Metabolic (energy) deficiency may be the cause of Parkinson Disease (PD)

haidut

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The dogma that PD is just a simple dopamine deficiency manifesting in genetically vulnerable individuals is quickly becoming untenable. It is well-known among clinicians that administering dopamine precursors such as L-Dopa, or selective dopamine agonists such as pramipexole has limited therapeutic effects for PD patients and invariably become ineffective after a few years of use. A few months ago, several studies identified serotonin excess as the primary driver of several key symptoms of PD such as tremors and psychosis. The role of serotonin in PD is corroborated by the fact that dopamine agonists that also possess serotonin antagonism properties such as bromocriptine, lisuride, methysergide, etc do not generally use effectiveness with prolonged use. Serotonin has a known, potent, anti-metabolic effect and anti-serotonin agents are now studied as possible treatments for obesity, diabetes, CVD, dementias, and even aging. The study below demonstrates that at its core, PD is likely an energetic deficiency disorder, which would explain both the serotonin excess seen in PD patients, as well as the positive effects of anti-serotonin/pro-dopamine drugs. It also opens the avenue to a number of metabolic therapies for PD, including reduction of endotoxin/LPS, and usage of OTC substances such as aspirin, naicinamide, progesterone, DHEA, testosterone/DHT, salt / baking soda, quinones (methylene blue, vitamin K, tetracyclines, etc), and anti-estrogenic substances (both OTC and pharma drugs), among others. Coincidentally, there is at least one study for any of the substances I mentioned above demonstrating robust therapeutic (and preventative) effect of said substance in a PD animal model. Some of them have already been tested in humans, but FDA demands that clinical trials with thousands of people be conducted before any of those substance can be used on PD patients, despite their proven safety and low cost.

Influence of energy deficiency on the subcellular processes of Substantia Nigra Pars Compacta cell for understanding Parkinsonian neurodegeneration - PubMed
IIT Madras Researchers find Energy Deficiency in some Brain Cells to be a major cause for Parkinson's Disease | Indian Institute of Technology Madras
"...Although it is known that PD is caused by the loss of dopaminergic cells in substantia nigra pars compacta (SNc), the decisive cause of this inexorable cell loss has not clearly been elucidated before. The IIT Madras researchers developed a computational model that showed that energy deficiency might be a major cause of SNc cell loss in Parkinson's Disease. This computational modelling was developed by Dr. Vignayanandam Ravindernath Muddapu, who completed his Ph.D. recently at IIT Madras, under the guidance of Prof. V. Srinivasa Chakravarthy, Department of Biotechnology, IIT Madras. Dr. Vignayanandam Ravindernath Muddapu has now joined the Blue Brain Project, an EPFL-linked research center for postdoctoral research. The findings of this research have been published recently in the prestigious peer-reviewed International Journal Nature Scientific Reports. Elaborating on the important findings of this research, Prof. V. Srinivasa Chakravarthy, Department of Biotechnology, IIT Madras, said, "While existing treatments manage PD symptoms - sometimes with great effect - a cure demands an understanding of the root cause of SNc cell loss. This is the main question addressed in our work: What is the major underlying cause of SNc cell loss in PD?" Further, Prof. V. Srinivasa Chakravarthy said, "It is quite remarkable that loss of neurons in a small nucleus like SNc can have wide-ranging, devastating effects in all the four major domains of brain function - sensory-motor, cognitive, affective, and autonomous. The sequence of the three computational studies suggests that metabolic deficiency within the basal ganglia circuit is the common underlying factor at the subcellular, cellular, and network level in PD. Thus, we have a reasonably comprehensive theory of the pathogenesis of Parkinson's disease." This research was undertaken at IIT Madras Computational Neuroscience Laboratory, which aims to build a simplified model of the whole brain and use it to develop applications in medicine and engineering. Prof. V. Srinivasa Chakravarthy is the head of Computational Neuroscience Laboratory. The computational model showed that: At the subcellular level, metabolic deficiency leads to changes like including alpha-synuclein aggregation, reactive oxygen species production, calcium elevation, and dopamine dysfunction, which are characteristic subcellular changes in Parkinson's disease."
 

mostlylurking

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The sequence of the three computational studies suggests that metabolic deficiency within the basal ganglia circuit is the common underlying factor at the subcellular, cellular, and network level in PD. Thus, we have a reasonably comprehensive theory of the pathogenesis of Parkinson's disease."
Dr. Costantini of Italy demonstrated via his successful treatment of over 4,000 patients that high dose thiamine solves the problem of metabolic deficiency in Parkinson's Disease. link to his site: HDT Therapy

"High-Dose Thiamine (HDT) therapy, administered at the right custom-corrected dose, improves fatigue and other symptoms in Parkinson’s Disease, as well as fatigue and disorder-specific symptoms in a number of other neurodegenerative (and related auto-immune and/or inflammatory) disorders.

What follows is a detailed explanation of how HDT therapy has been used for treating Parkinson’s Disease — both clinically and in studies — by Dr. Costantini."
At the subcellular level, metabolic deficiency leads to changes like including alpha-synuclein aggregation, reactive oxygen species production, calcium elevation, and dopamine dysfunction, which are characteristic subcellular changes in Parkinson's disease."
link to a list of Dr. Costantini's published papers: Published Study Articles
 

Birdie

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The dogma that PD is just a simple dopamine deficiency manifesting in genetically vulnerable individuals is quickly becoming untenable. It is well-known among clinicians that administering dopamine precursors such as L-Dopa, or selective dopamine agonists such as pramipexole has limited therapeutic effects for PD patients and invariably become ineffective after a few years of use. A few months ago, several studies identified serotonin excess as the primary driver of several key symptoms of PD such as tremors and psychosis. The role of serotonin in PD is corroborated by the fact that dopamine agonists that also possess serotonin antagonism properties such as bromocriptine, lisuride, methysergide, etc do not generally use effectiveness with prolonged use. Serotonin has a known, potent, anti-metabolic effect and anti-serotonin agents are now studied as possible treatments for obesity, diabetes, CVD, dementias, and even aging. The study below demonstrates that at its core, PD is likely an energetic deficiency disorder, which would explain both the serotonin excess seen in PD patients, as well as the positive effects of anti-serotonin/pro-dopamine drugs. It also opens the avenue to a number of metabolic therapies for PD, including reduction of endotoxin/LPS, and usage of OTC substances such as aspirin, naicinamide, progesterone, DHEA, testosterone/DHT, salt / baking soda, quinones (methylene blue, vitamin K, tetracyclines, etc), and anti-estrogenic substances (both OTC and pharma drugs), among others. Coincidentally, there is at least one study for any of the substances I mentioned above demonstrating robust therapeutic (and preventative) effect of said substance in a PD animal model. Some of them have already been tested in humans, but FDA demands that clinical trials with thousands of people be conducted before any of those substance can be used on PD patients, despite their proven safety and low cost.

Influence of energy deficiency on the subcellular processes of Substantia Nigra Pars Compacta cell for understanding Parkinsonian neurodegeneration - PubMed
IIT Madras Researchers find Energy Deficiency in some Brain Cells to be a major cause for Parkinson's Disease | Indian Institute of Technology Madras
"...Although it is known that PD is caused by the loss of dopaminergic cells in substantia nigra pars compacta (SNc), the decisive cause of this inexorable cell loss has not clearly been elucidated before. The IIT Madras researchers developed a computational model that showed that energy deficiency might be a major cause of SNc cell loss in Parkinson's Disease. This computational modelling was developed by Dr. Vignayanandam Ravindernath Muddapu, who completed his Ph.D. recently at IIT Madras, under the guidance of Prof. V. Srinivasa Chakravarthy, Department of Biotechnology, IIT Madras. Dr. Vignayanandam Ravindernath Muddapu has now joined the Blue Brain Project, an EPFL-linked research center for postdoctoral research. The findings of this research have been published recently in the prestigious peer-reviewed International Journal Nature Scientific Reports. Elaborating on the important findings of this research, Prof. V. Srinivasa Chakravarthy, Department of Biotechnology, IIT Madras, said, "While existing treatments manage PD symptoms - sometimes with great effect - a cure demands an understanding of the root cause of SNc cell loss. This is the main question addressed in our work: What is the major underlying cause of SNc cell loss in PD?" Further, Prof. V. Srinivasa Chakravarthy said, "It is quite remarkable that loss of neurons in a small nucleus like SNc can have wide-ranging, devastating effects in all the four major domains of brain function - sensory-motor, cognitive, affective, and autonomous. The sequence of the three computational studies suggests that metabolic deficiency within the basal ganglia circuit is the common underlying factor at the subcellular, cellular, and network level in PD. Thus, we have a reasonably comprehensive theory of the pathogenesis of Parkinson's disease." This research was undertaken at IIT Madras Computational Neuroscience Laboratory, which aims to build a simplified model of the whole brain and use it to develop applications in medicine and engineering. Prof. V. Srinivasa Chakravarthy is the head of Computational Neuroscience Laboratory. The computational model showed that: At the subcellular level, metabolic deficiency leads to changes like including alpha-synuclein aggregation, reactive oxygen species production, calcium elevation, and dopamine dysfunction, which are characteristic subcellular changes in Parkinson's disease."

Thanks for this. My husband has PD symptoms andI had been convinced it's not just a dopamine deficiency to be remedied with the PD drugs. I appreciate your concise list of lowering serotonin stuff: OTC substances such as aspirin, niacinamide, progesterone, DHEA, testosterone/DHT, salt / baking soda, quinones (methylene blue, vitamin K, tetracyclines, etc), and anti-estrogenic substances (both OTC and pharma drugs), among others.

Also, this, "The role of serotonin in PD is corroborated by the fact that dopamine agonists that also possess serotonin antagonism properties such as bromocriptine, lisuride, methysergide, etc do not generally lose effectiveness with prolonged use.

So far, as @mostlylurking advises, we have been using Dr Costantini's protocol for high dose thiamine this past year. It has relieved symptoms including chocking. After his first dose he was able to swallow pills again. His nighttime drooling decreased. His blurred speech improved.

But also has gynecomastia. This began about 5 years ago and has worsened. Recent blood labs show high estradiol. Of course, we knew this was probably a culprit, but it helps to see the labs in his case.

After spending the past 5 years trying a dietary approach with little acceptance by "the patient", I am looking at Exemestane after reading that @ecstatichamster and others have had good result with low doses for lowering estradiol (I think). Also have some bromocriptine that I'm considering. I'm foggy on it but seems it could cause problems in Parkinson's patients.

He has been taking some that are on your list: aspirin, niacin amide, 1 drop progesterone, DHEA occasionally, some salt, baking soda in oj, vitamin K, doxycycline 50mg 5days wk... He also has moderate prostate problems so he avoids antihistamines such as Benadryl which we think are contraindicated there. I anybody knows if cyproheptadine, also H1, I guess so maybe contraindicated.

Probably not enough salt and could up progesterone a little.
 

mostlylurking

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He has been taking some that are on your list: aspirin, niacin amide, 1 drop progesterone, DHEA occasionally, some salt, baking soda in oj, vitamin K, doxycycline 50mg 5days wk... He also has moderate prostate problems so he avoids antihistamines such as Benadryl which we think are contraindicated there. I anybody knows if cyproheptadine, also H1, I guess so maybe contraindicated.

Probably not enough salt and could up progesterone a little.
I'm not a doctor and I don't play one on TV, but it seems to me that your husband could benefit from a LOT more progesterone.

I've been taking about 40 mgs of progesterone in vitamin E (Progest-E = about 3/16-1/4 teaspoon) a day for about 6 years. It has been a life saver. RP has said that if there is a specific reason for it, men should also try it and not be concerned with side effects because it is very safe and clears the system pretty quickly. The idea is that gynecomastia is caused by high estrogen and progesterone lowers estrogen.

Here's a video for your consideration. I may not have it queued up at exactly the right spot so you may want to listen to some of the earlier show too.

View: https://youtu.be/zE_aBt6UYEo?t=9028
 

Birdie

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I'm not a doctor and I don't play one on TV, but it seems to me that your husband could benefit from a LOT more progesterone.

I've been taking about 40 mgs of progesterone in vitamin E (Progest-E = about 3/16-1/4 teaspoon) a day for about 6 years. It has been a life saver. RP has said that if there is a specific reason for it, men should also try it and not be concerned with side effects because it is very safe and clears the system pretty quickly. The idea is that gynecomastia is caused by high estrogen and progesterone lowers estrogen.

Here's a video for your consideration. I may not have it queued up at exactly the right spot so you may want to listen to some of the earlier show too.

View: https://youtu.be/zE_aBt6UYEo?t=9028

Thank you very much. This might be just what my husband needs. I'll send him your note. (He's not much for watching videos.) I don't think he needs a lot of eroding, just something to spur thought.

I didn't mean eroding. Got distracted. 3/16 to 1/4 tsp is more than I take too. I use 3 drops and rub it on gums. I have to drink tea after or else the progest-e choke. Will tell him and appreciate your comments.
 
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Progesterone is fantastic for men. Add a few mgs of DHEA and it is very good for promoting male androgens.
 

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Thanks ecstaticampster. He has a question for you guys. He says how old are you? He is 86 and I guess I need to figure out how much he needs for age and weight of 120 lbs.
 

Birdie

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I'm not a doctor and I don't play one on TV, but it seems to me that your husband could benefit from a LOT more progesterone.

I've been taking about 40 mgs of progesterone in vitamin E (Progest-E = about 3/16-1/4 teaspoon) a day for about 6 years. It has been a life saver. RP has said that if there is a specific reason for it, men should also try it and not be concerned with side effects because it is very safe and clears the system pretty quickly. The idea is that gynecomastia is caused by high estrogen and progesterone lowers estrogen.

Here's a video for your consideration. I may not have it queued up at exactly the right spot so you may want to listen to some of the earlier show too.

View: https://youtu.be/zE_aBt6UYEo?t=9028

I'm back here looking for more help for my husband. In the video, Georgi is talking about famotidine's lowering serotonin. The problem is that I understand that anti-histamines are contraindicated for men with prostatitis which my husband has. He stopped taking Benadryl for that reason. It's really too bad because it would seem that using famotidine would really help with his serotonin problem.

Still I might be able to get him to take more progest-E. 1/4 teaspoon sounds like an awful lot. I take that much, 4 big drops. I know gynecomastia is associated with high estrogen. What we have here is a case of possible patient resistance.

A quick search brought up this info connecting antihistamines and enlarged prostate:

Famotidine and Enlarged prostate - a phase IV clinical study of FDA data​

Summary:​

Enlarged prostate is found among people who take Famotidine, especially for people who are 60+ old, have been taking the drug for < 1 month.
The phase IV clinical study analyzes which people take Famotidine and have Enlarged prostate. It is created by eHealthMe based on reports of 56,645 people who have side effects when taking Famotidine from the FDA, and is updated regularly.


You should not use cyproheptadine if you have narrow-angle glaucoma, a stomach ulcer or obstruction, an enlarged prostate, urination problems, or if you are having an asthma attack.

I have been giving him a drop of cypro. I don't know if that's enough to be a problem, but I think I'll stop it to be on the safe side.
 

mostlylurking

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I'm back here looking for more help for my husband. In the video, Georgi is talking about famotidine's lowering serotonin. The problem is that I understand that anti-histamines are contraindicated for men with prostatitis which my husband has. He stopped taking Benadryl for that reason. It's really too bad because it would seem that using famotidine would really help with his serotonin problem.

Still I might be able to get him to take more progest-E. 1/4 teaspoon sounds like an awful lot. I take that much, 4 big drops. I know gynecomastia is associated with high estrogen. What we have here is a case of possible patient resistance.

A quick search brought up this info connecting antihistamines and enlarged prostate:

Famotidine and Enlarged prostate - a phase IV clinical study of FDA data​

Summary:​

Enlarged prostate is found among people who take Famotidine, especially for people who are 60+ old, have been taking the drug for < 1 month.
The phase IV clinical study analyzes which people take Famotidine and have Enlarged prostate. It is created by eHealthMe based on reports of 56,645 people who have side effects when taking Famotidine from the FDA, and is updated regularly.


You should not use cyproheptadine if you have narrow-angle glaucoma, a stomach ulcer or obstruction, an enlarged prostate, urination problems, or if you are having an asthma attack.

I have been giving him a drop of cypro. I don't know if that's enough to be a problem, but I think I'll stop it to be on the safe side.
Thank you for this information. Both my husband and I have been taking some Sambrosa nighttime cold & flu med due to catching the Omicron Covid a couple of weeks ago. There's an antihistamine in it; Doxylamine Succinate. I'll warn him about it as it seems to be slightly addictive; I've had some trouble sleeping without it now.

Isn't your husband taking thiamine? If yes, thiamine is known to lower high brain serotonin.

and
This second one explains that you need magnesium too. also this: "Serotonin in stomach and intestine increased in the excess-thiamine, magnesium-deficient group."

It would be nice if the patient would be willing to give a larger dose (1/4teas) of the progest-E a try for a few days (in the evening, before bed). Just a few days, to see if there's improvement.
 

mostlylurking

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@mostlylurking How does one know if thiamine is working to reduce serotonin? What are the signs to look out for?
Well, I'd look for improvement in the symptoms of high serotonin that you see now. For me, I stopped reacting negatively to high serotonin foods (bananas) and I became less tense and anxious. I had many improvements via high dose thiamine hcl plus magnesium (plus a b-complex supplement), some I'm sure were related to lowered serotonin, some unrelated to that.
 
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Well, I'd look for improvement in the symptoms of high serotonin that you see now. For me, I stopped reacting negatively to high serotonin foods (bananas) and I became less tense and anxious. I had many improvements via high dose thiamine hcl plus magnesium (plus a b-complex supplement), some I'm sure were related to lowered serotonin, some unrelated to that.
Thanks. Interesting that bananas are an issue for you. Just over 10 years ago I had a strange reaction after eating a banana. It doesn't happen anymore but I don't tend to eat them now. I do remember feeling very ill after eating pineapples last year, the same thing happened with kiwi. I used to be able to tolerate these before. They are both high in digestive enzymes so some of the discomfort could also be due to that. Anyway , it's good to know what to look out for.
 

mostlylurking

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Thanks. Interesting that bananas are an issue for you. Just over 10 years ago I had a strange reaction after eating a banana. It doesn't happen anymore but I don't tend to eat them now. I do remember feeling very ill after eating pineapples last year, the same thing happened with kiwi. I used to be able to tolerate these before. They are both high in digestive enzymes so some of the discomfort could also be due to that. Anyway , it's good to know what to look out for.
Kiwis and pineapples are also on the list of high serotonin foods. I react badly to them too. Kiwi has other things that are problematic; they make my mouth and lips break out as if I've chewed on poison ivy. I avoid them like the plague.

Here's a link: https://treehozz.com/are-bananas-high-in-serotonin
"While bananas contain serotonin, having one for a snack won't immediately lift your spirits. Unlike other forms, the serotonin found in bananas doesn't cross the blood-brain barrier,2? which means it can't get into the brain to supplement the serotonin that's naturally produced by the body.
Click here to know more about it.
Simply so, what fruits are high in serotonin?
Plantains, pineapple, bananas, kiwi fruit, plums, and tomatoes contain high amounts of serotonin. Moderate amounts can be found in avocados, dates, grapefruit, cantaloupe, and more. Eat a variety of fruits and vegetables every day to get the best health benefits."

I react badly to the whole list of foods mentioned. I have no idea if it's true that the foods listed raise serotonin but I've seen this list mentioned other places on line that make that claim. On many lists they focus on foods high in tryptophan. It seems they always encourage eating them to raise serotonin as if that's a good thing. Ha!
 
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Kiwis and pineapples are also on the list of high serotonin foods. I react badly to them too. Kiwi has other things that are problematic; they make my mouth and lips break out as if I've chewed on poison ivy. I avoid them like the plague.

Here's a link: https://treehozz.com/are-bananas-high-in-serotonin
"While bananas contain serotonin, having one for a snack won't immediately lift your spirits. Unlike other forms, the serotonin found in bananas doesn't cross the blood-brain barrier,2? which means it can't get into the brain to supplement the serotonin that's naturally produced by the body.
Click here to know more about it.
Simply so, what fruits are high in serotonin?
Plantains, pineapple, bananas, kiwi fruit, plums, and tomatoes contain high amounts of serotonin. Moderate amounts can be found in avocados, dates, grapefruit, cantaloupe, and more. Eat a variety of fruits and vegetables every day to get the best health benefits."

I react badly to the whole list of foods mentioned. I have no idea if it's true that the foods listed raise serotonin but I've seen this list mentioned other places on line that make that claim. On many lists they focus on foods high in tryptophan. It seems they always encourage eating them to raise serotonin as if that's a good thing. Ha!
This is interesting - the last time I had an avocado it went straight through me. My gut changed dramatically once I started bp meds, makes me wonder. It's good to know bananas are not as bad as some of the others - I think if they are well ripened, with spots, they can be good for the gut. I really like oranges/tangerines etc but my gut really struggles to get used to them.
 

mostlylurking

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This is interesting - the last time I had an avocado it went straight through me. My gut changed dramatically once I started bp meds, makes me wonder. It's good to know bananas are not as bad as some of the others - I think if they are well ripened, with spots, they can be good for the gut. I really like oranges/tangerines etc but my gut really struggles to get used to them.
Ray Peat does not speak very highly of bananas.
View: https://youtu.be/FiyW1y9Buo8?t=2926


He doesn't like avocados either; too much PUFA. He considers them a toxic food.

I eat a lot of oranges/tangerines too. I tolerate them pretty well.
 
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@mostlylurking thanks, I've heard peat talk about these fruits before. I'm still trying to figure out why I itch when I eat oranges/tangerines. I have access to organic grapes so I tend to eat more of them now.
 

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@mostlylurking thanks, I've heard peat talk about these fruits before. I'm still trying to figure out why I itch when I eat oranges/tangerines. I have access to organic grapes so I tend to eat more of them now.
I've learned that I do better if I eat organic oranges/tangerines. They aren't available often so I get what's available. I've noticed that some non-organic brands taste so bad I have to spit them out. They are flat out nasty; I think they have absorbed whatever was sprayed on them.

I eat peaches when they are available. The secret about peaches is that you have to buy them hard as rocks then set them out on the counter for 7-10 days until they smell like peaches and are ripe. Then you blanch them in boiling water for about 30-60 seconds and then slip the skins off and slice them up. They grow a lot of peaches locally but the peaches I buy from the grocery are from Georgia. Greed has set in at the local peach stands due to the plethora of tourists so the price for local peaches is double that for the grocery store peaches.

I also eat locally grown organic (I think) red plums when my friend gives me some. Delicious! It's a once a year thing.
 
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I've learned that I do better if I eat organic oranges/tangerines. They aren't available often so I get what's available. I've noticed that some non-organic brands taste so bad I have to spit them out. They are flat out nasty; I think they have absorbed whatever was sprayed on them.

I eat peaches when they are available. The secret about peaches is that you have to buy them hard as rocks then set them out on the counter for 7-10 days until they smell like peaches and are ripe. Then you blanch them in boiling water for about 30-60 seconds and then slip the skins off and slice them up. They grow a lot of peaches locally but the peaches I buy from the grocery are from Georgia. Greed has set in at the local peach stands due to the plethora of tourists so the price for local peaches is double that for the grocery store peaches.

I also eat locally grown organic (I think) red plums when my friend gives me some. Delicious! It's a once a year thing.
The quality of supermarket fruits is questionable. Thanks for the tips on peaches
 

mostlylurking

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The quality of supermarket fruits is questionable. Thanks for the tips on peaches
The blanching time might be shorter than what I said; may be more like 15-20 seconds. You'll get a feel for it. If you cook the skins too long they go mushy and don't stay together for easy removal.
 
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Peatness

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The blanching time might be shorter than what I said; may be more like 15-20 seconds. You'll get a feel for it. If you cook the skins too long they go mushy and don't stay together for easy removal.
Thanks
 

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