The Cause Of Baldness

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CLASH

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"Dietary intake. Despite a significant difference in BMI (Table 1), total energy intake, intake of carbohydrate, fat, and protein did not differ between NAFLD patients and controls (Table 2). However, regular leisurely physical activity was significantly less frequent in the group of NAFLD patients (50%) than in controls (100%). Total glucose and sucrose consumption did not differ between cases and controls. In contrast, total fructose intake, derived from free fructose and sucrose, was significantly higher by ;10 g/d in patients with NAFLD than in controls (Table 2)."

Both groups contained similar amounts of fructose, the NAFLD group consumed only 10 more grams a day of fructose and that was plus or minus 5, while the control group was plus or minus 3 on fructose consumption. The difference in intake was minimal especially considering the sucrose and glucose were only slightly highe in NAFLD. The reseaechers merely state a correlation of higher fructose intake and thus higher plasminogen activator inhibitor 1 mrna expression in the liver; levels in serum werent increased. What I see here is increased endotoxin associated with increased fatty liver disease. The fructose may play some role but i dont think this study shows that in any way. There wasnt even a correlation between fructose and endotoxin levels nor fatty liver disease. It seems more that an upper intestinal infection and a permeable intestinal mucosa is what leads to fatty liver disease due to the translocation of endotoxin. Fructose and carbohydrate are associated only in the fact that in this context they could be fermented by said bacteria leading to increased endotoxin. So i dont see any proof of fructose or glucose being toxic to the body itself. I see a bacterial infection of the upper intestine not being good for the body. Also these last points are shown in this research article. They are extensions. The article just shows increased fatty liver disease in association with endotoxin.
 

Wagner83

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There are many studies showing the dangers of excess fructose, link to insulin resistance etc but also studies showing the opposite often industry sponsored like Coca Cola, Nestlé etc. If one knows anything about how fructose is metabolized one knows not to overconsume it due to the heavy load on the liver.

https://www.dietdoctor.com/fructose-fatty-liver-sugar-toxin

10 Reasons Why Fructose Is Bad | Paleo Leap
I have seen very few studies which points to fructose being a reason for fatty liver, in rats and coupled with high fat then yes it's possible. In fact all human studies I have seen so far do not suggest bad effects. The only one who made a good argument against fructose overload here is tyw: Do Carbohydrates Turn Into Fat?
A few members here have reported large fructose intake without any deleterious effects, and I showed you a study which showed that fresher OJ greatly attenuated inflammatory markers and endotoxin release after a high fat - high carb meal .
 
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raypeatclips

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I have seen very few studies which points to fructose being a reason for fatty liver, in rats and coupled with high fat then yes it's possible. In fact all human studies I have seen so far do not suggest bad effects. The only one who made a good argument against fructose overload here is tyw: Do Carbohydrates Turn Into Fat?
A few members here have reported large fructose intake without any deleterious effects, and I showed you a study which showed that fresher OJ greatly attenuated inflammatory markers and endotoxin release after a high fat - high carb meal .

For what its worth, I feel drastically better eating more glucose sources (rice) that when my carbs were fructose containing source (juice, sugar, coke, fruit) I would say that someone that isn't feeling good eating a high fructose diet try more glucose as a replacement and see if their health improves regardless of whatever studies say.
 

eddiem991

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For what its worth, I feel drastically better eating more glucose sources (rice) that when my carbs were fructose containing source (juice, sugar, coke, fruit) I would say that someone that isn't feeling good eating a high fructose diet try more glucose as a replacement and see if their health improves regardless of whatever studies say.

Every cell in the body can use glucose as fuel, which is not the case with fructose.
 

Wagner83

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For what its worth, I feel drastically better eating more glucose sources (rice) that when my carbs were fructose containing source (juice, sugar, coke, fruit) I would say that someone that isn't feeling good eating a high fructose diet try more glucose as a replacement and see if their health improves regardless of whatever studies say.
Oh I agree with that, I think for me a glass of orange juice with my meals is nice. I don't like most of the fibers from fruits and avoid too much liquid or plain sugar, so choices are limited.
 
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The result in the orange juice study is due to the vitamin C and other antioxidants in the OJ... if it was just sugar water there would have been inflammation.

I think its pretty clear from the biochemistry that too much fructose can overwhelm the liver and cause ATP depletion, and if chronic, maybe even phosphorus deficiency . The fiber and antioxidants in whole fruits limit this danger. Also, eating starch and sugar together will saturate the sugar transporters in the intestine, diluting the fructose and protecting the liver.

Fructose Metabolism
Fructose Metabolism: Relation to Food Intake & Metabolic Dysfunction
 
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" The mechanism is due to the fact that fructokinase (KHK) rapidly phosphorylates fructose to fructose-1-phosphate resulting in marked ATP depletion. The activity of fructokinase (KHK) is not subject to feed-back inhibition such as is the case for glucose metabolism, thus the ATP depletion is profound. Since the majority of fructose metabolism occurs in the liver, the effects of this ATP depletion are exerted on numerous important hepatic metabolic processes. The depletion in ATP is also associated with intracellular phosphate depletion and dramatic increases in AMP generation. Both of the latter stimulate the activity of the purine nucleotide catabolic enzyme AMP deaminase increasing degradation of AMP ultimately to uric acid."
 
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" The mechanism is due to the fact that fructokinase (KHK) rapidly phosphorylates fructose to fructose-1-phosphate resulting in marked ATP depletion. The activity of fructokinase (KHK) is not subject to feed-back inhibition such as is the case for glucose metabolism, thus the ATP depletion is profound. Since the majority of fructose metabolism occurs in the liver, the effects of this ATP depletion are exerted on numerous important hepatic metabolic processes. The depletion in ATP is also associated with intracellular phosphate depletion and dramatic increases in AMP generation. Both of the latter stimulate the activity of the purine nucleotide catabolic enzyme AMP deaminase increasing degradation of AMP ultimately to uric acid."

Those are all things that make fructose a great tool. Lol.
 
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"When ATP levels fall there is a concomitant rise in AMP which results in activation of AMPK. Activation of AMPK results in phosphorylation and inhibition of ACC which then results in decreased malonyl-CoA levels in the hypothalamus."...

Malonyl-CoA basically acts as a signal of being in a fed state, and activates energy storage. Decreased levels, as found in fasted states, act to increase fatty acid oxidation.
 
D

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Don't forget that the vitamin D and mineralcorticoid receptors are the only ones shown to cause total balding in mice. Upregulation of the glucocorticoid receptor does not cause major hair issues.

Spironolactone was originally designed to antagonize the mineralcorticoid receptor.

Cortisol is usually referred to as a glucocorticoid, but it has equal affinity for the mineralcorticoid receptor.

Cyclosporines effects on hair is considered independent of it's immunosuppression effects. I don't necessarily agree that this is correct, as molecular mechanisms can be subjective at times and I haven't even examined the immunosuppressive mechanism. But it would certainly be expected to act on T-cells differently that keratinocytes. There are a few detailed studies on the mechanism of cyclosporine A, and it's cousin FK-506, directly on epidermal cells. Western and Southern blots have been made to see exactly which genes are shifted. From this data, most researchers agree that it works on the mineralcorticoid receptor in epidermal cells (keratinocytes).

Your saying low vitamin D causes balding?
 

Elephanto

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Reposting ITT for future reference.

Finasteride helps with hair loss in 2 ways :

1. Finasteride/Dutasteride have potent antibacterial effects.
Finasteride Activity Against Candida Albicans

and

2. DHT is triggered by chronic stress, it in turn triggers estrogen. High DHT isn't desirable but rather a symptom of systemic sickness.
Dihydrotestosterone (DHT) Activates Estrogen Receptor Alpha

I don't really believe in sebum being the main cause, but it doesn't help. I have seen high testosterone men (roiding) who produce a lot of sebum with perfect hairlines. Calcified scalps are found in deceased people who suffered from baldness. IGFBP3 is significantly lower in young men balding than their non-balding counterparts. Estrogen, Endotoxins and Vitamin D deficiency inhibit IGFBP3 and cause tissue calcification. The calcification is the main cause, cutting out blood circulation to hair follicles (in a way that is the only that can explain the horseshoe pattern), and it might be only enabled by an improper (narrow) skull structure. This can be changed with Vitamin K2, Pregnenolone, Boron and perhaps physical actions like mewing and hard chewing which have theoretical proofs supporting such influence. Decalcification reverses hair loss, with agents like high dose Magnesium, MSM, Taurine, Vitamin K2, D, Zinc, Boron and actions like rinsing the scalp with Apple Cider Vinegar and scalp massaging (like someone mentioned, inversion/headstand will also help). Endotoxins do the most of their damage when they enter the bloodstream by cause of intestinal permeability, so the avoidance of gut irritants and sufficiency of Vitamin D should be prioritary and perhaps Glutamine has to be supplemented in some cases.

Another thing that is important to prevent/reverse tissue calcification and is mentioned by Peat is adequate CO2. That's why 3 teaspoons a day of bicarbonate sodium (an hour after meals) was mentioned in a guide by someone who reversed hair loss (in his words it was because of its anti-candida property, I say why not both). Also bag breathing will help while you're still working on having a constant slow, controlled breathing. The shallow breathing/hyperventilation of stressed people is a sure way to deplete CO2 and increase calcification.

Endotoxin decreases serum IGFBP-3 and liver IGFBP-3 mRNA: comparison between Lewis and Wistar rats. - PubMed - NCBI

Estradiol, progesterone, and transforming growth factor alpha regulate insulin-like growth factor binding protein-3 (IGFBP3) expression in mouse en... - PubMed - NCBI

IGFBP-3 Interacts with the Vitamin D Receptor in Insulin Signaling Associated with Obesity in Visceral Adipose Tissue. - PubMed - NCBI

Effects of environmental stress on mRNA and protein expression levels of steroid 5alpha-Reductase isozymes in adult rat brain. - PubMed - NCBI

The study on lower IFGBP-3 in young balding men isn't easy to find anymore, I think it has been suppressed in search results by Google because it is too much of a paradigm-shifting information since it partly nullifies the DHT theory (I mean, DHT plays a role but you can achieve the same results and more by focusing on estrogen, the root cause of chronically high DHT (stress) and other signs of sickness without the brain-damaging and anti-androgenic effects of DHT deficiency) and that would also shift the paradigm of prostate cancer since low IGFBP3 is also found with the condition. It's probably still there, I can tell you that it was done by Mcgill University, the subjects were men in their 20s and was published in either the 90s or early 00's. Calcified scalps of deceased bald people was a study funded by L'Oréal.
 
D

Deleted member 5487

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Reposting ITT for future reference.

Finasteride helps with hair loss in 2 ways :

1. Finasteride/Dutasteride have potent antibacterial effects.
Finasteride Activity Against Candida Albicans

and

2. DHT is triggered by chronic stress, it in turn triggers estrogen. High DHT isn't desirable but rather a symptom of systemic sickness.
Dihydrotestosterone (DHT) Activates Estrogen Receptor Alpha

I don't really believe in sebum being the main cause, but it doesn't help. I have seen high testosterone men (roiding) who produce a lot of sebum with perfect hairlines. Calcified scalps are found in deceased people who suffered from baldness. IGFBP3 is significantly lower in young men balding than their non-balding counterparts. Estrogen, Endotoxins and Vitamin D deficiency inhibit IGFBP3 and cause tissue calcification. The calcification is the main cause, cutting out blood circulation to hair follicles (in a way that is the only that can explain the horseshoe pattern), and it might be only enabled by an improper (narrow) skull structure. This can be changed with Vitamin K2, Pregnenolone, Boron and perhaps physical actions like mewing and hard chewing which have theoretical proofs supporting such influence. Decalcification reverses hair loss, with agents like high dose Magnesium, MSM, Taurine, Vitamin K2, D, Zinc, Boron and actions like rinsing the scalp with Apple Cider Vinegar and scalp massaging (like someone mentioned, inversion/headstand will also help). Endotoxins do the most of their damage when they enter the bloodstream by cause of intestinal permeability, so the avoidance of gut irritants and sufficiency of Vitamin D should be prioritary and perhaps Glutamine has to be supplemented in some cases.

Another thing that is important to prevent/reverse tissue calcification and is mentioned by Peat is adequate CO2. That's why 3 teaspoons a day of bicarbonate sodium (an hour after meals) was mentioned in a guide by someone who reversed hair loss (in his words it was because of its anti-candida property, I say why not both). Also bag breathing will help while you're still working on having a constant slow, controlled breathing. The shallow breathing/hyperventilation of stressed people is a sure way to deplete CO2 and increase calcification.

Endotoxin decreases serum IGFBP-3 and liver IGFBP-3 mRNA: comparison between Lewis and Wistar rats. - PubMed - NCBI

Estradiol, progesterone, and transforming growth factor alpha regulate insulin-like growth factor binding protein-3 (IGFBP3) expression in mouse en... - PubMed - NCBI

IGFBP-3 Interacts with the Vitamin D Receptor in Insulin Signaling Associated with Obesity in Visceral Adipose Tissue. - PubMed - NCBI

Effects of environmental stress on mRNA and protein expression levels of steroid 5alpha-Reductase isozymes in adult rat brain. - PubMed - NCBI

The study on lower IFGBP-3 in young balding men isn't easy to find anymore, I think it has been suppressed in search results by Google because it is too much of a paradigm-shifting information since it partly nullifies the DHT theory (I mean, DHT plays a role but you can achieve the same results and more by focusing on estrogen, the root cause of chronically high DHT (stress) and other signs of sickness without the brain-damaging and anti-androgenic effects of DHT deficiency) and that would also shift the paradigm of prostate cancer since low IGFBP3 is also found with the condition. It's probably still there, I can tell you that it was done by Mcgill University, the subjects were men in their 20s and was published in either the 90s or early 00's. Calcified scalps of deceased bald people was a study funded by L'Oréal.

Perfect

Thanks you.

I Will get to work

Whats the best way to approach the antimicrobial aspect of the gut?
 

Travis

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Your saying low vitamin D causes balding?

That could imply that a concentration of zero could cause balding, yet the vitamin D receptor transcribes for only one hair keratin—i.e. keratin 33. The vitamin D receptor is involved in hair growth, to a degree, yet I don't think it's worth much considering.
 

Elephanto

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@Amarsh213

BTW that's the guide I'm refering to :
https://forum.bodybuilding.com/showthread.php?t=160444941&pagenumber=1 (the pictures got 404'd apparently)
But I'd be cautious about many of the dosages used (for instance Selenium is detrimental past 100mcg a day or Zinc past 50mg) and wouldn't take Omega 3s (O6 avoidance + Vit E will suffice), Iodine or green tea extract. I think he just took a stack of everything he could find on hairloss forums. Some of the reasons he takes the supps for are wrong imo. Like his avoidance of grains, I think he was doing Keto. (really avoiding gluten, oats, potatoes will do the job since the reason in my opinion is their intestinal permeability increasing properties). As you can see he also takes a lot of coconut oil, which "completetly abolishes the response to endotoxin" in a study posted by haidut. Also avoiding alcohol will help in this regard and taking some Apple Cider Vinegar internally. Really many of the supps work in this way and in lowering nitric oxide, you can also add ginger, the occasional green tea and some herbs tisane like chamomille.

Another guy with full hairline restoration I contacted from this thread years ago only ate white rice with coconut oil. He also did headstands, and told me he felt it was cracking and flattening a kind of "calcified mount" on top of his head.
 
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Luckytype

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That could imply that a concentration of zero could cause balding, yet the vitamin D receptor transcribes for only one hair keratin—i.e. keratin 33. The vitamin D receptor is involved in hair growth, to a degree, yet I don't think it's worth much considering.

Another way to consider this for some that may have tunnel vision regarding hairloss is that making sure vitamin D for its hormonal actions is at an appropriate level, and in some cases of long term deficiency will affect a few people but its likely not the cause of a majority of hair loss in mostpeople; despite playing a supporting metabolic role and sometimes a very dominate role in a few cases.

In other words, likely not the cause of all hair loss and shouldnt be megadosed but Vit D should be given attention for other important metabolic actions.
 

Travis

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Another way to consider this for some that may have tunnel vision regarding hairloss is that making sure vitamin D for its hormonal actions is at an appropriate level, and in some cases of long term deficiency will affect a few people but its likely not the cause of a majority of hair loss in mostpeople; despite playing a supporting metabolic role and sometimes a very dominate role in a few cases.

In other words, likely not the cause of all hair loss and shouldnt be megadosed but Vit D should be given attention for other important metabolic actions.

Yes, even though its initially plausible based on a few observations—e.g. (1) synthetic vitamin D analogues can cause hair growth; (2) vitamin D knockout rats are hairless; and (3) head pattern balding is reminiscent of shadows formed by hats, of course worn primarily by men—quite a bit of vitamin D is distributed by the bloodstream to the head, to compensate, and other shaded areas do have hair.

Perhaps vitamin D is not even needed at all? The rats in the study had lost an entire transcription factor—or had it inactivated somehow—and one responsible for dimerizing with retinoic acid receptors. It could be more that the RAR had lost a dimer partner than a consequence of vitamin D transcription per se. I think this is findoutable becaues vitamin D knockout and vitamin D knockdown rats are common, used in dozens of studies that are completely unrelated to hair. What would it mean if only knockout mutations in the vitamin D receptor RAR-binding domain caused hair loss? and never mutations placed in the vitamin D binding domain?

Vitamin D may be more important that I imagine, and is worth considering, but don't people that absolutely never wear hats also get hair loss?
 

Luckytype

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Yes, even though its initially plausible based on a few observations—e.g. (1) synthetic vitamin D analogues can cause hair growth; (2) vitamin D knockout rats are hairless; and (3) head pattern balding is reminiscent of shadows formed by hats, of course worn primarily by men—quite a bit of vitamin D is distributed by the bloodstream to the head, to compensate, and other shaded areas do have hair.

Perhaps vitamin D is not even needed at all? The rats in the study had lost an entire transcription factor—or had it inactivated somehow—and one responsible for dimerizing with retinoic acid receptors. It could be more that the RAR had lost a dimer partner than a consequence of vitamin D transcription per se. I think this is findoutable becaues vitamin D knockout and vitamin D knockdown rats are common, used in dozens of studies that are completely unrelated to hair. What would it mean if only knockout mutations in the vitamin D receptor RAR-binding domain caused hair loss? and never mutations placed in the vitamin D binding domain?

Vitamin D may be more important that I imagine, and is worth considering, but don't people that absolutely never wear hats also get hair loss?

Absolutely, and if we consider the way a blanket sits on a car when people hastily use it as a car cover that should provide a reconsideration in scalp mechanics. Then consider the rats along with infants. Same pattern of baldness but aside from the obvious incredible prolactin levels of newborns and that physiological stress of entering the world..are they dealing with scalp calcification - absolutely not.

The complexity of this for those concerned continues to have so many facets that unfortunately people get isolated upon. Is tissue changing? Yes. Is it fibrotic, in some cases yes.

But what nobody is considering or articulating is that a compromised energy pattern or system of cell replacement(our body), loses its integrity in whole or in part it then becomes susceptible to the figurative and literal environment. As such is the case with the obvious things - thyroid issues, vitamin issues, inability to buffer stressors. Once energy balance and thus physical structural integrity is restored, once the scalp doesnt have to physically fight gravity, once every cell becomes resistant to regular epigenetic change, hair growth will reoccur.

There is a reason why grass can grow in flexible soil but not in clay. The soil is relaxed, clay is high energy with limited flexibility unless forced
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

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