. Relaxations and subintimal smooth muscle hyperpolarizations evoked by cyclopiazonic acid were depressed by the gap junction inhibitor 2-aminoethoxydiphenyl borate, whose effects were prevented by 5-MTHF and BH(4), but not by their oxidized forms folic acid and 7,8-dihydrobiopterin. Analogously, 5-MTHF and BH(4), but not folic acid or 7,8-dihydrobiopterin, attenuated the depression of subintimal hyperpolarization by a connexin-mimetic peptide targeted against Cx37 and Cx40 ((37,40)Gap 26) and the depression of subadventitial hyperpolarization by a peptide targeted against Cx43 ((43)Gap 26), thus reflecting the known differential expression of Cx37 and Cx40 in the endothelium and Cx43 in the media of the rabbit iliac artery. The inhibitory effects of 2-aminoethoxydiphenyl borate and (37,40)Gap 26 against subintimal hyperpolarization were prevented by catalase, which destroys H(2)O(2). 5-MTHF and BH(4) thus appear capable of modulating electrotonic signaling by means of myoendothelial and smooth muscle gap junctions by reducing oxidant stress, potentially conferring an ability to reverse the endothelial dysfunction found in disease states through mechanisms that are independent of NO.

 

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5-Methyltetrahydrofolate Rapidly Improves Endothelial Function and Decreases Superoxide Production in Human Vessels
Effects on Vascular Tetrahydrobiopterin Availability and Endothelial Nitric Oxide Synthase Coupling

http://circ.ahajournals.org/cgi/content ... 14/11/1193

 

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Folic acid reverts dysfunction of endothelial nitric oxide synthase.
Stroes ES, van Faassen EE, Yo M, Martasek P, Boer P, Govers R, Rabelink TJ.
Source

Department of Vascular Medicine, University Hospital Utrecht, The Netherlands. e.stroes@digd.azu.nl
Abstract

5-methyltetrahydrofolate (MTHF), the active form of folic acid, has been reported to restore NO status in hypercholesterolemic patients. The mechanism of this effect remains to be established. We assessed the effects of L- and D-MTHF on tetrahydrobiopterin (BH(4))-free and partially BH(4)-repleted endothelial NO synthase (eNOS). Superoxide production of eNOS and the rate constants for trapping of superoxide by MTHF were determined with electron paramagnetic resonance using 5-diethoxyphosphoryl-5-methyl-1-pyrroline-N-oxide (DEPMPO) as spin trap for superoxide. NO production was measured with [(3)H]arginine-citrulline conversion or nitrite assay. The rate constants for scavenging of superoxide by L- and D-MTHF were similar, 1.4 x 10(4) ms(-1). In BH(4)-free eNOS, L- and D-MTHF have no effect on enzymatic activity. In contrast, in partially BH(4)-repleted eNOS, we observe a 2-fold effect of MTHF on the enzymatic activity. First, superoxide production is reduced. Second, NO production is enhanced. In cultured endothelial cells, a similar enhancement of NO production is induced by MTHF. In the present study, we show direct effects of MTHF on the enzymatic activity of NO synthase both in recombinant eNOS as well as in cultured endothelial cells, which provides a plausible explanation for the previously reported positive effects of MTHF on NO status in vivo.

 

[thinninghairsucks]

They were given food that is deficient in magnesium supplements. The result was that they lost hair in bunches. When they were fed a low biotin diet they became hairless. But, when they were fed the food rich in Vitamin B the got back their hair. Similar studies conducted on human beings found that Vitamin B improves the quality of hair.