Ray Peat Email Advice Depository

[UG Krishnamurti]

​	Jan 8, 2022, 4:23 AM

Q: Hello Dr. Peat

Is there any new research about losing sense of smell and taste due to covid. It's a 100% loss of smell and taste for me and this point.

RP: Trace minerals (e.g., having sea food once a week) and coffee have helped to improve the sense of smell in some studies.
Study he shared

 

[UG Krishnamurti]

​	Sun, Jan 9, 8:47 PM

Q: Hello Dr. Peat

I don't understand why I have sudden bursts of black moles on my face?

When I used high doses of VIT D I put my body in some kind of a stress mode. The experience of mast cell activation, high histamine, calcemia etc... Just days after that I've started getting black moles on my face and they don't stop even now - 6 months after.

What is the cause of this?

RP: Usually, a sudden multiplication of moles is a sign of hypothyroidism.

 

[UG Krishnamurti]

​	Thu, Feb 3, 12:46 AM

Q: Hello Dr. Peat

You once mentioned that radiation at higher altitude or in airplane is bigger or has bigger waves or something like that - therefore it is less dangerous than low level radiation because it cannot penetrate the tissues and you mention some Russian researcher if I remember correctly.

Would you mind sharing some studies which support that?

Much love

RP: You can find the research under “linear energy transfer,” high energy radiation, cosmic rays, etc. It’s well known basic science, but medical people rarely understand it.

 

[UG Krishnamurti]

​	Tue, Mar 8, 12:53 AM

Q: Hello Dr. Peat

What would be the difference between the people whose cells take up too much calcium leading to cell death and excitotoxicity and people who don't experience these calcium issues - where the calcium remains outside of the cell.

Why would the cell take up too much calcium?

I know you've said CO2 would expel excess calcium from the cell but would the lack of CO2 also cause the cells to retain it? Are there any other mechanisms through which this could happen?

Much love

RP: Yes, the lack of CO2 increases lactate; too little vitamin D and/or calcium in the diet increased parathyroid hormone, increasing lactate and intracellular calcium.

 

[UG Krishnamurti]

​	Sat, Mar 19, 1:10 AM

Q: Hello Dr. Peat

When I increase my fruit and cheese consumption I usually get motion sick quite often and tonight I wondered why for the first time.

I started reading about the drug that always helped me in these situations since I was a kid. The main ingredient of the drug is diphenhydramine - an antihistamine - which is also one of the main ingredients of benadryl.

Do you know if diphenhydramine is a safe thing to consume on a daily basis or at least several times a week in order to keep my histamine under control and what is the mechanism of action there - why would antihistamine help me with motion sickness?

Much love

RP: Histamine activates the parasympathetic nervous system, which is involved in nausea. Pure diphenhydramine is better than Benadryl. Cyproheptadine is another antihistamine. Histamine supports wakefulness, and too little lowers alertness.

Q: Thank you Dr. Peat

Do you think Cyproheptadine would be safer than diphenhydramine?
Would the minimal those of these substances be safe to use long term?

RP: My experience has been that cyproheptadine had a reparative effect, so that after a few days using a milligram, a half or fourth worked as well, and then I didn’t need it again for a long time.

 

[UG Krishnamurti]

​	Thu, Apr 7, 12:21 AM

Q: Hello Dr. Peat

This study found that when mice were injected with LPS brain serotonin levels dropped while staying the same in the control group.
While also stating that histamine rose in the brain - to block the effect of serotonin.

Do you think that histamine acts as a protective mechanism against high levels of serotonin? Histamine could be a key player in depression, according to study in mice

RP: No.

 

[UG Krishnamurti]

​	Apr 13, 2022, 12:34 AM

Q: Hello Dr. Peat

What do you think about the study which claims that Inhibition of succinate dehydrogenase by malonate promotes adult cardiomyocyte proliferation, revascularization, and heart regeneration.

Is malonate safe? I never heard of it before.

Malonate Promotes Adult Cardiomyocyte Proliferation and Heart Regeneration - PubMed

RESULTS: Our results demonstrate that injection of succinate into neonatal mice results in inhibition of cardiomyocyte proliferation and regeneration. Our evidence also shows that inhibition of SDH by malonate treatment after birth extends the window of cardiomyocyte proliferation and regeneration in juvenile mice. Remarkably, extending malonate treatment to the adult mouse heart after myocardial infarction injury results in a robust regenerative response within 4 weeks after injury via promoting adult cardiomyocyte proliferation and revascularization. Our metabolite analysis after SDH inhibition by malonate induces dynamic changes in adult cardiac metabolism.

RP: //shared a study//

Br J Pharmacol. 2005 Feb; 144(4): 528–537.
Malonate induces cell death via mitochondrial potential collapse and delayed swelling through an ROS-dependent pathway
Francisco J Fernandez-Gomez,1 Maria F Galindo,1 Maria Gómez-Lázaro,1 Victor J Yuste,2 Joan X Comella,2 Norberto Aguirre,3 and Joaquín Jordán1,4,*
Abstract
Herein we study the effects of the mitochondrial complex II inhibitor malonate on its primary target, the mitochondrion.
Malonate induces mitochondrial potential collapse, mitochondrial swelling, cytochrome c (Cyt c) release and depletes glutathione (GSH) and nicotinamide adenine dinucleotide coenzyme (NAD(P)H) stores in brain-isolated mitochondria.
Although, mitochondrial potential collapse was almost immediate after malonate addition, mitochondrial swelling was not evident before 15 min of drug presence. This latter effect was blocked by cyclosporin A (CSA), Ruthenium Red (RR), magnesium, catalase, GSH and vitamin E.
Malonate added to SH-SY5Y cell cultures produced a marked loss of cell viability together with the release of Cyt c and depletion of GSH and NAD(P)H concentrations. All these effects were not apparent in SH-SY5Y cells overexpressing Bcl-xL.
When GSH concentrations were lowered with buthionine sulphoximine, cytoprotection afforded by Bcl-xL overexpression was not evident anymore.
Taken together, all these data suggest that malonate causes a rapid mitochondrial potential collapse and reactive oxygen species production that overwhelms mitochondrial antioxidant capacity and leads to mitochondrial swelling. Further permeability transition pore opening and the subsequent release of proapoptotic factors such as Cyt c could therefore be, at least in part, responsible for malonate-induced toxicity.

Introduction
Mitochondria are involved in a number of important cellular functions, including essential pathways of intermediate metabolism, amino-acid biosynthesis, fatty acid oxidation and steroid metabolism. Of key importance is the role of mitochondria in oxidative phosphorylation and apoptosis. Thus, mitochondria are considered the headquarters in apoptosis pathways (for a review, see Susin et al., 1998; Kroemer & Reed, 2000; Jordan et al., 2003). Many apoptotic stimuli cause either functional or morphological mitochondrial alterations such as collapse of the transmembranal potential or swelling. Hallmarks of these mitochondrial alterations are increased free radical production and release of cytochrome c (Cyt c) from mitochondria to the cytosol through the permeability transition pore (PTP) (Kroemer & Reed, 2000; Vila & Przedborski, 2003). The Bcl-2 family of proteins, which is implicated in the regulation of apoptosis by modulating PTP aperture, comprises members that have either antiapoptotic (such as Bcl-2 and Bcl-xL) or proapoptotic (such as Bax and Bak) effects (Brenner et al., 2000; Gross, 2001). In this sense, Bcl-2 or Bcl-xL overexpression has been shown to confer protection to cells exposed to apoptotic stimuli including staurosporine (Yuste et al., 2002), 6-hydroxydopamine (6-OHDA) (Galindo et al., 2004), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyride (MPTP) (Yang et al., 1998) or 3-nitorpropionic acid (3-NP) (Bogdanov et al., 1999).
There is substantial evidence indicating that oxidative stress plays a role in the progression of a constellation of neurological disorders. Mitochondria have been proposed to be the main source of reactive oxygen species (ROS) in neuronal cells. Cells contain antioxidant systems to block ROS overproduction, including glutathione (GSH) and nicotinamide adenine dinucleotide coenzyme (NADH/NAD+) and its derivatives (NADPH/NADP+) (NAD(P)H), which play a crucial role as part of the primary cellular defence against oxidative stress. It has been shown that GSH levels in the cerebrospinal fluid decline during aging (Cudkowicz et al., 1999). The involvement of GSH in the control of cell death in neurodegenerative diseases is striking and it has been suggested that GSH depletion might be an upstream biochemical event in neurodegeneration (Dexter et al., 1989a, 1989b). We and others have also observed a GSH depletion after different apoptotic stimuli including 6-OHDA (Galindo et al., 2004), veratridine (Jordan et al., 2002), MPTP (Selley, 1998) or malonate (Ehrhart & Zeevalk, 2003).
On the other hand, it is clear that impairment of mitochondrial energy metabolism is the key pathogenic factor in a number of neurodegenerative disorders (see review by Schon & Manfredi, 2003). Accordingly, toxins that affect mitochondria are being used as pharmacological tools to mimic several of these diseases. Among others, 3-NP, MPTP, rotenone and malonate are well-established mitochondrial complex inhibitors frequently used to investigate the key cellular pathways that provoke neurodegeneration in Parkinson's or Huntington's diseases (Browne & Beal, 2002).
Malonate has been shown to cause dose-dependent neurotoxicity both ‘in vivo' and ‘in vitro' by inhibition of succinate dehydrogenase and depletion of striatal ATP (Beal et al., 1993; Greene & Greenamyre, 1995; Stokes et al., 2001, Van Westerlaak et al., 2001) resulting in neuronal depolarization and secondary excitotoxicity (Henshaw et al., 1994; Greene & Greenamyre, 1996). In a recent study by Schulz et al. (1998), it was suggested that malonate toxicity involves neurons dying not only by secondary excitotoxicity but also by delayed caspase activation and apoptosis (Schulz et al., 1998). Thus, the exact mechanism by which malonate induces toxicity remains unclear.
The aim of this study was to analyse the role played by mitochondria in the mechanisms underlying malonate-induced cell death. We used isolated mitochondrial preparations to study the effect of malonate on this organelle. We present evidence showing that malonate induces mitochondrial potential collapse and depletion of mitochondrial antioxidant defence which leads to mitochondrial swelling and release of proapoptotic proteins including Cyt c. The role of the antiapoptotic protein Bcl-xL in these processes is also addressed.

Q: Should we worry about the fact that small amounts of malic acids are found in many fruits and vegetables:

Malonic acid

Malonic acid is found in small amounts in sugar beet and green wheat, being formed by oxidative degradation of malic acid. Malonic acid has been identified in celery, parsnip, green pepper, tangerine, beet, oats, tabasco, chili, orange, grapefruit, lime, melon, cantaloupe, sunflower, barley, prickly pear, Indian fig, ginseng, black bean, kidney bean, green bean, peach, corn, Scotch pine, alfalfa, banana, tobacco plant, and juniper.

RP: Malic acid is o.k.; malonic acid is what makes unripe apples toxic.

 

[UG Krishnamurti]

​	Apr 14, 2022, 1:11 AM

Q: Hello Dr. Peat

I'm planning to buy a property with some land in Serbia, my home country, to try to gain independence from the system and move away from environmental pollution and toxins as much as possible. Growing my own food and raising animals.

What would you look for in a house or a property if you were to buy one yourself?

Unfortunately the area where I'm planning to buy a house has a low altitude [100-200m] so higher CO2 is not achievable at the moment.

Much love

RP: I would look for a stone house, good soil and sun exposure, and a reliable water source, with good neighbors.

Q: I don't think I will ever find a stone house here in Serbia :)

Bricks and building blocks are the most common here. The old houses are made out of mud.

Do you think bricks or blocks are ok?
What do you think about modular homes?

Much love

RP: I think mud is best, bricks next, then cement blocks.

 

[UG Krishnamurti]

Tue, Apr 19, 12:14 AM

Q: Hello Dr. Peat

Do you know what would reduce radiation from using the laptop in your lap or on your knees from time to time, besides the obvious one like stop using the laptop in that manner?

RP: Stopping it is the only protection.

Q: Thank you. Do you think buying a property in the countryside - 370m away from the cell tower - is safe?

RP: I think that’s a safe distance.

 

[UG Krishnamurti]

​	Sat, May 7, 9:21 PM

Q: Hello Dr. Peat

Can you tell me what damages the kidney which leads to renal insufficiency and then to ESKD?

Is it the body constantly trying to balance out the blood acidity to maintain the proper pH?
Endotoxins?

RP: It comes from poisoning from things produced in the intestine by bacteria, resulting from poor digestion. Acid balancing isn’t a problem.

 

[UG Krishnamurti]

​	Tue, May 31, 12:06 AM

Q: Hello Dr. Peat

After experimenting with glycine last night (1g in OJ) I heard a LOUD scream in my ear while I was sleeping. Woke me up and scared me :)
I Knew it was "in my head" because my extremely alert dog was sleeping.
I also woke up with an extremely dry mouth, grogginess and fatigue.
It also seems that glycine clogs my nose even more.

What do you think is behind this mechanism? Increasing glutamate? Methylation issues?

Much love

RP: A large amount of any amino acid can interfere with protein synthesis.

Q: Do you think 1g is a large amount of glycine? I had a similar experience to hearing strange sounds (usually when I sleep) when I was using gelatin and some GABAergic teas.

You think impaired protein synthesis could induce these symptomes?

RP: Chemically pure substances are often disturbing to tissues.

 

[UG Krishnamurti]

​	Sun, Jun 26, 2:20 AM

Q: Hello Dr. Peat

Whole oats or flattened oats? Oat meal or porridge? Which would be a better choice? How would you prepare them?

Much love

RP: Rolled oats or oat bran either would be be o.k., people vary in their response. The grain should be added to boiling water, and allowed to simmer for several minutes.

// Sunday, Jun 26th is the last day we spoke. I knew you were feeling under the weather so I stopped bothering you and actually tried doing my own research more extensively. You offered me the framework. You offered us all the framework. Thank you for always trying to help this poor fool out and sorry we bothered you with our silly questions. Let me end it in a way I always ended our emails: "Much love Dr. Peat". Much love indeed //

 

[windinthepines]

[2009]

At 12:32 PM 12/21/2009, you wrote:

Dr. Peat,
I have a question for you about fructose and glucose. If I understand your work correctly, you suggest that we should favor fructose over glucose. I understand that fructose takes longer to absorb than glucose, and that the speed at which a sugar is absorbed might be a sign of some potential dangers, but I was under the impression that fructose raises blood sugar slower than glucose only because it must first be metabolized by the liver. I've also read that the liver must process fructose in much the same way that it processes alcohol, and that fructose might be considered a poison as well. There seems to be a startling increase in the number of cases of 'non alcoholic fatty liver syndrome,' and I wonder if a corresponding increase in fructose consumption could at least partially account for it.

===Sucrose is what I recommend, because starch is pure glucose, and usually doesn't have the appropriate minerals associated with it. Fructose just doesn't occur naturally in practical amounts; well aged jerusalem artichokes are the only food I know of that contains it without balancing glucose, and it's rare to find them properly aged.

Historically, it looks like fruit was available only seasonally (even in the tropics). I've seen it suggested that it's healthier to binge
on fruit at infrequent intervals than to consume it every day. Also, from what I can tell, plenty of the groups studied by Weston A. Price consumed a lot of glucose, but none consumed a lot of fructose.

====With a good liver, a person can store a lot of glycogen, but I don't know of any advantage in having sugar intermittenly. I suppose there are some places in the tropics without much variety of fruit, but many places have fruits in all seasons. Cactus fruit in desert areas, guavas in slightly moister areas, for example. At my place in Michoacan even the apples and peaches make two crops a year, and various berries, custard apples, citrus fruits are never far.

I know that you wrote that there's nothing inherently wrong with consuming a lot of starch, but that when available superior foods should replace starch. Maybe I'm looking at this all the wrong way: if we can't consume more than 35% of our total calories as protein, then the remaining 65% needs to be composed of sugar and fat. Should we be replacing starch with fruit, or starch with saturated fat?

====A little saturated fat, especially with the shorter chains, is helpful. I don't think any amount of starch is beneficial, and without fat undercooked starch can be persorbed.

I did notice that there's some information out there on the beneficial effects of saturated fat on fatty liver disease. Could it be that
fructose only damages the liver in the presence of PUFA?

====PUFA damage the liver.

Carbohydr Res. 2009 Sep 8;344(13):1676-81. Epub 2009 Jun 3.
Protective role of fructose in the metabolism of astroglial C6 cells exposed to hydrogen peroxide.
Spasojevi I, Baji A, Jovanovi K, Spasi M, Andjus P.
Center for Laser Microscopy, Faculty of Biology, University of Belgrade,
Belgrade, Serbia. [email protected]
Astroglial cells represent the main line of defence against oxidative damage
related to neurodegeneration. Therefore, protection of astroglia from an excess
of reactive oxygen species could represent an important target of the treatment
of such conditions. The aim of our study was to compare the abilities of glucose
and fructose, the two monosaccharides used in diet and infusion, to protect C6
cells from hydrogen peroxide (H(2)O(2))-mediated oxidative stress. It was
observed using confocal microscopy with fluorescent labels and the MTT test that
fructose prevents changes of oxidative status of the cells exposed to H(2)O(2)
and preserves their viability. Even more pronounced protective effects were
observed for fructose 1,6-bis(phosphate). We propose that fructose and its
intracellular forms prevent H(2)O(2) from participating in the Fenton reaction
via iron sequestration. As fructose and fructose 1,6-bis(phosphate) are able to
pass the blood-brain barrier, they could provide antioxidative protection of
nervous tissue in vivo. So, in contrast to the well-known negative effects of
frequent consumption of fructose under physiological conditions, acute infusion
or ingestion of fructose or fructose 1,6-bis(phosphate) could be of benefit in
the cytoprotective therapy of neurodegenerative disorders related to oxidative
stress.

J Physiol 1987 Sep;253(3 Pt 1):G390-6
Fructose prevents hypoxic cell death in liver.
Anundi I, King J, Owen DA, Schneider H, Lemasters JJ, Thurman RG.
Perfusion of livers from fasted rats with nitrogen-saturated buffer caused
hepatocellular damage within 30 min. Lactate dehydrogenase (LDH) was released at
maximal rates of approximately 300 U . g-1 . h-1 under these conditions, and
virtually all cells in periportal and pericentral regions of the liver lobule
were stained with trypan blue. Infusion of glucose, xylitol, sorbitol, or
mannitol (20 mM) did not appreciably change the time course or extent of damage
due to perfusion with nitrogen-saturated perfusate. However, fructose (20 mM)
completely prevented damage assessed by LDH release, trypan blue uptake, and
ultrastructural changes for at least 2 h of perfusion. Neither glucose, xylitol,
sorbitol, nor mannitol (20 mM) increased lactate formation above basal levels
during hypoxia. On the other hand, fructose (0.4-20 mM) caused a
concentration-dependent increase in lactate formation that reached maximal rates
of approximately 180 mumol . g-1 . h-1. The dose-dependent increase in
glycolytic lactate production from fructose correlated well with cellular
protection reflected by decreases in LDH release. ATP:ADP ratios were also
increased from 0.4 to 1.8 in a dose-dependent manner by fructose. The results
indicate that fructose protects the liver against hypoxic cell death by the
glycolytic production of ATP in the absence of oxygen.

J Biol Chem 1987 Jul 15;262(20):9529-34
Gluconeogenesis from fructose predominates in periportal regions of the liver
lobule.
Anundi I, Kauffman FC, Thurman RG.
Gluconeogenesis from fructose was studied in periportal and pericentral regions
of the liver lobule in perfused livers from fasted, phenobarbital-treated rats.
When fructose was infused in increasing concentrations from 0.25 to 4 mM,
corresponding stepwise increases in glucose formation by the perfused liver were
observed as expected. Rates of glucose and lactate production from 4 mM fructose
were around 100 and 75 mumol/g/h, respectively. Rates of fructose uptake were
around 190 mumol/g/h when 4 mM fructose was infused. 3-Mercaptopicolinate, an
inhibitor of phosphoenolpyruvate carboxykinase, decreased glucose formation from
fructose maximally by 20% suggesting that a fraction of the lactate formed from
fructose is used for glucose synthesis. A good correlation (r = 0.92) between
extra oxygen consumed and glucose produced from fructose was observed. At low
fructose concentrations (less than 0.5 mM), the extra oxygen uptake was much
greater than could be accounted for by glucose synthesis possibly reflecting
fructose 1-phosphate accumulation. Furthermore, fructose diminished ATP/ADP
ratios from about 4.0 to 2.0 in periportal and pericentral regions of the liver
lobule indicating that the initial phosphorylation of fructose via fructokinase
occurs in both regions of the liver lobule. Basal rates of oxygen uptake
measured with miniature oxygen electrodes were 2- to 3-fold higher in periportal
than in pericentral regions of the liver lobule during perfusions in the
anterograde direction. Infusion of fructose increased oxygen uptake by 65
mumol/g/h in periportal areas but had no effect in pericentral regions of the
liver lobule indicating higher local rates of gluconeogenesis in hepatocytes
located around the portal vein. When perfusion was in the retrograde direction,
however, glucose was synthesized nearly exclusively from fructose in upstream,
pericentral regions. Thus, gluconeogenesis from fructose is confined to
oxygen-rich upstream regions of the liver lobule in the perfused liver.

Res Commun Chem Pathol Pharmacol 1987 Jan;55(1):111-6
Total protection from hypoxic liver damage by fructose.
Anundi I, King J, Owens DA, Schneider H, Lemasters JJ, Thurman RG.
The purpose of these experiments was to evaluate the effect of carbohydrates on
hypoxic cell death in the perfused rat liver. Lactate dehydrogenase (LDH) was
released maximally at rates up to 300 U/g/h after 40 to 60 min of hypoxia in
control livers from fasted rats or in livers perfused with glucose (20 mM).
Fructose (20 mM) prevented the release of LDH completely. Rates of anaerobic
glycolysis indexed by release of lactate were around 150 mumol/g/h in livers
perfused with fructose but were undetectable in livers perfused with glucose.
The results demonstrate that fructose prevents hypoxic damage in the liver
presumably by providing glycolytic ATP in the absence of oxygen.

Hepatology 1991 Feb;13(2):297-303
Differences in glycolytic capacity and hypoxia tolerance between hepatoma cells
and hepatocytes.
Hugo-Wissemann D, Anundi I, Lauchart W, Viebahn R, de Groot H.
Klinische Forschergruppe Leberschadigung, Institut fur Physiologische Chemie I,
Heinrich-Heine-Universitat, Dusseldorf, Federal Republic of Germany.
Viability, glycolytic capacity and energy metabolism under anaerobic conditions
were studied in the hepatoma cell lines HTC, FU5 and HepG2 and in rat and human
hepatocytes using glucose and fructose as glycolytic precursors. During 6 hr of
anaerobic incubation without additional substrate, viability decreased rapidly
in FU5 and HTC cells, whereas viability of HepG2 cells was not significantly
affected. In all tumor cells, 10 mmol/L glucose prevented hypoxic cell injury
almost completely. Lactate formation from glucose was about five times higher
than in hepatocytes under these circumstances. ATP content of the tumor cells
remained almost constant under anaerobic conditions in the presence of glucose.
Ten millimoles per liter of fructose diminished glycolysis in the hepatoma cells
compared with glucose, ranging from 87% reduction in HTC cells to 43% reduction
in HepG2 cells. Accordingly, ATP content decreased rapidly in the FU5 and slowly
in the HepG2 cells. Viability was strongly diminished in the HTC and FU5 cells
in the presence of fructose, whereas in the HepG2 cells no effect of fructose on
viability was detectable. In contrast to the hepatoma cells, rat and human
hepatocytes exhibited higher rates of anaerobic glycolysis in the presence of
fructose and thus were able to maintain their viability under these conditions.
These differences in glycolytic capacity, energy metabolism and hypoxia
tolerance of hepatoma cells compared with hepatocytes may be used for the
treatment of liver cancer by isolated liver perfusion and ex situ revision of
the organ.

Am J Physiol 1989 Jul;257(1 Pt 1):G58-64
Hypoxic liver cell death: critical Po2 and dependence of viability on glycolysis.
Anundi I, de Groot H.
Institut fur Physiologische Chemie I, Universitat Dusseldorf, Federal Republic
of Germany.
Viability of isolated hepatocytes was not significantly dependent on oxygen at
oxygen partial pressures (Po2) from 70 to 0.3 mmHg. The critical Po2 for
induction of hypoxic cell death was close to 0.1 mmHg and was distinct from the
value at which mitochondrial function becomes impaired (2-5 mmHg). Hypoxic
damage in hepatocytes from fasted rats occurred within 1 h but was delayed by
the addition of fructose, which increased rates of lactate formation from about
1 to 12 nmol.10(6) cells-1.min-1. Hepatocytes from fed rats maintained viability
for almost 180 min of anaerobic incubation and then rapidly became damaged.
Addition of fructose prevented hypoxic cell damage also in these hepatocytes.
Rates of lactate formation were 11-15 nmol.10(6) cells-1.min-1 and were
increased two- to threefold by fructose. The rapid initial degradation of
glycogen and the release of glucose were delayed with fructose, which also could
have contributed to sustained glycolytic rates. Further, under conditions in
which lactate production was high, e.g., in the fed state, there was also a
significantly better preservation of cellular ATP levels.

 

[windinthepines]

[2013]

Me:

You probably already saw it in the news, but a few months ago there were stories about an unusually old man who had been using aspirin/caffeine tablets everyday for years. I don't know strength the tablets that he was using, but it seemed like it would have been quite a large dose of aspirin. I thought of your articles when I saw it.

(The Social Climber: World's Oldest Man Credits Longevity to Anacin, Bananas)

RP:
Thanks, that's closely related to my next (January) newsletter.

 

[windinthepines]

[2013]

Me:

When you mention having taken 100,000 units of vitamin A a day in the past, do you mean orally? Would the equivalent dose on the skin be 400,000 to 500,000 units?

RP:

Yes, it was oral. Emanuel Cheraskin's study involved some people taking
100,000 units orally, too. Vitamin A is light sensitive, so I've used it
only on my feet, where sunlight wouldn't reach it under my shoes.

Me:

I recently started taking more thyroid, 50mcg of T3, which has fixed my insomnia. My pulse is 85 to 100 in the day, and I seem to need much more food and vitamin A (acne, dandruff). I've been putting 100,000 units on my wrists and arms at night to avoid light, but I think some of it is absorbing into my clothes, and I still have acne and dandruff. Wouldn't a lot of it come off into your socks?

RP:

Yes, it's much more efficient to take it orally, but around 1980 vitamin A started giving me migraines, I think from sulfite contaminating it.

 

[windinthepines]

[2013]

Me:

When you were taking large amounts of pregnenolone daily, did your need for vitamin A decrease? Can you substitute taking pregnenolone instead of vitamin A? When I recently tried a gram of pregnenolone a day, it seemed to affect my dandruff and acne situation, making my skin dryer like vitamin A does.

RP:

Yes, I stopped taking vitamin A then.

 

[windinthepines]

[2013]

Me:

Hi, was wondering if you have seen this pregnenolone powder from "Health Natura." It has a certificate of analsyis on the website. Maybe it's better than the other products?

healthnatura.com

RP:

Everything I've seen lately has been described as >99%; the absence of
excipients is important, then trying a sample is the only way to be sure.

Me:

I ordered some of this pregnenolone to try. I've used pregnenolone from a few other places. Is there anything specific to watch for when I try it, symptoms from impurities?

RP:

Nasal congestion, headache, sore throat, and/or hemorrhoids are common reactions to impurities.

 

[windinthepines]

[2013]

Me:

I had been rereading some of your articles that dealt with insomnia. A few months ago, as an experiment, I started taking 50mcg of T3 in many small doses: for a time this reversed my long-standing insomnia. Right now I'm taking one 25mcg cynomel pill, and one half of a cynoplus pill: I still have insomnia with this dose. Is this because the cynomel is more effective? Might increasing the dose of cynoplus help? I will probably try this anyway, but wanted to get your thoughts. I have been trying to make sure to get the necessary minerals: now I am drinking a gallon of milk a day, with orange juice and coffee.

RP:

The cynoplus should be divided, too, with about a quarter of it at
bedtime. If that ~8 mcg of T3 isn't enough, a little cynomel could be
added. The T4 during the night reduces the rise in TSH that usually
happens at night.

 

[windinthepines]

[2013]

Me:
I read horse meat is sometimes sold as beef in Europe, and thought of your MS article. Do you know if the same substitutions are happening in the US or Mexico? It seems like people here might be able to make money doing so.


RP:

I read horse meat is sometimes sold as beef in Europe, and thought of your MS article. Do you know if the same substitutions are happening in the US or Mexico? It seems like people here might be able to make money doing so.

====================================
Me:
I read about using progesterone after head injuries. If I carried a bottle of Progest-E with me, how much would I want to use if I injured my head? For instance, if I got into a car accident, would I want to immediately eat a whole bottle?


RP:

No, a fourth to half a teaspoonful (100 to 200 mg) would be a moderately
anesthetic and protective dose.

====================================

Me:

I was used 1mg DHEA in olive oil for a few days. It made me feel extremely confident and energetic. All my anxiety and fatigue were gone. But I felt a little too 'speedy,' like I wanted to do everything really fast, and my memory was a little worse than normal. My chest/breast area felt sore for no reason. I tried to keep my pulse high with cynomel and took extra aspirin. But could some of the speedy feeling be from the DHEA turning into estrogen.

RP:

It doesn't seem likely that such a small amount, with aspirin and cynomel, could increase estrogen. Does pregnenolone cause any of the good effects of the DHEA?


=================================

Me:

I've been having digestion problems for years, sometimes diarrhea a few times a day, even after changing my diet and trying all sorts of things. Is there anything to try, other than carrots, antibiotics, and anti-serotinin drugs? I was wondering if some type of restricted diet high in gelatin or glycine might permanently help.

RP:

Have you tried elimination diets, for example nothing but milk and carrots for a few days, or orange juice and eggs, to see if you can identify problem foods?

=================================

Me:

I saw a study that said cyproheptadine was more effective than benzodiazepine drugs. Have you heard of anyone using it for insomnia? Or is there anything good to use for insomnia, besides benadryl? I have been trying sugar, T3, T4, beandryl, aspirin, and magnesium.

RP:

It works extremely well, but it's important to start with a much smaller dose than is usually recommended, 1 mg, or even less, can be effective, and 4 mg sometimes makes people goofy the next day. I know people who use it for nocturnal episodes of asthma or epilepsy-like episodes.

Me:

Is there a preferred brand or source for cyproheptadine?

RP:

I had some that a doctor got in a US drugstore that was good, but I don't know the brand; I got some from a drugstore in India that tasted odd and didn't seem as effective.

Me:

I took cyproheptadine last night. It was from an online pharmacy, maybe from India. It put me to sleep like benadryl. There was a period of morning grogginess today, but it feels preferable to benadryl, which makes me depressed. I also feel relaxed and less anxious. Is cyproheptadine OK to use everyday, or will it eventually cause problems?

RP:

I think it's safe to keep using in small amounts.

 

[windinthepines]

[2013]

Me:

[Seems like I respond differently to thyroid supplementation than before. I get cold hands and feet, and feel anxious. I have serious insomnia problems]

RP:
If you have been sleeping in the daytime a light deficiency might be involved. Have you had any blood tests?

Me:

[Gibberish]

RP:

The stress hormones are higher during the dark phase, so maybe your light environment isn't bright enough.


===============================

Me:
I'm taking 1.5 cytomel tablets a day. Sometimes when I take my 1/6th pill pieces of cytomel, my pulse rises to 90, but my feet are very cold, and I feel tired. Does that mean that I'm not making steroids for some reason?

RP:

Do you know what your cholesterol level is? Various nutritional deficiencies could be involved.

Me:

About four years ago my cholesterol was high 200s. After a few years of using thyroid, my level was 160 this past winter.

RP:

Things that increase temperature but not pulse rate are progesterone, sodium, sugar, and balanced protein.

Me:


I've been trying to figure out why I now respond to cytomel differently than in the past. 2mcg with a meal makes my feet extremely cold. Along with the cold feet, I now get anxious and depressed instead of happy and calm. Even having a cup of sugar in milk doesn't make my feet warmer. I've been eating more protein, almost a gallon of milk, and eating liver for more vitamin A. Is there another nutrient that I could check, to see if I have some deficiency?

RP:

Selenium (reliably present in sea food) is essential for good thyroid function. Have you tried other products, such as Armour or Cynoplus or Proloid-S?

=========================================

Me:


Hi Ray,

I was hoping you could clarify your view on something for me.

I was listening to Colin Wilson talk about how he thinks we can will ourselves into different states of consciousness. He was describing how he overcame a series of panic attacks by essentially deciding to do so.

If I'm panicking, I decide to drink milk and sugar, and take more thyroid, and that seems to calm me down. I was interested in your phrase that went something like 'consciousness is the interface between the outside world and you'. Sorry if I don't have that quite right.

So I was thinking that the purpose of consciousness is to decide to how to modify our bodies by deciding what external substances to include and what to exclude.

It seems like you and Wilson both see that humans can decide to induce the next evolutionary phase. But to some extent Wilson thinks about the mind and body as separate.

Do I have this all backwards?

RP:

He went straight from the hopelessness of being an English working class kid into the world of literature, which was like a ghost world that was permitted to float above the real world of exploitation and oppression. He found that he could function and even excel in that world, which touched reality only in ways that didn't challenge the system. He was absolutely right about the importance of intentionality, of choosing to function rather than to not function, but he excluded the kinds of choice that would have led him to engage with issues of politics and science. The way we cause our body to interact with the world includes everything.