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question to droddy and others

+5
ngb
DeadlyDevice
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egodust
researchingeverything
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Post  researchingeverything Thu Apr 10, 2014 8:29 am

why you dont recommend krill oil, curcumin and quercetin?
do you think fish oil is bad for the health?

wouldnt be an onion soup rich in quercetin a great food for us?

also you recommend coffee...but caffeine can interfere with zinc absorption of zinc by as much as 50 percent

also not sure..but i dont think you dont talk about glutathione

your suggestions are for all types of hair loss?

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Post  egodust Thu Apr 10, 2014 8:43 am

researchingeverything wrote:
why you dont recommend krill oil, curcumin and quercetin?
do you think fish oil is bad for the health?

all of these are COX-1 and COX-2 inhibitors, the Peat protocol contains inhibitors in the form of plant food, i.e. beta-carotene will also inhibit COX-2 but won't give EPA and DHA.

researchingeverything wrote:
wouldnt be an onion soup rich in quercetin a great food for us?

tbh, therapeutic levels of quercetin cannot be found from food, parsley is probably better as it contains
vanadium and other trace minerals

researchingeverything wrote:
also you recommend coffee...but caffeine can interfere with zinc absorption of zinc by as much as 50 percent

there are pros and cons, caffeine is associated with higher levels of SHBG which bind to DHT and that is good for
hair - it is also associated with better insulin response which is also good for hair.

Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3012180/

Too much Zinc is bad for hair because it suppresses Copper - which is needed to absorb Zinc in the first place
but at the right dosage to suppress 5ar activity.

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Post  droddy Fri Apr 11, 2014 9:43 am

I look at hair loss in the context of energy metabolism. More specifically, glucose to carbon dioxide through the mitochondria.

researchingeverything wrote:why you dont recommend krill oil,


Unsaturated fats significantly interfere with energy metabolism.

researchingeverything wrote:curcumin and quercetin?


These things are 'shots in the dark'. There are more physiologically appropriate therapies like nutrition, thyroid hormone, vitamin D, vitamin K, and maybe aspirin.

researchingeverything wrote:do you think fish oil is bad for the health?


Unsaturated fats significantly interfere with energy metabolism.

researchingeverything wrote:also you recommend coffee...


Coffee is a source of magnesium, and the caffeine seems to be a potent anti-inflammatory. However, I can see how if not used properly coffee could cause problems, for instance if it was consumed along without sugar and fat.

researchingeverything wrote:your suggestions are for all types of hair loss?

Discussions about whether a person’s hair loss is androgenic, androgen-independent, or age-related have neglected the possibility that pattern hair loss does not begin in advanced age or when a genetic code is triggered. Rather, I think that pattern hair loss—of any kind—is the result of a life-long development process involving stress, energy and aging.
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Post  DeadlyDevice Fri Apr 11, 2014 9:28 pm

Has anyone with MPB messaged you saying that they have actually regrown hair with your methods, droddy?

There are like 2 people on this entire forum that I've seen get regrowth, one of them is doing manuals, and the other was loaded with different supplements and possibly had hair loss related to steroids or what not.

So I am wondering, what is the success rate of your approach?

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Post  droddy Sat Apr 12, 2014 4:47 am

DeadlyDevice wrote:Has anyone with MPB messaged you saying that they have actually regrown hair with your methods, droddy?

So I am wondering, what is the success rate of your approach?

Time will tell how fruitful the new paradigm is (my book just came out last December), but I've been sent a more than a few anecdotes from people who have said that they've stopped their hair loss and caused it to thicken up.

The great thing about what I'm saying is that you don't have to take my word for it: Measuring your pulse rate and body temperature over the span of a week is probably good enough to estimate where the metabolic rate is at. Some people invest in lab work to test their TSH, prolactin, parathyroid hormone, carbon dioxide, and other hormones associated with baldness and bone health.

For what it's worth here are reviews of my book: http://amzn.to/1c9Ndhv
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Post  ngb Sat Apr 12, 2014 5:04 am

So 30 calories of Krill oil will significantly interfere with energy metabolism and offer no health benefits? The most krill or fish oil I've seen anyone recommending is 5 grams. This fanatical avoidance of all PUFA seems a little chicken little-ish to me.

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Post  droddy Sat Apr 12, 2014 5:27 am

ngb wrote:So 30 calories of Krill oil will significantly interfere with energy metabolism and offer no health benefits?  The most krill or fish oil I've seen anyone recommending is 5 grams.  This fanatical avoidance of all PUFA seems a little chicken little-ish to me.

I don't know what "chicken little-ish" means, but all food contains PUFA.

If the accumulation of PUFA, overtime, caused baldness it's probably reasonable to avoid it as much as possible.
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Post  Manoko Sat Apr 12, 2014 5:46 am

droddy wrote:
ngb wrote:So 30 calories of Krill oil will significantly interfere with energy metabolism and offer no health benefits?  The most krill or fish oil I've seen anyone recommending is 5 grams.  This fanatical avoidance of all PUFA seems a little chicken little-ish to me.

I don't know what "chicken little-ish" means, but all food contains PUFA.

If the accumulation of PUFA, overtime, caused baldness it's probably reasonable to avoid it as much as possible.

Danny Roddy, would you be so kind as to look at the regimen described in this thread: https://immortalhair.forumotion.com/t10092-supposed-regrowth-protocol

I tend to think it might have a link with the diet you advocate on Hair Like a Fox, and wanted to simply have your opinion on it, see it through a "Peat-prism".

Thank you. Smile

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Post  ngb Sat Apr 12, 2014 6:30 am

droddy wrote:
ngb wrote:So 30 calories of Krill oil will significantly interfere with energy metabolism and offer no health benefits?  The most krill or fish oil I've seen anyone recommending is 5 grams.  This fanatical avoidance of all PUFA seems a little chicken little-ish to me.

I don't know what "chicken little-ish" means, but all food contains PUFA.

If the accumulation of PUFA, overtime, caused baldness it's probably reasonable to avoid it as much as possible.

Could you explain how PUFA accumulates?

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Post  droddy Sat Apr 12, 2014 7:00 am

[quote="ngb"][quote="droddy"]
ngb wrote:Could you explain how PUFA accumulates?

Body fat reflects the types of fats consumed over a life time. In stress, fat is liberated into the blood (i.e., lipolysis). If these fats were primarily saturated, the stress response would be self-limiting, however, unsaturated fats appear to intensify the stress response.

Gerontology. 1993;39(1):7-18.
Modulation of membrane phospholipid fatty acid composition by age and food restriction.
Laganiere S, Yu BP.
Phospholipids from liver mitochondrial and microsomal membrane preparations were analyzed to further assess the effects of age and lifelong calorie restriction on membrane lipid composition. Results showed that the major phospholipid classes, phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylinositol and cardiolipin did not vary significantly with age or diet. The fatty acid composition of the phospholipids was determined in PC and PE and ages of 6, 12 and 24 months. The data revealed characteristic patterns of age-related changes in ad libitum (AL) fed rats: membrane levels of long-chain polyunsaturated fatty acids, 22:4 and 22:5, increased progressively, while membrane linoleic acid (18:2) decreased steadily with age. Levels of 18:2 fell by approximately 40%, and 22:5 content almost doubled making the peroxidizability index increase with age. In addition, levels of 16:1 and 18:1 decreased significantly with age, indicating a possible change in delta 9-desaturase activity coefficient. Food restriction resulted in a significant increase in levels of essential fatty acids while attenuating levels of 22:4, 22:5, 22:6 and peroxidizability. We concluded that the membrane-stabilizing action of long-term calorie restriction relates to the selective modification of membrane long-chain polyunsaturated fatty acids during aging.


Modulation of cardiac mitochondrial membrane fluidity by age and calorie intake.
Lee J, Yu BP, Herlihy JT.
The aim of the present study was to determine the effects of dietary restriction (DR) on the age-related changes in membrane fluidity, fatty acid composition and free radical damage of mitochondrial membranes obtained from the rat left ventricle. Mitochondrial membrane preparations were obtained from the left ventricles of 6- and 24-month-old, male, Fischer 344 rats that were allowed to eat throughout their life either ad lib (Group A) or only 60% of the amount consumed by the ad lib fed group (Group B). Our results show that the membrane fluidity of the 24 month Group A hearts was less than that of the 6 month group A hearts. No differences in membrane fluidity were observed between the 6 and 24 month DR groups. The fatty acid composition of the mitochondrial membranes of the two ad lib fed groups differed: the long-chain polyunsaturated 22:4 fatty acid was higher in the older group, although linoleic acid (18:2) was lower. DR eliminated the differences. No statistically significant difference in the overall polyunsaturated fatty acid content was noted. However, the peroxidizability index was higher in the membranes of the 24 month Group A hearts but not in the 24 month Group B hearts. Finally, the degree of lipid damage, as assessed in vitro by the induced production of reactive oxygen species, was elevated in the 24 month Group A hearts. No difference was observed between the young and old DR groups. Considered together, these results suggest that DR maintains the integrity of the cardiac mitochondrial membrane fluidity by minimizing membrane damage through modulation of membrane fatty acid profile.

Ophthalmic Res. 1999;31(4):273-9.
Age-related accumulation of free polyunsaturated fatty acids in human retina.
Nourooz-Zadeh J, Pereira P.
The present study reports composition of free (nonesterified) as well as total (sum of free and esterified) fatty acids (FAs) in human retina (n = 13). For free fatty acid (FFA) analysis, retina tissue was homogenized, total lipids were partitioned with ethyl acetate and subsequently applied onto a aminopropyl (NH2) cartridge to isolate FFAs from the bulk of other lipids. FFAs were converted to methyl ester derivatives and analysed by gas chromatography using flame ionization detector. Analysis of FFAs revealed that the mean percentage composition of the major components including palmitic acid (PA), stearic acid (SA), oleic acid (OA), arachidonic acid (AA) and docosahexaenoic acid (DHA) were 17.2, 36.7, 15.6, 8.8 and 14.2%, respectively. There were significant correlations between age of the donors’ and the content of both free AA and DHA (rPearson = 0.69, p = 0.005, and rPearson = 0.64, p = 0.009). The mean percentage of total PA, SA, OA, AA and DHA were 22.6, 23.2, 17.7, 11.4 and 21.9%, respectively. There was no association between age and any of the major FAs. The present study provides the first evidence for the presence of FFAs in the human retina as well as an age-related accumulation of polyunsaturated fatty acids (PUFAs). The latter finding suggests an alteration in the metabolism of retinal PUFAs which can be due to an increase of oxidative stress and/or decrease of antioxidant defences during ageing.


Ann Nutr Metab. 1989;33(6):315-22.
Adipose tissue levels of fatty acids and tocopherol in young and old women.
Schäfer L, Overvad K, Thorling EB, Velander G.
Tocopherol concentration and fatty acid composition were determined in samples of subcutaneous adipose tissue from 33 young and 28 old women. Young women exhibited more saturated fatty acids and less monounsaturated fatty acids than old women (p less than 0.01). Adipose tissue tocopherol correlated with plasma tocopherol, with r = 0.49 and p less than 0.01, when the data for young and old were combined. A negative association was found between adipose tissue tocopherol and the n-3/n-6 fatty acid ratio in the old women (r = 0.42; p less than 0.05), suggesting that the tocopherol content of adipose tissue is determined not only by the intake of the nutrient but also by the tissue fatty acid composition.


Ann Nutr Metab. 2007;51(5):433-8. Epub 2007 Nov 20.
Three-year tracking of fatty acid composition of plasma phospholipids in healthy children.
Guerra A, Demmelmair H, Toschke AM, Koletzko B.
OBJECTIVES:
The fatty acid composition of plasma phospholipids reflects the dietary fatty acid intake as well as endogenous turnover. We aimed at investigating the potential tracking of plasma phospholipid fatty acid composition in children that participated in a prospective cohort study.
METHODS:
26 healthy children participated in a longitudinal study on health risks and had been enrolled after birth. All children were born at term with birth weights appropriate for gestational age. Follow-up took place at ages 24, 36 and 60 months. At each time point a 24-hour dietary recall was obtained, anthropometric parameters were measured and a blood sample for phospholipid fatty acid analysis was taken.
RESULTS:
Dietary intake of saturated (SFA), monounsaturated (MUFA) and polyunsaturated (PUFA) fatty acids at the three time points were not correlated. We found lower values for plasma MUFA and the MUFA/SFA ratio at 60 months compared to 24 months. In contrast, total PUFA, total n-6 and n-6 long-chain polyunsaturated fatty acids (LC-PUFA) were higher at 60 months. Significant averaged correlation coefficients (average of Pearson’s R for 24 versus 36 months and 36 versus 60 months) were found for n-6 LC-PUFA (r = 0.67), n-6/n-3 LC-PUFA ratio (r = 0.59) and arachidonic acid/linoleic acid ratio (r = 0.64). Partial tracking was found for the docosahexaenoic acid/alpha-linolenic acid ratio (r = 0.33). Body mass index and sum of skinfolds Z-scores were similar in the three evaluations.
CONCLUSIONS:
A significant tracking of n-6 LC-PUFA, n-6 LC-PUFA/n-3 LC-PUFA ratio, arachidonic acid/linoleic acid ratio and docosahexaenoic acid/alpha-linolenic acid ratio may reflect an influence of individual endogenous fatty acid metabolism on plasma concentrations of some, but not all, fatty acids.
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Post  droddy Tue Apr 15, 2014 11:38 am

Manoko wrote:Danny Roddy, would you be so kind as to look at the regimen described in this thread: https://immortalhair.forumotion.com/t10092-supposed-regrowth-protocol

There doesn't seem to be any rhyme or reason to the supplements/drugs listed.
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Post  Shinobi Tue Apr 15, 2014 8:55 pm

droddy wrote:
ngb wrote:
droddy wrote:
ngb wrote:Could you explain how PUFA accumulates?

Body fat reflects the types of fats consumed over a life time. In stress, fat is liberated into the blood (i.e., lipolysis). If these fats were primarily saturated, the stress response would be self-limiting, however, unsaturated fats appear to intensify the stress response.

Gerontology. 1993;39(1):7-18.
Modulation of membrane phospholipid fatty acid composition by age and food restriction.
Laganiere S, Yu BP.
Phospholipids from liver mitochondrial and microsomal membrane preparations were analyzed to further assess the effects of age and lifelong calorie restriction on membrane lipid composition. Results showed that the major phospholipid classes, phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylinositol and cardiolipin did not vary significantly with age or diet. The fatty acid composition of the phospholipids was determined in PC and PE and ages of 6, 12 and 24 months. The data revealed characteristic patterns of age-related changes in ad libitum (AL) fed rats: membrane levels of long-chain polyunsaturated fatty acids, 22:4 and 22:5, increased progressively, while membrane linoleic acid (18:2) decreased steadily with age. Levels of 18:2 fell by approximately 40%, and 22:5 content almost doubled making the peroxidizability index increase with age. In addition, levels of 16:1 and 18:1 decreased significantly with age, indicating a possible change in delta 9-desaturase activity coefficient. Food restriction resulted in a significant increase in levels of essential fatty acids while attenuating levels of 22:4, 22:5, 22:6 and peroxidizability. We concluded that the membrane-stabilizing action of long-term calorie restriction relates to the selective modification of membrane long-chain polyunsaturated fatty acids during aging.


Modulation of cardiac mitochondrial membrane fluidity by age and calorie intake.
Lee J, Yu BP, Herlihy JT.
The aim of the present study was to determine the effects of dietary restriction (DR) on the age-related changes in membrane fluidity, fatty acid composition and free radical damage of mitochondrial membranes obtained from the rat left ventricle. Mitochondrial membrane preparations were obtained from the left ventricles of 6- and 24-month-old, male, Fischer 344 rats that were allowed to eat throughout their life either ad lib (Group A) or only 60% of the amount consumed by the ad lib fed group (Group B). Our results show that the membrane fluidity of the 24 month Group A hearts was less than that of the 6 month group A hearts. No differences in membrane fluidity were observed between the 6 and 24 month DR groups. The fatty acid composition of the mitochondrial membranes of the two ad lib fed groups differed: the long-chain polyunsaturated 22:4 fatty acid was higher in the older group, although linoleic acid (18:2) was lower. DR eliminated the differences. No statistically significant difference in the overall polyunsaturated fatty acid content was noted. However, the peroxidizability index was higher in the membranes of the 24 month Group A hearts but not in the 24 month Group B hearts. Finally, the degree of lipid damage, as assessed in vitro by the induced production of reactive oxygen species, was elevated in the 24 month Group A hearts. No difference was observed between the young and old DR groups. Considered together, these results suggest that DR maintains the integrity of the cardiac mitochondrial membrane fluidity by minimizing membrane damage through modulation of membrane fatty acid profile.

Ophthalmic Res. 1999;31(4):273-9.
Age-related accumulation of free polyunsaturated fatty acids in human retina.
Nourooz-Zadeh J, Pereira P.
The present study reports composition of free (nonesterified) as well as total (sum of free and esterified) fatty acids (FAs) in human retina (n = 13). For free fatty acid (FFA) analysis, retina tissue was homogenized, total lipids were partitioned with ethyl acetate and subsequently applied onto a aminopropyl (NH2) cartridge to isolate FFAs from the bulk of other lipids. FFAs were converted to methyl ester derivatives and analysed by gas chromatography using flame ionization detector. Analysis of FFAs revealed that the mean percentage composition of the major components including palmitic acid (PA), stearic acid (SA), oleic acid (OA), arachidonic acid (AA) and docosahexaenoic acid (DHA) were 17.2, 36.7, 15.6, 8.8 and 14.2%, respectively. There were significant correlations between age of the donors’ and the content of both free AA and DHA (rPearson = 0.69, p = 0.005, and rPearson = 0.64, p = 0.009). The mean percentage of total PA, SA, OA, AA and DHA were 22.6, 23.2, 17.7, 11.4 and 21.9%, respectively. There was no association between age and any of the major FAs. The present study provides the first evidence for the presence of FFAs in the human retina as well as an age-related accumulation of polyunsaturated fatty acids (PUFAs). The latter finding suggests an alteration in the metabolism of retinal PUFAs which can be due to an increase of oxidative stress and/or decrease of antioxidant defences during ageing.


Ann Nutr Metab. 1989;33(6):315-22.
Adipose tissue levels of fatty acids and tocopherol in young and old women.
Schäfer L, Overvad K, Thorling EB, Velander G.
Tocopherol concentration and fatty acid composition were determined in samples of subcutaneous adipose tissue from 33 young and 28 old women. Young women exhibited more saturated fatty acids and less monounsaturated fatty acids than old women (p less than 0.01). Adipose tissue tocopherol correlated with plasma tocopherol, with r = 0.49 and p less than 0.01, when the data for young and old were combined. A negative association was found between adipose tissue tocopherol and the n-3/n-6 fatty acid ratio in the old women (r = 0.42; p less than 0.05), suggesting that the tocopherol content of adipose tissue is determined not only by the intake of the nutrient but also by the tissue fatty acid composition.


Ann Nutr Metab. 2007;51(5):433-8. Epub 2007 Nov 20.
Three-year tracking of fatty acid composition of plasma phospholipids in healthy children.
Guerra A, Demmelmair H, Toschke AM, Koletzko B.
OBJECTIVES:
The fatty acid composition of plasma phospholipids reflects the dietary fatty acid intake as well as endogenous turnover. We aimed at investigating the potential tracking of plasma phospholipid fatty acid composition in children that participated in a prospective cohort study.
METHODS:
26 healthy children participated in a longitudinal study on health risks and had been enrolled after birth. All children were born at term with birth weights appropriate for gestational age. Follow-up took place at ages 24, 36 and 60 months. At each time point a 24-hour dietary recall was obtained, anthropometric parameters were measured and a blood sample for phospholipid fatty acid analysis was taken.
RESULTS:
Dietary intake of saturated (SFA), monounsaturated (MUFA) and polyunsaturated (PUFA) fatty acids at the three time points were not correlated. We found lower values for plasma MUFA and the MUFA/SFA ratio at 60 months compared to 24 months. In contrast, total PUFA, total n-6 and n-6 long-chain polyunsaturated fatty acids (LC-PUFA) were higher at 60 months. Significant averaged correlation coefficients (average of Pearson’s R for 24 versus 36 months and 36 versus 60 months) were found for n-6 LC-PUFA (r = 0.67), n-6/n-3 LC-PUFA ratio (r = 0.59) and arachidonic acid/linoleic acid ratio (r = 0.64). Partial tracking was found for the docosahexaenoic acid/alpha-linolenic acid ratio (r = 0.33). Body mass index and sum of skinfolds Z-scores were similar in the three evaluations.
CONCLUSIONS:
A significant tracking of n-6 LC-PUFA, n-6 LC-PUFA/n-3 LC-PUFA ratio, arachidonic acid/linoleic acid ratio and docosahexaenoic acid/alpha-linolenic acid ratio may reflect an influence of individual endogenous fatty acid metabolism on plasma concentrations of some, but not all, fatty acids.

Danny, thanks a lot for these studies but it seems it state opposite of what you want to show.. for exemple it clearly state a decrease in linoleic PUFA w6.. You confuse unsaturate fatty acid long chain and medium chain. As people confuse saturate faty acid long and medium chain.

Thus, there is plenty of studies wich clearly show a positiv corelation between specific unsaturate faty acid and health artery concern. CS made a great post years back about it.

Really you seems to mistaken in this war.

http://www.ncbi.nlm.nih.gov/pubmed/24727233

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Post  researchingeverything Wed Apr 16, 2014 2:54 am

hi danny where you get the vitamin k2 from? what you think about carrot juice?

do you think that glutathione and growth hormone are important for hair?
we can optimize those with diet and lifestyle too...

btw I lost 7 kg after removing bread, grains, quinoa, oatmeal fried foods and pasta etc etc

if I stop eating rice i will lose much more muscle and weight for sure...
i dont want to lose more hair but i want to look strong and muscular..with your diet will be difficult..

i think the problem is that in the last years i have given lots of carbs and food to my body...so my body and metabolism
changed during these years because of eating so much food and carbs...


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Post  theseeker86 Wed Apr 16, 2014 3:14 am

Carbs are positive or negative for hair?

I've been meaning to read hair like a fox, seems like it has some interesting stuff packed in there.

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Post  AS54 Wed Apr 16, 2014 4:04 am

To the contrary, I think the Peat diet could be very conducive for muscle building, although it would be a little more difficult on the wallet getting your protein from a larger proportion of seafood versus cheaper things like whey protein and beef. Its the PUFA limitations that make the Peat diet somewhat difficult in that respect, but it could be done. Gelatin is another option. Peat's diet certainly isn't low in protein. I believe - and correct me if I'm wrong - he gets upwards of 120 g daily. Milk and cheeses are rich in protein as well.

To be honest, I'm not sure how Peat feels about whey proteins. I have to believe he'd disagree with using them, some of the free aminos present which he's not a fan of.
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