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Dear Carnivore Dieters, A Muscle Meat Only Diet is Extremely Healing Because it is a Low "vitamin A" Diet. This is Why it Works so Well...
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Ray Peat Email Advice Depository
- Thread starter charlie
- Start date
BrunoI send an email to Dr Peat asking about magnesium requirement. This is his reply.
Q: Do you have any recommendation for daily intake of magnesium? Is RDA of 420 mg for adult sufficient?
Ray Peat :With the average diet, that amount is enough. Good thyroid function, and plenty of calcium, potassium, and sodium can decrease the amount of magnesium needed.
Q: Do you have any recommendation for daily intake of magnesium? Is RDA of 420 mg for adult sufficient?
Ray Peat :With the average diet, that amount is enough. Good thyroid function, and plenty of calcium, potassium, and sodium can decrease the amount of magnesium needed.
5magicbeans
Member
- Joined
- Mar 6, 2013
- Messages
- 120
- Age
- 59
Response from the "Mr. Darcy" of energy protection
I think Ray Peat is amazing.
His graciousness in responding to all of us sets a precedence for the possibilities of a new type of "community" that is not much unlike his idea that "energy and structure are interdependent, at every level".
Anywho, here is his response to some of my questions regarding headaches, lab tests and finding a useful form of Emodin.
"I think prolactin and TSH would be worth checking. I have had bad headaches when I used vitamin A orally, and even getting a little on my lips was enough to do it. It could be that the Nutrisorb-A was the cause, if you used it orally. I use it only on my legs and feet.
It's hard now (since the FDA's anticascara action) to find a standardized aged cascara product, but Western Botanical and (in Italy) Farmalabor are two sources that I know of. (Naturlich Kost Ko-op in Millersburg, Ohio, has cascara, but I think FDA is currently preventing them from doing business.) The Chinese rhubarb products are probably standardized, but I have never used them. An amount slightly less than a laxative dose has beneficial systemic effects."
I think Ray Peat is amazing.
His graciousness in responding to all of us sets a precedence for the possibilities of a new type of "community" that is not much unlike his idea that "energy and structure are interdependent, at every level".
Anywho, here is his response to some of my questions regarding headaches, lab tests and finding a useful form of Emodin.
"I think prolactin and TSH would be worth checking. I have had bad headaches when I used vitamin A orally, and even getting a little on my lips was enough to do it. It could be that the Nutrisorb-A was the cause, if you used it orally. I use it only on my legs and feet.
It's hard now (since the FDA's anticascara action) to find a standardized aged cascara product, but Western Botanical and (in Italy) Farmalabor are two sources that I know of. (Naturlich Kost Ko-op in Millersburg, Ohio, has cascara, but I think FDA is currently preventing them from doing business.) The Chinese rhubarb products are probably standardized, but I have never used them. An amount slightly less than a laxative dose has beneficial systemic effects."
Hashimoto Diagnosis:
Ray Peat does not believe that "Hashimoto" is really an autoimmune disease.
He mentioned in earlier audio interviews that antibodies used to diagnose Hashimoto
are not an autoimmune reaction. To be sure what he meant by antibody tests i asked him following question.
Ray Peat does not believe that "Hashimoto" is really an autoimmune disease.
He mentioned in earlier audio interviews that antibodies used to diagnose Hashimoto
are not an autoimmune reaction. To be sure what he meant by antibody tests i asked him following question.
mandance
Member
- Joined
- Jul 5, 2013
- Messages
- 473
Ray Peat response to low testosterone and high cholesterol
The problem with chicken is that the fat is highly unsaturated, and the meat provides very little calcium. Milk and cheese have a much better ratio of calcium to phosphate. Having the carrots raw (shredded, with a little olive oil, vinegar, and salt) would help with the hormone balance, and protect the intestine against inflammation. Supplementing pregnenolone wouldn't have the risk of the DHEA being converted to estrogen, which tends to happen when thyroid function is low. A small supplement of Armour thyroid or the equivalent could quickly lower the cholesterol, and since cholesterol is converted by thyroid into pregnenolone and DHEA, that would probably help the testosterone. Some shellfish (oysters, shrimp, squid, etc.) or low fat fish would provide trace minerals that might be lacking in your diet. Several eggs per week, or liver once a week, can help with other nutrients that are probably deficient in your present foods. Well cooked potatoes, with butter or cream, fruit, and well cooked greens are other foods have vitamins and minerals that are helpful.
Ray Peat guidance on dosing thyroid
Cynoplus (www.farmaciadelnino.com has a good price) is cheaper than Armour, and an eighth to a fourth of a tablet would be a reasonable amount to start with; thyroxine's half-life in the body is two weeks, so the effect is cumulative, and if you get the desired effects in less than two weeks the dose should probably be reduced.
At the beginning, once a day, but if your temperature and pulse and symptoms aren't just right after two weeks you could add another dose at a different time of day. Change of seasons affects the amount of thyroid you need, sometimes it isn't needed after using it for a while, but it's always good to watch for signs of change.
The body makes up to about 4 mcg of T3 in an hour, so each dose should be small, with food to delay absorption. Are you having orange juice and milk in your diet? Sometimes a B vitamin deficiency, especially B1, can cause the fog. A supplement of 10 mg. is often enough to improve focus and prevent fatigue.
When you take T3 without food, it enters the blood stream very suddenly, and the liver is likely to detect an excessive amount, causing it to produce enzymes to eliminate it. The result can be a decrease in T3 for the rest of the day, especially at night if you took it in the morning. Have you tried rebreathing into a paper bag, to see if the increased CO2 affects the fog?
Ray Peat on SSRIs
It takes time to adapt to decreasing those drugs, keeping sugar up and inflammation down, including bag breathing, should help.
Starting with a little, a sixth or fourth of a tablet, of cynoplus in the evening would be the best way to try it.
The problem with chicken is that the fat is highly unsaturated, and the meat provides very little calcium. Milk and cheese have a much better ratio of calcium to phosphate. Having the carrots raw (shredded, with a little olive oil, vinegar, and salt) would help with the hormone balance, and protect the intestine against inflammation. Supplementing pregnenolone wouldn't have the risk of the DHEA being converted to estrogen, which tends to happen when thyroid function is low. A small supplement of Armour thyroid or the equivalent could quickly lower the cholesterol, and since cholesterol is converted by thyroid into pregnenolone and DHEA, that would probably help the testosterone. Some shellfish (oysters, shrimp, squid, etc.) or low fat fish would provide trace minerals that might be lacking in your diet. Several eggs per week, or liver once a week, can help with other nutrients that are probably deficient in your present foods. Well cooked potatoes, with butter or cream, fruit, and well cooked greens are other foods have vitamins and minerals that are helpful.
Ray Peat guidance on dosing thyroid
Cynoplus (www.farmaciadelnino.com has a good price) is cheaper than Armour, and an eighth to a fourth of a tablet would be a reasonable amount to start with; thyroxine's half-life in the body is two weeks, so the effect is cumulative, and if you get the desired effects in less than two weeks the dose should probably be reduced.
At the beginning, once a day, but if your temperature and pulse and symptoms aren't just right after two weeks you could add another dose at a different time of day. Change of seasons affects the amount of thyroid you need, sometimes it isn't needed after using it for a while, but it's always good to watch for signs of change.
The body makes up to about 4 mcg of T3 in an hour, so each dose should be small, with food to delay absorption. Are you having orange juice and milk in your diet? Sometimes a B vitamin deficiency, especially B1, can cause the fog. A supplement of 10 mg. is often enough to improve focus and prevent fatigue.
When you take T3 without food, it enters the blood stream very suddenly, and the liver is likely to detect an excessive amount, causing it to produce enzymes to eliminate it. The result can be a decrease in T3 for the rest of the day, especially at night if you took it in the morning. Have you tried rebreathing into a paper bag, to see if the increased CO2 affects the fog?
Ray Peat on SSRIs
It takes time to adapt to decreasing those drugs, keeping sugar up and inflammation down, including bag breathing, should help.
Starting with a little, a sixth or fourth of a tablet, of cynoplus in the evening would be the best way to try it.
J
j.
Guest
I asked Ray Peat about persorption, and how to reduce it.
Ray Peat said:
J
j.
Guest
As I add more and more incandescent lights to see how I feel, is there an approximate number of watts which is prudent to not go over?
Ray Peat said:
Dr Peat
You wrote in vitamin E article that liver is a rich source of vitamin E. But USDA data shows
100 grams of beef liver has only 0.4 mg of E.
Is this a correct number? Do You know what is the real value? Would over cooking liver destroy vitamin E?
You wrote in vitamin E article that liver is a rich source of vitamin E. But USDA data shows
100 grams of beef liver has only 0.4 mg of E.
Is this a correct number? Do You know what is the real value? Would over cooking liver destroy vitamin E?
4peatssake
Member
- Joined
- Feb 7, 2013
- Messages
- 2,055
- Age
- 63
Could you give us some clarity and help us to understand your thoughts about potatoes, when time permits?
Ray Peat said:
Dan W
Member
- Joined
- Jan 22, 2013
- Messages
- 1,528
Thanks to Zachariah Salazar for this one, regarding an article by Mercola about starch and acrylamide:
Ray Peat said:
Dan W
Member
- Joined
- Jan 22, 2013
- Messages
- 1,528
Thanks to Martin Brown on the Facebook group:
Martin said:
Ray Peat said:
Q:
I saw a reply you gave to someone in an email saying starch in aspirin was okay as long as it did not cause issues such as asthma, hemorrhoids or headaches. Do you think the starch in aspirin is the reason asthmatics may have issues with aspirin and that pure aspirin powder would not cause an asthmatic problems?
I saw a reply you gave to someone in an email saying starch in aspirin was okay as long as it did not cause issues such as asthma, hemorrhoids or headaches. Do you think the starch in aspirin is the reason asthmatics may have issues with aspirin and that pure aspirin powder would not cause an asthmatic problems?
Ray Peat said:
Q: All the studies i have seen claims that Heme iron absorption is not changed by other factors like tea and coffee. Do you know of any study that shows coffee inhibiting heme iron absorption? I found this study showing beef liver has 13 percent heme iron and beef meat has 64 % heme iron. If this is true then muscle meat is more harmful than liver in terms of iron absorption . http://www.ncbi.nlm.nih.gov/pubmed/19475341
Here is his response. It seems like fresh meat has ferrous iron, the bad kind and older meat will be in ferric form, the good kind. There is another reason to avoid iron rich animal foods
Here is his response. It seems like fresh meat has ferrous iron, the bad kind and older meat will be in ferric form, the good kind. There is another reason to avoid iron rich animal foods
Re: Coffee ,estrogen and cortisol
I send Ray Peat the abstract of that study showing Estradiol is increased 70% with 500 mg caffeine daily and got his response. Original study is http://www.ncbi.nlm.nih.gov/pubmed/11591405
Early follicular phase hormone levels in relation to patterns of alcohol, tobacco, and coffee use.
Lucero J, Harlow BL, Barbieri RL, Sluss P, Cramer DW.
Abstract
OBJECTIVE:
To examine the effects of alcohol, caffeine, and tobacco use on early follicular phase FSH, LH, E2, and sex hormone-binding globulin (SHBG).
DESIGN:
Cross-sectional study.
SETTING:
Academic medical center.
PATIENT(S):
Four hundred ninety-eight women selected from the general population, ages 36-45, who were not currently pregnant, breast feeding, or using exogenous hormones.
INTERVENTION(S):
A general questionnaire assessing demography, anthropometry, and smoking habits and a standardized dietary questionnaire assessing food and beverage frequencies, including sources of alcohol and caffeine.
MAIN OUTCOME MEASURE(S):
FSH, LH, E2, and SHBG levels measured during the early follicular phase of the menstrual cycle.
RESULT(S):
Significant associations observed in a univariate analysis included age > or =40 and current smoking associated with higher FSH; higher body mass index (BMI) associated with lower SHBG levels; and daily alcohol use, cholesterol consumption greater than the median, and coffee use >1 cup/d associated with higher E2 levels. In a multivariate model, total caffeine use was significantly associated with E2 levels after adjustment for age, BMI, total calories, current smoking, alcohol, cholesterol consumption, and day of sampling. Early follicular phase E2 increased from 28.2 pg/mL for women consuming < or =100 mg of caffeine to 45.2 pg/mL for women consuming > or =500 mg of caffeine per day, about a 70% increase.
CONCLUSION(S):
Coffee consumption and total caffeine use may increase early follicular phase E2 levels independent of related habits of alcohol or tobacco use."
[ modereator edit: discussion in Coffee [Cortisol, Estrogen] ]
I send Ray Peat the abstract of that study showing Estradiol is increased 70% with 500 mg caffeine daily and got his response. Original study is http://www.ncbi.nlm.nih.gov/pubmed/11591405
Early follicular phase hormone levels in relation to patterns of alcohol, tobacco, and coffee use.
Lucero J, Harlow BL, Barbieri RL, Sluss P, Cramer DW.
Abstract
OBJECTIVE:
To examine the effects of alcohol, caffeine, and tobacco use on early follicular phase FSH, LH, E2, and sex hormone-binding globulin (SHBG).
DESIGN:
Cross-sectional study.
SETTING:
Academic medical center.
PATIENT(S):
Four hundred ninety-eight women selected from the general population, ages 36-45, who were not currently pregnant, breast feeding, or using exogenous hormones.
INTERVENTION(S):
A general questionnaire assessing demography, anthropometry, and smoking habits and a standardized dietary questionnaire assessing food and beverage frequencies, including sources of alcohol and caffeine.
MAIN OUTCOME MEASURE(S):
FSH, LH, E2, and SHBG levels measured during the early follicular phase of the menstrual cycle.
RESULT(S):
Significant associations observed in a univariate analysis included age > or =40 and current smoking associated with higher FSH; higher body mass index (BMI) associated with lower SHBG levels; and daily alcohol use, cholesterol consumption greater than the median, and coffee use >1 cup/d associated with higher E2 levels. In a multivariate model, total caffeine use was significantly associated with E2 levels after adjustment for age, BMI, total calories, current smoking, alcohol, cholesterol consumption, and day of sampling. Early follicular phase E2 increased from 28.2 pg/mL for women consuming < or =100 mg of caffeine to 45.2 pg/mL for women consuming > or =500 mg of caffeine per day, about a 70% increase.
CONCLUSION(S):
Coffee consumption and total caffeine use may increase early follicular phase E2 levels independent of related habits of alcohol or tobacco use."
[ modereator edit: discussion in Coffee [Cortisol, Estrogen] ]
Last edited by a moderator:
mandance
Member
- Joined
- Jul 5, 2013
- Messages
- 473
Ray Peats response to getting off antidepressant use.
Keeping the metabolic rate and cholesterol up is important, so that repair and adaptation will be quick. Progesterone reduces pain and anxiety, and pregnenolone would be the most convenient supplement for men, but it's hard to find products without allergens. Combining progesterone and DHEA or testosterone can produce the stabilizing effect without suppressing the libido. Benadryl and cyproheptadine are probably both helpful. Withdrawal from morphine and SSRIs and migraine involve some similar processes.
Psychopharmacologia 1973, Volume 28, Issue 2, pp 165-170
Suppression of the drug-induced morphine withdrawal syndrome by cyproheptadine
Klaus Opitz, Ingrid Reimann
In rats treated with gradually increasing amounts of morphine hydrochloride until they tolerated fatal doses, levallorphan precipitated acute body weight loss and elicited a variety of other typical withdrawal symptoms. Cyproheptadine markedly reduced this b.w. loss and abolished the drug-induced withdrawal syndrome. Fenfluramine also suppressed the major signs of the levallorphan-induced morphine withdrawal; however the combination of the three drugs proved to be very toxic. Since both agents interfere with different hypothalamic feeding mechanisms these results are accordant with the hypothesis of Kerr and Pozuelo (1971) that morphine dependence and tolerance are due to a functional disorganization of the hypothalamic centers concerned wit the regulation of food intake.
Psychopharmacologia Psychopharmacologia Look
Acta Physiol Pharmacol Bulg. 1976;2(2):68-74.
Pharmacological analysis of certain mechanisms of morphine addiction.
Ovcharov R, Bantoutova I, Kobourova K.
The effects of L-Dopa, Methysergid, Diphenhydramine hydrochloride and LSD on the development of morphine dependence and the abstience syndrome after its withdrawal, were tested in experiments on 200 male Wistar albino rats. L-Dopa had no efect on the development of physical morphine dependence, while Methysergid prevented its development. Applied in rats during the abstinence syndrome, LSD intensified their aggressivity with no influence on the analgesic effect of morphine. Diphenhydramine reduced the aggressiveness of the rats during the abstinence syndrome. Biochemical tests show that in morphine-tolerant rats there was an increase in the content of brain serotonin, less of dopamine and no changes in noradrenaline. The significance of the brain levels of serotonin, dopamine and noradrenaline for the development of physical morphine-dependence is discussed. It is pointed out that serotonin and dopamine play an important role both for the origin of the physical morphine dependence, and in the abstinence syndrome after its withdrawal.
Drug Alcohol Depend. 1976 Feb;1(3):221-39.
Central serotonergic mechanisms and development of morphine dependence.
Blasig J, Papeschi R, Gramsch C, Herz A.
The effects of different manipulations of brain serotonin (5-HT) content on the
development of morphine dependence were investigated in rats, which were
implanted with morphine pellets for 40 days. Serotonin content was decreased by
(a) short or long term inhibition of tryptophan hydroxylase with
para-chlorophenylalanine (PCPA), (b) by short or long term degeneration of 5-HT
containing nerve terminals with 5,6-dihydroxytryptamine or (c) by degeneration of
5-HT containing nerve terminals by lesioning of midbrain raphe nuclei. With all
methods used, the frequency of withdrawal jumping was significantly reduced,
while other withdrawal signs remained more or less unchanged. Additional
administration of 5-HTP to chronically PCPA treated rats did not reverse the PCPA
effect. Since chronic reduction of 5-HT level during the whole time of morphine
exposure changed withdrawal symptomatology in nearly the same way as did a
decrease in 5-HT level during the time of withdrawal only, it is suggested that
serotonergic mechanisms are not linked to the basic processes underlying
dependence development but that they are only involved in the nervous pathways
mediating the expression of some withdrawal signs.
PMID: 138583 [PubMed - indexed for MEDLINE]
Clin Exp Pharmacol Physiol. 1976 Nov-Dec;3(6):587-98.
Physical dependence in the rat induced by slow release morphine: dose-response,
time course and brain biogenic amines.
Laska JF, Fennessy MR.
1. Physical dependence was induced in rats by administration of a slow release
morphine emulsion (morphine SR), and assessed by scoring abstinence signs and
temperature changes after i.p. administration of naloxone (5 mg/kg). Three groups
of rats received doses of 75, 100 or 150 mg/kg of morphine SR. Dependence was
evaluated in each of these groups after 24, 48 and 72 h. 2. The effect of these
treatments at the different times on brain levels of serotonin,
5-hydroxyindoleacetic acid, noradrenaline and dopamine was determined. 3. A
ceiling level of dependence was reached 24 h after 75 and 100 mg/kg and 48 h
after 150 mg/kg of morphine SR. 4. These different treatments produced no
significant effect on the brain levels of noradrenaline, dopamine or serotonin.
The levels of 5-hydroxyindoleacetic acid were significantly raised in
morphine-dependent rats and the changes correlated well with the changes in
abstinence behaviour and temperature after naloxone. 5. The results suggest that
a relationship exists between serotonin turnover and physical dependence on
morphine.
Naunyn Schmiedebergs Arch Pharmacol. 2002 Mar;365(3):210-9. Epub 2002 Feb 1.
Supersensitivity of 5-HT1A autoreceptors and alpha2-adrenoceptors regulating
monoamine synthesis in the brain of morphine-dependent rats.
Sastre-Coll A, Esteban S, García-Sevilla JA.
Laboratory of Neuropharmacology, Associate Unit of the Institute Cajal/CSIC,
Department of Biology, University of the Balearic Islands, Cra. Valldemossa Km
7.5, 07071 Palma de Mallorca, Spain.
The sensitivity of 5-HT1A serotonin receptors and alpha2-adrenoceptors
(autoreceptors and heteroreceptors) modulating brain monoamine synthesis was
investigated in rats during morphine treatment and after naloxone-precipitated
withdrawal. The accumulation of 5-hydroxytryptophan (5-HTP) and
3,4-dihydroxyphenylalanine (DOPA) after decarboxylase inhibition was used as a
measure of the rate of tryptophan and tyrosine hydroxylation in vivo. Acute
morphine (3-100 mg/kg, 1 h) increased the synthesis of 5-HTP/5-HT in various
brain regions (15%-35%) and that of DOPA/dopamine (DA) in striatum (28%-63%), but
decreased the synthesis of DOPA/noradrenaline (NA) in hippocampus and cortex
(20%-33%). Naloxone (2-60 mg/kg, 1 h) did not alter the synthesis of 5-HTP or
DOPA in brain. Tolerance to the inhibitory effect of morphine on DOPA/NA
synthesis and a sensitization to its stimulatory effects on DOPA/DA and
5-HTP/5-HT synthesis were observed after chronic morphine and/or in
morphine-withdrawn rats. In morphine-dependent rats (tolerant and withdrawn
states) the inhibitory effects of the 5-HT1A agonists 8-OH-DPAT and buspirone
(0.1 mg/kg, 1 h), and that of the alpha2-adrenoceptor agonist clonidine (0.1
mg/kg, 1 h), on the synthesis of 5-HTP/5-HT were potentiated (25%-50%). Moreover,
the effect of 8-OH-DPAT was antagonized by WAY 100135, a selective 5-HT1A
antagonist. In morphine-dependent rats (tolerant state), the inhibitory effects
of clonidine on the synthesis of DOPA/NA (hippocampus, hypothalamus) and DOPA/DA
(striatum) also were potentiated (35%-55%). In summary, we conclude that morphine
addiction is associated with supersensitivity of 5-HT1A serotonin receptors and
alpha2-adrenoceptors (autoreceptors and heteroreceptors) that modulate the
synthesis of monoamines in brain.
Psychopharmacology (Berl). 1979 Oct;65(2):205-9.
Morphine abstinence and serotonin supersensitivity in man: analogies with the
mechanism of migraine?
Sicuteri F, Del Bianco PL, Anselmi B.
Supersensitivity to serotonin during migraine attack has been previously
observed. Since the attack has been attributed to a critical lowering of
morphine-like factors, we can expect serotonin supersensitivity during morphine
abstinence. Slight signs of morphine abstinence have also been induced in
volunteers after mild (10-24 mg/day) and limited (3 days) treatment. To evaluate
the sensitivity to serotonin, dopamine, noradrenaline, and tyramine in the smooth
muscle of the hand dorsal vein, in vivo, the computerized venotest was applied
before, during, and 24 h after withdrawal of morphine. Venous sensitivity to
serotonin and dopamine (but not to noradrenaline and tyramine) increased 10- to
20-fold after morphine withdrawal. Venous monoamine supersensitivity in morphine
abstinence, similar to that observed during migraine attacks, could be indirect
evidence of an analogous mechanism in both conditions.
Agents Actions. 1975 Dec;5(5):476-83.
The possible role of brain histamine and H1 and H2 receptors in the development
of morphine tolerance and physical dependence in mice.
Wong CL, Roberts MB.
The possible role of brain histamine in the mechanisms of morphine tolerance and
physical dependence is under investigation in mice. L-histidine and histamine,
given during the 'withdrawal' phase, significantly increase tolerance to the
analgesic effects of morphine but reduce the degree of physical dependence.
Metiamide significantly inhibits tolerance but has no consistent effect on
physical dependence. These results suggest that H2 receptors may be involved in
the development of morphine tolerance. Mepyramine does not significantly affect
tolerance, and with regard to dependence there is an effect only on body weight
loss, which is increased. However, combined treatment with metiamide and
mepyramine inhibits tolerance significantly more than metiamide alone; and
withdrawal jumping is also reduced more significantly by combined treatment than
by the separate administration of these drugs. It is suggested that brain
histamine is definitely implicated in the mechanisms of the 'withdrawal' phase of
morphine tolerance and physical dependence in mice, with H2 receptors probably
playing the more important part.
Adv Biochem Psychopharmacol. 1980;22:523-33.
Dopamine and 5-HT supersensitivity in nonorganic central pain and in morphine
abstinence: fortuitous or renal analogy?
Sicuteri F, Anselmi B, Del Bianco PL.
Unexplained pain, such as central panalgesia, might be the most common clinical
expression of a deficiency, central in nature, of the endorphin system. Acute
natural opioid deficiency is comparable to morphine withdrawal in addicts
characterized by vegetative, psychic disorder and the appearance of pain. An
impressive supersensitivity (up to 1000 fold) to dopamine and 5-HT of the smooth
muscle (hand dorsal vein: venotest) is detected both in central panalgesia
sufferers and in addicts during spontaneous (withdrawal) or pharmacological
(naloxone) abstinence. A 5-HT and dopamine supersensitivity, of less intensity,
however, (10-30 fold), is found during migraine attacks: on these occasions,
morphine-like factors in CSF appear reduced or undetectable, reinforcing the
chemical analogy between morphine abstinence and migraine attacks. In the present
study, evidence of opiate receptors in the human vein is also provided: 5-HT
venospasms, inhibited by morphine, promptly emerge when naloxone is inoculated
locally.
Headache. 1976 Sep;16(4):145-59.
Hypothesis: migraine, a central biochemical dysnociception.
Sicuteri F.
Headache. 1979 May;19(4):232-3.
Phenomenal similarities of migraine and morphine abstinence.
Sicuteri F.
Keeping the metabolic rate and cholesterol up is important, so that repair and adaptation will be quick. Progesterone reduces pain and anxiety, and pregnenolone would be the most convenient supplement for men, but it's hard to find products without allergens. Combining progesterone and DHEA or testosterone can produce the stabilizing effect without suppressing the libido. Benadryl and cyproheptadine are probably both helpful. Withdrawal from morphine and SSRIs and migraine involve some similar processes.
Psychopharmacologia 1973, Volume 28, Issue 2, pp 165-170
Suppression of the drug-induced morphine withdrawal syndrome by cyproheptadine
Klaus Opitz, Ingrid Reimann
In rats treated with gradually increasing amounts of morphine hydrochloride until they tolerated fatal doses, levallorphan precipitated acute body weight loss and elicited a variety of other typical withdrawal symptoms. Cyproheptadine markedly reduced this b.w. loss and abolished the drug-induced withdrawal syndrome. Fenfluramine also suppressed the major signs of the levallorphan-induced morphine withdrawal; however the combination of the three drugs proved to be very toxic. Since both agents interfere with different hypothalamic feeding mechanisms these results are accordant with the hypothesis of Kerr and Pozuelo (1971) that morphine dependence and tolerance are due to a functional disorganization of the hypothalamic centers concerned wit the regulation of food intake.
Psychopharmacologia Psychopharmacologia Look
Acta Physiol Pharmacol Bulg. 1976;2(2):68-74.
Pharmacological analysis of certain mechanisms of morphine addiction.
Ovcharov R, Bantoutova I, Kobourova K.
The effects of L-Dopa, Methysergid, Diphenhydramine hydrochloride and LSD on the development of morphine dependence and the abstience syndrome after its withdrawal, were tested in experiments on 200 male Wistar albino rats. L-Dopa had no efect on the development of physical morphine dependence, while Methysergid prevented its development. Applied in rats during the abstinence syndrome, LSD intensified their aggressivity with no influence on the analgesic effect of morphine. Diphenhydramine reduced the aggressiveness of the rats during the abstinence syndrome. Biochemical tests show that in morphine-tolerant rats there was an increase in the content of brain serotonin, less of dopamine and no changes in noradrenaline. The significance of the brain levels of serotonin, dopamine and noradrenaline for the development of physical morphine-dependence is discussed. It is pointed out that serotonin and dopamine play an important role both for the origin of the physical morphine dependence, and in the abstinence syndrome after its withdrawal.
Drug Alcohol Depend. 1976 Feb;1(3):221-39.
Central serotonergic mechanisms and development of morphine dependence.
Blasig J, Papeschi R, Gramsch C, Herz A.
The effects of different manipulations of brain serotonin (5-HT) content on the
development of morphine dependence were investigated in rats, which were
implanted with morphine pellets for 40 days. Serotonin content was decreased by
(a) short or long term inhibition of tryptophan hydroxylase with
para-chlorophenylalanine (PCPA), (b) by short or long term degeneration of 5-HT
containing nerve terminals with 5,6-dihydroxytryptamine or (c) by degeneration of
5-HT containing nerve terminals by lesioning of midbrain raphe nuclei. With all
methods used, the frequency of withdrawal jumping was significantly reduced,
while other withdrawal signs remained more or less unchanged. Additional
administration of 5-HTP to chronically PCPA treated rats did not reverse the PCPA
effect. Since chronic reduction of 5-HT level during the whole time of morphine
exposure changed withdrawal symptomatology in nearly the same way as did a
decrease in 5-HT level during the time of withdrawal only, it is suggested that
serotonergic mechanisms are not linked to the basic processes underlying
dependence development but that they are only involved in the nervous pathways
mediating the expression of some withdrawal signs.
PMID: 138583 [PubMed - indexed for MEDLINE]
Clin Exp Pharmacol Physiol. 1976 Nov-Dec;3(6):587-98.
Physical dependence in the rat induced by slow release morphine: dose-response,
time course and brain biogenic amines.
Laska JF, Fennessy MR.
1. Physical dependence was induced in rats by administration of a slow release
morphine emulsion (morphine SR), and assessed by scoring abstinence signs and
temperature changes after i.p. administration of naloxone (5 mg/kg). Three groups
of rats received doses of 75, 100 or 150 mg/kg of morphine SR. Dependence was
evaluated in each of these groups after 24, 48 and 72 h. 2. The effect of these
treatments at the different times on brain levels of serotonin,
5-hydroxyindoleacetic acid, noradrenaline and dopamine was determined. 3. A
ceiling level of dependence was reached 24 h after 75 and 100 mg/kg and 48 h
after 150 mg/kg of morphine SR. 4. These different treatments produced no
significant effect on the brain levels of noradrenaline, dopamine or serotonin.
The levels of 5-hydroxyindoleacetic acid were significantly raised in
morphine-dependent rats and the changes correlated well with the changes in
abstinence behaviour and temperature after naloxone. 5. The results suggest that
a relationship exists between serotonin turnover and physical dependence on
morphine.
Naunyn Schmiedebergs Arch Pharmacol. 2002 Mar;365(3):210-9. Epub 2002 Feb 1.
Supersensitivity of 5-HT1A autoreceptors and alpha2-adrenoceptors regulating
monoamine synthesis in the brain of morphine-dependent rats.
Sastre-Coll A, Esteban S, García-Sevilla JA.
Laboratory of Neuropharmacology, Associate Unit of the Institute Cajal/CSIC,
Department of Biology, University of the Balearic Islands, Cra. Valldemossa Km
7.5, 07071 Palma de Mallorca, Spain.
The sensitivity of 5-HT1A serotonin receptors and alpha2-adrenoceptors
(autoreceptors and heteroreceptors) modulating brain monoamine synthesis was
investigated in rats during morphine treatment and after naloxone-precipitated
withdrawal. The accumulation of 5-hydroxytryptophan (5-HTP) and
3,4-dihydroxyphenylalanine (DOPA) after decarboxylase inhibition was used as a
measure of the rate of tryptophan and tyrosine hydroxylation in vivo. Acute
morphine (3-100 mg/kg, 1 h) increased the synthesis of 5-HTP/5-HT in various
brain regions (15%-35%) and that of DOPA/dopamine (DA) in striatum (28%-63%), but
decreased the synthesis of DOPA/noradrenaline (NA) in hippocampus and cortex
(20%-33%). Naloxone (2-60 mg/kg, 1 h) did not alter the synthesis of 5-HTP or
DOPA in brain. Tolerance to the inhibitory effect of morphine on DOPA/NA
synthesis and a sensitization to its stimulatory effects on DOPA/DA and
5-HTP/5-HT synthesis were observed after chronic morphine and/or in
morphine-withdrawn rats. In morphine-dependent rats (tolerant and withdrawn
states) the inhibitory effects of the 5-HT1A agonists 8-OH-DPAT and buspirone
(0.1 mg/kg, 1 h), and that of the alpha2-adrenoceptor agonist clonidine (0.1
mg/kg, 1 h), on the synthesis of 5-HTP/5-HT were potentiated (25%-50%). Moreover,
the effect of 8-OH-DPAT was antagonized by WAY 100135, a selective 5-HT1A
antagonist. In morphine-dependent rats (tolerant state), the inhibitory effects
of clonidine on the synthesis of DOPA/NA (hippocampus, hypothalamus) and DOPA/DA
(striatum) also were potentiated (35%-55%). In summary, we conclude that morphine
addiction is associated with supersensitivity of 5-HT1A serotonin receptors and
alpha2-adrenoceptors (autoreceptors and heteroreceptors) that modulate the
synthesis of monoamines in brain.
Psychopharmacology (Berl). 1979 Oct;65(2):205-9.
Morphine abstinence and serotonin supersensitivity in man: analogies with the
mechanism of migraine?
Sicuteri F, Del Bianco PL, Anselmi B.
Supersensitivity to serotonin during migraine attack has been previously
observed. Since the attack has been attributed to a critical lowering of
morphine-like factors, we can expect serotonin supersensitivity during morphine
abstinence. Slight signs of morphine abstinence have also been induced in
volunteers after mild (10-24 mg/day) and limited (3 days) treatment. To evaluate
the sensitivity to serotonin, dopamine, noradrenaline, and tyramine in the smooth
muscle of the hand dorsal vein, in vivo, the computerized venotest was applied
before, during, and 24 h after withdrawal of morphine. Venous sensitivity to
serotonin and dopamine (but not to noradrenaline and tyramine) increased 10- to
20-fold after morphine withdrawal. Venous monoamine supersensitivity in morphine
abstinence, similar to that observed during migraine attacks, could be indirect
evidence of an analogous mechanism in both conditions.
Agents Actions. 1975 Dec;5(5):476-83.
The possible role of brain histamine and H1 and H2 receptors in the development
of morphine tolerance and physical dependence in mice.
Wong CL, Roberts MB.
The possible role of brain histamine in the mechanisms of morphine tolerance and
physical dependence is under investigation in mice. L-histidine and histamine,
given during the 'withdrawal' phase, significantly increase tolerance to the
analgesic effects of morphine but reduce the degree of physical dependence.
Metiamide significantly inhibits tolerance but has no consistent effect on
physical dependence. These results suggest that H2 receptors may be involved in
the development of morphine tolerance. Mepyramine does not significantly affect
tolerance, and with regard to dependence there is an effect only on body weight
loss, which is increased. However, combined treatment with metiamide and
mepyramine inhibits tolerance significantly more than metiamide alone; and
withdrawal jumping is also reduced more significantly by combined treatment than
by the separate administration of these drugs. It is suggested that brain
histamine is definitely implicated in the mechanisms of the 'withdrawal' phase of
morphine tolerance and physical dependence in mice, with H2 receptors probably
playing the more important part.
Adv Biochem Psychopharmacol. 1980;22:523-33.
Dopamine and 5-HT supersensitivity in nonorganic central pain and in morphine
abstinence: fortuitous or renal analogy?
Sicuteri F, Anselmi B, Del Bianco PL.
Unexplained pain, such as central panalgesia, might be the most common clinical
expression of a deficiency, central in nature, of the endorphin system. Acute
natural opioid deficiency is comparable to morphine withdrawal in addicts
characterized by vegetative, psychic disorder and the appearance of pain. An
impressive supersensitivity (up to 1000 fold) to dopamine and 5-HT of the smooth
muscle (hand dorsal vein: venotest) is detected both in central panalgesia
sufferers and in addicts during spontaneous (withdrawal) or pharmacological
(naloxone) abstinence. A 5-HT and dopamine supersensitivity, of less intensity,
however, (10-30 fold), is found during migraine attacks: on these occasions,
morphine-like factors in CSF appear reduced or undetectable, reinforcing the
chemical analogy between morphine abstinence and migraine attacks. In the present
study, evidence of opiate receptors in the human vein is also provided: 5-HT
venospasms, inhibited by morphine, promptly emerge when naloxone is inoculated
locally.
Headache. 1976 Sep;16(4):145-59.
Hypothesis: migraine, a central biochemical dysnociception.
Sicuteri F.
Headache. 1979 May;19(4):232-3.
Phenomenal similarities of migraine and morphine abstinence.
Sicuteri F.
mandance
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Ray Peat continued:
I knew someone who had been addicted to morphine and alcohol for 30 years, who was drinking quarts of beer and wine daily when he didn't have morphine, who had an opportunity for a good job if he could get sober. Starting progesterone at bedtime (and stopping the wine), he said it was the first time he didn't have a hangover in the morning. He used enough progesterone to neuter most people, but said it didn't affect his sex function; he was taking a lot of Cytomel and magnesium, but wasn't drunk again as long as I knew him, and his general health improved.
I knew someone who had been addicted to morphine and alcohol for 30 years, who was drinking quarts of beer and wine daily when he didn't have morphine, who had an opportunity for a good job if he could get sober. Starting progesterone at bedtime (and stopping the wine), he said it was the first time he didn't have a hangover in the morning. He used enough progesterone to neuter most people, but said it didn't affect his sex function; he was taking a lot of Cytomel and magnesium, but wasn't drunk again as long as I knew him, and his general health improved.
mandance
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More Peat
It depends on how much pregnenolone you can assimilate. People would use progesterone in amounts needed to stop the withdrawal symptoms, but pregnenolone doesn't have the powerful effects of progesterone, even in multi-gram quantities, so it's just a matter of seeing what it can do. As I understand the mechanism (migraine, withdrawal, etc.), estrogen-histamine-serotonin rise on a background of hypothyroid liver malfunction, cytomel (and/or sugar, selenium, B vitamins) allows the liver and other detoxifying systems to lower them, and the lower they are, the less progesterone or pregnenolone it takes to block the symptoms.
Again, talking about withdrawing from antidepressants.
It depends on how much pregnenolone you can assimilate. People would use progesterone in amounts needed to stop the withdrawal symptoms, but pregnenolone doesn't have the powerful effects of progesterone, even in multi-gram quantities, so it's just a matter of seeing what it can do. As I understand the mechanism (migraine, withdrawal, etc.), estrogen-histamine-serotonin rise on a background of hypothyroid liver malfunction, cytomel (and/or sugar, selenium, B vitamins) allows the liver and other detoxifying systems to lower them, and the lower they are, the less progesterone or pregnenolone it takes to block the symptoms.
Again, talking about withdrawing from antidepressants.
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