Serum Paroxonase 1 level may be an Indicator and Predictor of the Severity of Androgenetic Alopecia

jamesbooker1975

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New study , Dec 2021 :

Serum Paroxonase 1 level may be an Indicator and Predictor of the Severity of Androgenetic Alopecia
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Abstract​

Background: Androgenetic alopecia (Androgenetic Alopecia) is a common stressful form of hair loss caused by androgen excess, genetic factors, and exposure to oxidative stress (OS) with the formation of reactive oxygen species (ROS). Paraoxonase 1 (PON1) is an enzyme synthesized in the liver bound to high-density lipoproteins to prevent lipid peroxidation.
Aim: The aim of our work is to estimate serum PON1 level in patients with Androgenetic Alopecia and correlate its levels with disease severity which may help in determining if there is a role of ROS in pathogenesis of Androgenetic Alopecia.
Subjects and methods: This study was carried out as a case and control on 40 patients with Androgenetic Alopecia (diagnosed by typical clinical and dermoscopic finding) versus 40 control subjects. Blood samples were taken from all subjects to assess serum PON1enzyme using enzyme-linked immunosorbent assay kits.
Results: There was a significant decrease in serum PON1 concentration level in Androgenetic Alopecia patients in comparison to controls, in addition, there was a significant decrease correlated with Androgenetic Alopecia severity (P < 0,001). The study proved that PON1 is considered highly sensitive and specific for Androgenetic Alopecia cases and a good predictive factor of Androgenetic Alopecia in healthy subjects.
Conclusion: This is the first study done to reveal that the level of PON1 significantly decreased in Androgenetic Alopecia patients, which may give additional proof that OS has role in the pathogenesis of Androgenetic Alopecia and hence may help in the management of Androgenetic Alopecia by adding antioxidants in treatment.
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whatevr

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People have taken tocopherols & tocotrienols, glutathione, NAC, astaxanthin and many other antioxidants without success.

What I love about studies like these though is that it throws a wrench in the broscience argument that balding men are the same as everyone else, but they just somehow miraculously have "DHT-sensitive folllicles". Systemic differences prove that whatever is causing Androgenetic Alopecia is present over the entire body, the hair follicle likely just manifests it the strongest.

EDIT: Apparently it's not just a mild difference either. Non balding people have 3 times as much PON1 on average.

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trialAcc

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People have taken tocopherols & tocotrienols, glutathione, NAC, astaxanthin and many other antioxidants without success.

What I love about studies like these though is that it throws a wrench in the broscience argument that balding men are the same as everyone else, but they just somehow miraculously have "DHT-sensitive folllicles". Systemic differences prove that whatever is causing Androgenetic Alopecia is present over the entire body, the hair follicle likely just manifests it the strongest.
I would think this was obvious as soon as they realized that people with Androgenetic Alopecia are significantly more at risk for heart disease. It's clearly an auto immune or chronic inflammatory condition that has yet to fully get the respect it deserved from the medical community.
 

coolio

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There is a lot more correlation than causation evidence though.

It's like saying that being thinner (body mass) correlates with being unhealthy. That's true. Many health problems & drug addictions & stress problems cause people to lose weight. But a person can also be thin (within reason) and be perfectly healthy.

Both hair loss and being thin are influenced by genetics & lifestyle/health to varying degrees. If genetics is giving your hair a severe ***-kicking then you will go bald even without any other contributing issues.
 

whatevr

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The patients' serum paraoxonase 1 (PON 1) activity was increased by 83%, whereas serum LDL basal oxidative state and LDL susceptibility to copper ion-induced oxidation were both significantly reduced, by 90% and 59%, respectively, after 12 months of PJ consumption, compared to values obtained before PJ consumption.

Lol pomegranate juice here we come.
 

zaman

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The patients' serum paraoxonase 1 (PON 1) activity was increased by 83%, whereas serum LDL basal oxidative state and LDL susceptibility to copper ion-induced oxidation were both significantly reduced, by 90% and 59%, respectively, after 12 months of PJ consumption, compared to values obtained before PJ consumption.

Lol pomegranate juice here we come.

That's what I found too, and immediately began searching for pomegranate extract
 

whatevr

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That's what I found too, and immediately began searching for pomegranate extract

I wouldn't hold my breath as I haven't found any anecdotal reports of hair growth from the people taking this stuff. The interesting thing though is that it seems to help with prostate cancer and reducing PSA, another androgen-driven condition.
 

coolio

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I seem to remember a debunking of that pomegranate juice thing a few years later. Conflict-of-interest or bad methodology or something.
 

Dimitri001

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People have taken tocopherols & tocotrienols, glutathione, NAC, astaxanthin and many other antioxidants without success.

What I love about studies like these though is that it throws a wrench in the broscience argument that balding men are the same as everyone else, but they just somehow miraculously have "DHT-sensitive folllicles". Systemic differences prove that whatever is causing Androgenetic Alopecia is present over the entire body, the hair follicle likely just manifests it the strongest.

EDIT: Apparently it's not just a mild difference either. Non balding people have 3 times as much PON1 on average.

View attachment 174751
That's not necessarily true, because castration will stop Androgenetic Alopecia, so it is very possible that the only difference is something DHT-related (although it seems that in the absence of PRLR activation, DHT alone isn't enough - which is functioning abnormally in bald men, IDK).

I'm not sure that the fact that bald men also have some other systemic difference means that that systemic difference does anything as far as Androgenetic Alopecia is concerned. My understanding is that most genes affect multiple things.
 

whatevr

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That's not necessarily true, because castration will stop Androgenetic Alopecia, so it is very possible that the only difference is something DHT-related (although it seems that in the absence of PRLR activation, DHT alone isn't enough - which is functioning abnormally in bald men, IDK).

I'm not sure that the fact that bald men also have some other systemic difference means that that systemic difference does anything as far as Androgenetic Alopecia is concerned. My understanding is that most genes affect multiple things.

Fair point. What seems to be apparent is that we are witnessing an aberrant response of the body to androgens, what is less clear is which changes are merely correlational and causative, but what is apparent is that they are systemic, not limited to the follicle.

For instance, even this PON1 seems to be influenced by androgens:

Liver PON1 mRNA expression is influenced by genetic and environmental factors, and both androgens and proinflammatory mediators decrease liver PON1 expression (bin Ali et al., 2003). Of interest, both androgen excess and proinflammatory genotypes are associated with PCOS (Peral et al., 2002; Villuendas et al., 2002; Escobar-Morreale et al., 2003). Serum PON1 activity has been reported to be lower in male mice (bin Ali et al., 2003). Following castration of male mice, hepatic PON1 mRNA had increased by 170%. In our study, we noted a significant negative correlation between serum total testosterone levels and serum PON1 activity in the PCOS group (r = –0.54; P <0.01).

Interestingly enough similar study has been done in female Androgenetic Alopecia patients, they also found reduced levels of PON1:

 
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trialAcc

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e.g. this routine seems cool and exciting, because it's lots of experimental stuff

View attachment 174784
but in reality could be a ticket to lots of further hair loss because nothing in it has any guarantee of working

different philosophy I guess
Ah yes so your philosophy is that you'd rather take a bunch of things move the needle maybe 1% each (at best) but have concrete human studies that tell you it's 1% then then try things that could move the needle 50% but only have validated human application in similar indications.

Unfortunately for you, your philosophy is the reason why the most interesting hair loss products year after year are garbage shampoos and onion juice creams instead of anything useful for people who didn't start finasteride the second they started losing hair and not get sides.
 

waynakyo

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I have seen some really crappy studies coming from that university.
I think people should add the journal in which the paper is published. People underestimate how crappy and useless some studies are.
All I am sayiing I wouldnt change my diet for a paper like that
 

whatevr

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I have seen some really crappy studies coming from that university.
I think people should add the journal in which the paper is published. People underestimate how crappy and useless some studies are.
All I am sayiing I wouldnt change my diet for a paper like that

Here you go then, a study from a university in Poland which shows reduced PON1 levels even in female androgenic alopecia:

 

whatevr

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Drink up boyos!

Responsibly, though. Light drinking (1-2 shots of moderate strength alcohol) will increase your serum paroxonase by up to 395% compared to non-drinkers, enough to compensate for the discrepancy in the OP study.

Getting shitfaced (>6 drinks per day), on the other hand, will lower it even further by up to 45% compared to non-drinkers. Not good.
 

zaman

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I started on Pomegranate extract on the basis of increasing paroxonase and progesterone. Apparently it's not a simple matter whether Pomegranate is estrogenic. It reduces estradiol and acts as a SERM, and in women reduces both Estrone and Testosterone. If it were estrogenic though, I don't know why people use it for ED. I keep seeing 'hormone balancing'.

Anyway, I will also be starting Alfatradiol too soon.

I haven't been taking anything recently so will be able to report any progress or lack thereof.
 

Squeegee 2.0

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The Search for Dietary Supplements to Elevate or Activate Circulating Paraoxonases​


Abstract​

Low levels of paraoxonase 1 (PON1) have been associated with the development of several pathological conditions, whereas high levels have been shown to be anti-atherosclerotic in mouse models. These findings suggest that PON1 could be a good surrogate biomarker. The other members of the family, namely PON2 and PON3, the role of which has been much less studied, deserve more attention. This paper provides a systematic review of current evidence concerning dietary supplements in that regard. Preliminary studies indicate that the response to dietary supplements may have a nutrigenetic aspect that will need to be considered in large population studies or in clinical trials. A wide range of plant preparations have been found to have a positive action, with pomegranate and some of its components being the best characterized and Aronia melanocarpa one of the most active. Flavonoids are found in the composition of all active extracts, with catechins and genistein being the most promising agents for increasing PON1 activity. However, some caveats regarding the dose, length of treatment, bioavailability, and stability of these compounds in formulations still need to be addressed. Once these issues have been resolved, these compounds could be included as nutraceuticals and functional foods capable of increasing PON1 activity, thereby helping with the long-term prevention of atherosclerosis and other chronic ailments.

Table 1​

Plant preparations found to increase serum PON1 in different experimental designs.
Extract​
Experimental Model​
Dose​
Effect​
References​
Eucommia ulmoides Oliver leaf​
Diabetic C57BL/KsJ-db/db mice​
400 mg/kg bw​
↑ 22%​
[21]​
Murraya koenigii
Streptozotocin-induced diabetic mice​
150 mg/kg​
↑ 105%​
[22]​
Grape seed extracts​
Streptozotocin-induced diabetic rats​
100 mg/kg​
↑ 86%​
[23]​
Red wine polyphenol extract​
Heterozygous Cbs-deficient mice​
100 mg/kg​
↑ 20%​
[25]​
Sambucus nigra
Apoe-deficient mice​
200 mg/kg​
↑ 20%​
[26]​
Aronia melanocarpa
Apoe-deficient mice​
6 mg/kg​
↑ 39%​
[27]​
Onion extract​
Mercuric chloride-induced oxidative insult in male Wistar rats​
20 mg/kg​
↑ 30%​
[28]​
Aronia melanocarpa
Rats on a high-fructose and high-fat diet​
Not reported​
↑ 65%​
[29]​
Cornelian cherry​
Rats on a high-fructose and high-fat diets​
Not reported​
↑ 45%​
[30]​
Genistein​
Arthritic rats​
20 mg/kg​
↑ 230%​
[33]​
Euterpe oleracea Mart​
Female Fischer rats on high-cholesterol, high-fat diets​
2 mg/kg​
↑ 60%​
[34]​
Avocado​
Male Wistar rats​
28 g/kg​
↑ 33%​
[35]​
Ilex paraguariensis
Healthy volunteers​
0.5 L of extract​
↑ 10%​
[37]​
Cranberry extract with vitamin C and zinc​
Healthy volunteers​
2 g/day (300 mg/day)​
↑ 67%​
[38]​
Zingiber officinale
Type 2 diabetic patients​
3 g​
↑ 28%​
[39]​
Salvia miltiorrhiza
Type 2 diabetic patients​
Not reported​
Increased PON1 activity​
[40]​
Origanum onites
Hyperlipidemic patients​
Not reported​
↑ 14%​
[41]​
 
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