Ray Peat Email Advice Depository

[windinthepines]

[2014]

Me:

I was very interested in your discussion of the visual systems in Mind
and Tissue. I've been trying to observe my own sight processes,
thinking about the box and triangle diagrams you included, but I'm
having trouble. What can I do to observe this process? Thanks.

Peat:

The motion after-effect is easiest to notice, when you have been
traveling and watching scenery come toward you for a while, or if you
watch an Archimedes spiral rotating on a turntable, until there is an
after-effect (when the real movement stops) of apparent motion in the
opposite direction. If you close your eyes during the several seconds
when the after-effect would be occurring, you might be able to see what
looks like flowing sand.

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

Me:

I was reading about the old LSD studies and saw that they were also
using carbogen (maybe a strong mixture?) to induce a psychedelic
experience. I remember you talking about a friend who, because of a
bad regulator, used more CO2 then he intended on a patient, with the
result being that the patient regained his voice. In a situation like
that, or in other CO2 healing situations, does the person have any
sort of drug like experience? Does the intoxication (I don't know what
to call it, maybe unusual state) mean something is going wrong
physiologically?

Peat:

That person was very unconscious. I don't know of any psychedelic
effects from too much CO2.

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

Me:

Do you have any experience with Gerovital supplements of procaine hydrocloride?

Peat:


Yes, recently a woman in her sixties with multiple joint, muscle, and
nerve pains started taking it in the conventional Ana Aslan form, with
additives, and now she's limber, and says her joints are rubbery and
painless. I have seen amazing things with just plain procaine, and would
talk about it more, except that it can be very allergenic for some
people. Lidocaine has enough overlap with it to be valuable.

Me:

That's really interesting. I recently ordered some GH3 to try for my
intestines and insomnia. I haven't found anything really good to read
about it though.

Peat:

Two big studies done in the US around 1960 didn't get published,
probably because they provided very strong confirmation for Aslan's
research. (I got a copy of the one done at Edgemoor Geriatric Hospital
in Santee, California, but have probably lost it.)

 

[windinthepines]

[2014]

Me:

[...]
With its high altitude and pollution, is
Mexico City a healthy place to live? [Moving to MX and teaching English]

RP:

There are places with less smog than Mexico City, that have language
schools, but the altitude is still beneficial in DF. In Mexico, pay for
English teachers is low.

Me:

Thanks. I was wondering what Ivan Illich might say about teaching
English. Probably that it's arrogant and presumptuous, unless I intent
to take the experience selfishly, trying to learn Spanish, trying to
learn from the people there. [...] Do you know people who manage to somehow escape
the 40 hour work week?

RP:

I started a language school in Mexico City in 1962, and I had friends
who made a fair living by giving private classes. The rent for the
school building meant that I had to teach 8 classes a day and not eat
much, so then I got a job at the state university and got slightly
better pay, but was required to use the "embassy method," which was
probably like delivering pizzas, except no tips. It's an opportunity to
learn Spanish, and in Mexico it was a chance to get to know interesting
people. At least when I was there, the people who could afford to study
English weren't the people Illich talked about. One was a taxi driver,
who learned English to become a guide at the Museo de Antropologia,
others were middle class, doctors, actors, politicians. I have heard
that the immigration people are much more organized now in Mexico, but
in Coeneo, Michoacan, when I declined to teach a class in a friend's
school because I didn't have work papers, he said "there are no
immigration people here," so it's probably easier for undocumented
people in small towns. There, students offered to pay a dollar or two
each per hour in a group class, and room and board cost about
$300/month, so it wouldn't be stressful work.

Me:

That's very helpful, thanks. I had read that the immigration paper
process is difficult, and that you need to be in the Mexico to look
for a job, but I didn't know that small towns might be a better place
to look. I have some Mexican friends at work, who might have ideas on
which towns to look in, although when I mentioned Michoacan, they
told me it's a dangerous drug state, and that I shouldn't go there. I
guess it's a change of routine and place I'm looking for, also a
chance for interactions that are richer than just handing over a pizza
box. Around 300/month is great, and would be less stressful than
trying to pay rent in this area.

RP:

It's the southern part of Michoacan, Tierra Caliente/Nueva Italia,
that's dangerous, but it was dangerous long before the drug cartel took
over.

Me:

[...] Does your friend still have his
language school in Coeneo?

RP:

It's sort of an adult education school, largely for young school
dropouts, and when I tried teaching a class there the noise from a class
next door made it hard to hear--cement block walls, and windows,
transmit and echo the sound. English is always of interest, so classes
could be held in the teacher's house, or in any quiet place.

Me:

[...]

RP:

Someone always wants an English teacher, but pay in a place like that
depends on how many students sign up, so being there and getting
acquainted would be necessary. Finding someone to be your Spanish tutor
would be a way to start, and in small towns word spreads quickly. I know
the school's owner by his first name, Juvenal, but I don't know his last
name, and so don't know how to contact him by mail or phone. One of the
reasons that English teachers usually go to the big cities is that lots
of city people know some English, and in small towns not many do (except
in places like Coeneo in the winter, when large numbers of men come back
from working in the US), so it takes some time to make living arrangements.

Me:

[...]

RP:

I think arranging a trip with the intention of learning Spanish is the
right way, English students always find you. When I was 18 I spent the
summer taking classes at Mexico City College; I didn't speak any
Spanish, but one of the first taxi rides I took, the driver asked me to
tutor him, just being there for an hour now and then for him to speak
English with. Doing that kind of private tutoring, or small groups,
avoids the issue of having work papers. If you haven't had a Spanish
course, it's really helpful to find a textbook with a vocabulary list of
a couple of thousand words, and to memorize as many as possible before
going.

 

[windinthepines]

[2014]

Me:

Sorry to quote you, but at http://peatarian.com/peatexchanges I read
about LSD that, "It acts as a learning experience, and can affect your
general attitudes; if the amount is excessive, causing depletion of
brain glycogen, I think it can lead to prolonged defensive attitudes,
probably with a rebound of serotonin."

I read about James Fadiman's study in the '60s that used LSD for
technical problem solving. They had good results and I think used
100mcg LSD. But I think they were only giving it one time per person.
Now he talks about even smaller doses-- I think around 5-20mcg. Some
of the other research I was reading was using much larger doses,
around 400mcg. What might be an excessive amount?

Peat:

I think the right amount is something like 5 to 20; 400 is much too much.

Me:

Would small doses of something like mescaline (in cactus) be
healthful, like LSD?

Peat:

One of the old medical writers in Mexico reported that the local people
used it for treating heart disease. I think that probably relates to an
antistress effect. The good thing about cyproheptadine is that it's legal.

Science. 1976 May 21;192(4241):801-3.
Lysergic acid diethylamide- and mescaline-induced attenuation of the
effect of punishment in the rat.
Schoenfeld RI.
At a dose as low as 1 microgram per kilogram of body weight, lysergic
acid diethylamide (LSD) significantly decreased the suppressive effect
of electric shock on licking behavior of the rat. Attenuation of
punishment was also obtained with mescaline, but neither
dimethyltryptamine nor delta9-tetrahydrocannabinol was active in this
test. Cyproheptadine and alpha-propyldopacetamide, drugs that interfere
with the function of neurons that contain serotonin, have a behavioral
effect similar to that of LSD and mescaline, which suggests that the
attenuation of punishment produced by these hallucinogens may result
from decreased activity of such neurons.

Me:
There was an article about one of the few legal licensed peyote
growers; he said he took a small amount of the peyote for his heart
condition. I don't know why, but I think buying San Pedro cactus is
legal in the US. [Note, not legal to prepare or consume, I believe.]

Is the punishment in that experiment analogous to signals we get from
our culture, at work, from the bank, from defensive and aggressive
people?

Peat:

I think it is; stresses reduce spontaneity.

 

[windinthepines]

[2014]

Me:

Is there a particular nutrient that could be deficient if someone gets muscle tension when increasing thyroid supplements?

RP:

Usually magnesium. Cells contain more when they have thyroid.

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

Me:

Would it be safe to use more than 4 mg of cyproheptadine for insomnia and IBS? Someone mentioned I could use 16 mg. I found some studies that use these doses, but I have always seen you refer to the smaller doses, and was wondering what your reasoning was. Thanks.

RP:

I have known people who did well with 12 mg/day, and know that some
people use much more, but until you know your sensitivity to it, it's
best to start with the minimal doses. Even 4 mg at night can make some
people too torpid to function the next morning.

Me:

I tried 12mg of cyproheptadine for a couple day. It made me feel and think differently, but didn't make me tired, or let me fall asleep. The day after, I was a little muted, but got more errands done than usual. Are high or low levels of serotonin responsible for a person's reaction to the drug? Or is insomnia always from an underenergized brain, from lack of thyroid?

RP:

I think thyroid and the dependent neurosteroids are the basic things, and that the reactive adrenaline, serotonin, nitric oxide, and prostaglandins are the immediately involved things. Keeping endotoxin absorption low can often make a big difference, with diet or antibiotics.

Me:

Would daily cyproheptadine eventually permanently lower serotonin levels?

RP:

I think it could lower stress, allowing other healing processes to correct it.

Me:

The larger doses are making me feel a lot less anxious overall.

So anit-serotonin drugs don't necessarily act on serotonin directly? I thought they generally had a chemical structure somewhat similar to serotonin, allowing some type of interference.

RP:

Cyproheptadine's effect is mainly by blocking the effects, rather than inhibiting its formation, but by reducing inflammation, it can break a vicious circle, affecting the whole system.

 

[Elderflower j58]

My email to Dr Peat and his answer.

Dear Dr Peat
I hope you can advise me I have a very large ovarian cyst measuring 26 cm which I am having removed surgically on the 29th of December.
My problem is it's bad enough having to have the surgery but they are trying to force me into a full hysterectomy which I do not want.
I understand because I am 64 there may be a chance of cancer but I am willing to take my chances and keep hold of my organs.Their reasoning for the full hysterectomy is that is more or less the protocol for women of my age... and my uterus and ovaries are pretty much useless which I know is not true.

Please correct me if I'm wrong, but from my research I have found out that this cyst has been growing for over a year possibly longer and would I not be in a worse state of health if it was cancer?
They say it is that complex cyst.


My TSH is 4.7 which I know makes me hypothyroid but because I have a long-standing heart condition I was never prescribed any thyroid medication and I was a bit scared to do it myself because of all the scaremongering around the heart and the thyroid.

Any guidance or advice would be gratefully received Dr Peat.



Dr Peats answer


High TSH in itself is deeply involved as a causal factor in heart and circulatory disease, and in ovarian malfunctions including cysts. What kind of heart problem was it? Have they measured various relevant hormones and vitamin D? Did they describe the composition of the cyst? A cancer of that size would be likely to have major toxic effects on your physiology, including weight loss and high serum lactate and cortisol. With such a large cyst, removing the rest of that ovary would seem reasonable, but not removal of the other ovary and uterus. Surgery is tolerated much better when thyroid function is normal.



Acta Obstet Gynecol Scand. 1997 May;76(5):478-83.
Estradiol, gonadotropins, and tumor markers in ovarian cyst fluid
T Reimer, B Gerber, S Kunkel, K Luettich
Background: The study was designed to improve the discrimination between functional and neoplastic ovarian cysts in order to avoid unnecessary surgery.
Methods: Concentrations of tumor markers (CA 125, CEA, CASA, CA 72-4) and hormones (estradiol, FSH, LH) in cyst fluid were detected by enzyme immuno- or immunoradiometric assays. Wilcoxon test was used to evaluate the correlation of cyst fluid markers and histology.
Results: One hundred and thirty-eight ovarian cyst aspirates were investigated. Seventy-one patients (51.5%) had functional cysts whereas 67 (48.5%) had benign (n=59) or malignant (n=8) cystic tumors. Statistically significant correlations of CA 125 (p<0.0005) and CASA (p<0.02) with neoplastic histology were found. No significant correlation could be detected between CA 72-4, CEA, or hormone values and histology. Elevated estradiol concentrations are suspicious for functional cysts in premenopausal age. Low FSH and LH levels seem to be an indicator for functional cysts in peri- and postmenopausal age.
Conclusions: The assessed analytes could not reliably distinguish between functional and neoplastic ovarian cysts. Our results indicate that CA 125 is a marker for neoplastic histology in a proportion of ovarian cysts. The use of FSH and LH in the diagnosis of postmenopausal blastomas needs further investigation.

Dear Dr Peat
Thank you so much for your prompt response to my problem.
I have attached a photo of my care plan. There may be some info in there that you can decipher?
I had a face-to-face appointment with my gynecologist yesterday Friday the 17th she seemed to me to be avoiding what I would call slightly good news regarding my condition but very reluctantly agreed to my wishes which are just the removal of cyst and my left ovary as it is enveloped by the cyst. The news which I think is good... is what she did not mention and had painted a pretty poor picture the week before.
That my womb uterus cervix could have Cancer or cancer markers or abnormal cells , and other parts of my body could have cancer markers, these parts of my body were not mentioned at all and when I asked her was my womb uterus cervix showing anything abnormal she said they were fine .
She does want to do a biopsy on the smaller 5cm cyst that is on my right ovary I'm not sure this would be to my advantage according to your excellent estrogen progesterone and menopausal articles what do you think
To put it crudely I think best left alone and not poked.
Another small piece of good news she said my TSH has gone down from 4.7 or 8 I am not sure to 2.6.
I know this is still not ideal but surely a good thing that it has lowered some what,
and d a very kind nurse who was sorting out my blood test agreed to add on progesterone and oestrogen as this is not normal just a special request.
When I asked the gynecologist why oestrogen and progesterone was not included in testing as especially unopposed oestrogen has a lot to do with cancerous cysts she brushed me aside
And continued to convince me regarding a hysterectomy.


DR PEAT'S ANSWER


You’re right about biopsies tending to activate inert abnormal cells. Progesterone protects against the stress of surgery, and reduces the risk of metastasis if any cancer cells are present. Hypothyroidism/high TSH reliably causes hypercholestolemia and excessive clotting; doctors who don’t know that shouldn’t work in medicine. 5,000 IU of vitamin D is o.k. until you get a blood test for it. If you eat eggs regularly, and milk and cheese, you probably get enough vitamin A; when thyroid function is low, the need for vitamin A is low, since it isn’t being used at the normal rate.

These conversations are from December 2021

 

[dfspcc20]

Q: What do you think could explain the out-of-season increase in RSV cases this summer (2021)? Especially among children.
RP: I think the emphasis on vaccinating babies for influenza starting at 6 months is a factor, weakening their resistance to other respiratory infections.

Q: What can be done to help ensure proper healing and union of a potential fracture? Specifically fractures that are known for delayed healing and nonunion (such as John's Fracture of the foot). Thinking red light, CO2, thyroid, vitamin D & enough calcium, aspirin would be good recommendations. Anything else?
RP: Ultrasound treatments can stimulate healing.

 

[Roni123@]

Beauty

 

[Advocate2021]

i am copying and pasting from my emails:

Ray Peat <[email protected]>​	Jul 7, 2021, 9:25 PM
to me

If it didn’t anesthetize your throat I think the dose was o.k. Lidocaine is usually a compact powder, it could be 100 mg.

On Jul 7, 2021, at 8:17 PM, melissa wrote:
Wow excited to try daily for a while. i do not currently have a scale and simply took a 1/32 tsp of the powder from a 25 G bag. But i do not think actually that there are 1,000 servings that way, so wondering if i am actually taking more than 25mg. have to see if i can find info relaying the number of mg of lidocaine in 1/32 tsp. it seems all powders are different.

Do you have any idea how many miligrams of pharmaceutical grade lidocaine powder would be 1/32 tsp?
On Wed, Jul 7, 2021 at 9:01 PM Ray Peat <[email protected]> wrote:

I think the invigorating effect is from reducing inflammation that drains energy. I think that dose is safe to use daily for a while. I recently gathered these articles for someone with high circulating cancer cells post-mastectomy; I think they suggest how important the anti-inflammatory anti-stress effects can be. It prevents excitatory calcium overload of cells.

Review Front Med (Lausanne). 2017 Dec 20;4:235.
The Amide Local Anesthetic Lidocaine in Cancer Surgery-Potential Antimetastatic Effects and Preservation of Immune Cell Function? A Narrative Review
Thiên-Nga Chamaraux-Tran 1 2 , Tobias Piegeler 3
Free PMC article
Abstract
Surgical removal of the primary tumor in solid cancer is an essential component of the treatment. However, the perioperative period can paradoxically lead to an increased risk of cancer recurrence. A bimodal dynamics for early-stage breast cancer recurrence suggests a tumor dormancy-based model with a mastectomy-driven acceleration of the metastatic process and a crucial role of the immunosuppressive state during the perioperative period. Recent evidence suggests that anesthesia could also influence the progress of the disease. Local anesthetics (LAs) have long been used for their properties to block nociceptive input. They also exert anti-inflammatory capacities by modulating the liberation or signal propagation of inflammatory mediators. Interestingly, LAs can reduce viability and proliferation of many cancer cells in vitro as well. Additionally, retrospective clinical trials have suggested that regional anesthesia for cancer surgery (either with or without general anesthesia) might reduce the risk of recurrence. Lidocaine, a LA, which can be administered intravenously, is widely used in clinical practice for multimodal analgesia. It is associated with a morphine-sparing effect, reduced pain scores, and in major surgery probably also with a reduced incidence of postoperative ileus and length of hospital stay. Systemic delivery might therefore be efficient to target residual disease or reach cells able to form micrometastasis. Moreover, an in vitro study has shown that lidocaine could enhance the activity of natural killer (NK) cells. Due to their ability to recognize and kill tumor cells without the requirement of prior antigen exposure, NKs are the main actor of the innate immune system. However, several perioperative factors can reduce NK activity, such as stress, pain, opioids, or general anesthetics. Intravenous lidocaine as part of the perioperative anesthesia regimen would be of major interest for clinicians, as it might bear the potential to reduce the risk of cancer recurrence or progression patients undergoing cancer surgery. As a well-known pharmaceutical agent, lidocaine might therefore be a promising candidate for oncological drug repurposing. We urgently need clinical randomized trials assessing the protective effect of lidocaine on NKs function and against recurrence after cancer surgery to achieve a "proof of concept.”

Br J Anaesth. 2018 Oct;121(4):962-968.
Lidocaine inhibits cytoskeletal remodelling and human breast cancer cell migration
G D'Agostino, A Saporito, V Cecchinato, Y Silvestri, A Borgeat, L Anselmi, M Uguccioni
Free article
Abstract
Background: The metastatic potential of breast cancer cells has been strongly associated with overexpression of the chemokine CXCL12 and the activity of its receptor CXCR4. Lidocaine, a local anaesthetic that can be used during breast cancer excision, inhibits the growth, invasion, and migration of cancer cells. We therefore investigated, in a breast cancer cell line, whether lidocaine can modulate CXCL12-induced responses.
Methods: Intracellular calcium, cytoskeleton remodelling, and cell migration were assessed in vitro in MDA-MB-231 cells, a human breast cancer epithelial cell line, after exposure to lidocaine (10 μM or 100 μM).
Results: Lidocaine (10 or 100 μM) significantly inhibited CXCR4 signalling, resulting in reduced calcium release (Fluo 340 nm/380 nm, 0.76 mean difference, p<0.0001), impaired cytoskeleton remodelling (F-Actin fluorescence mean intensity, 21 mean difference, P=0.002), and decreased motility of cancer cells, both in the scratch wound assay (wound area at 21 h, -19%, P<0.0001), and in chemotaxis experiments (fluorescence mean intensity, 0.16, P=0.0047). The effect of lidocaine was not associated with modulation of the CD44 adhesion molecule.
Conclusions: At clinical concentrations, lidocaine significantly inhibits CXCR4 signalling. The results presented shed new insights on the molecular mechanisms governing the inhibitory effect of lidocaine on cell migration.
Keywords: CXCL12; CXCR4; breast cancer; cell migration; lidocaine.
Copyright © 2018 The Authors. Published by Elsevier Ltd.. All rights reserved.

BMC Cancer. 2018 Jun 19;18(1):666.
Effects of local anesthetics on breast cancer cell viability and migration
Ru Li 1 , Chunyun Xiao 1 , Hengrui Liu 1 , Yujie Huang 1 2 , James P Dilger 1 3 , Jun Lin 4 5
Free PMC article
Abstract
Background: Breast cancer accounts for nearly a quarter of all cancers in women worldwide, and more than 90% of women diagnosed with breast cancer undergo mastectomy or breast-conserving surgery. Retrospective clinical studies have suggested that use of regional anesthesia leads to improved patient outcomes. Laboratory studies have reported that breast cancer cells are inhibited by some local anesthetics at millimolar concentration. Here, we present a comprehensive analysis of the effects of six common local anesthetics on two human breast cancer cell lines. We used concentrations ranging from those corresponding to plasma levels during regional block by local anesthetic (plasma concentration) to those corresponding to direct infiltration of local anesthetic.
Methods: Human breast cancer cell lines, MDA-MB-231 and MCF7, were incubated with each of six local anesthetics (lidocaine, mepivacaine, ropivacaine, bupivacaine, levobupivacaine, and chloroprocaine) (10 μM ~ 10 mM) for 6 to 72 h. Assays for cell viability, cytotoxicity, migration, and cell cycle were performed.
Results: High concentrations (> 1 mM) of local anesthetics applied to either MDA-MB-231 or MCF7 cells for 48 h significantly inhibited cell viability and induced cytotoxicity. At plasma concentrations (~ 10 μM) for 72 h, none of the local anesthetics affected cell viability or migration in either cell line. However, at 10 × plasma concentrations, 72-h exposure to bupivacaine, levobupivacaine or chloroprocaine inhibited the viability of MDA-MB-231 cells by > 40% (p < 0.001). Levobupivacaine also inhibited the viability of MCF7 cells by 50% (p < 0.001). None of the local anesthetics affected the viability of a non-cancerous breast cell line, MCF10A. MDA-MB-231 cell migration was inhibited by 10 × plasma concentrations of levobupivacaine, ropivacaine or chloroprocaine and MCF7 cell migration was inhibited by mepivacaine and levobupivacaine (p < 0.05). Cell cycle analysis showed that the local anesthetics arrest MDA-MB-231 cells in the S phase at both 1 × and 10 × plasma concentrations.
Conclusions: Local anesthetics at high concentrations significantly inhibited breast cancer cell survival. At 10 × plasma concentrations, the effect of local anesthetics on cancer cell viability and migration depended on the exposure time, specific local anesthetic, specific measurement endpoint and specific cell line.
Keywords: Breast Cancer cells; Cell cycle; Cell migration; Cell viability; Local anesthetics.
Conflict of interest statement
Authors’ information
Chunyun Xiao is currently in the Master of Clinical Nutrition coordinated program at University of Texas Southwestern Medical Center, Dallas, Texas, USA.

Cancers (Basel). 2019 Sep 22;11(10):1414. doi: 10.3390/cancers11101414.
Effects of Lidocaine and Src Inhibition on Metastasis in a Murine Model of Breast Cancer Surgery
Thomas P Wall 1 2 , Peter D Crowley 3 , Aislinn Sherwin 4 , Andrew G Foley 5 , Donal J Buggy 6 7 8
Free PMC article
Abstract
Breast cancer recurs in 20% of patients following intended curative resection. In vitro data indicates that amide local anaesthetics, including lidocaine, inhibit cancer cell metastasis by inhibiting the tyrosine kinase enzyme Src. In a murine breast cancer surgery model, systemic lidocaine reduces postoperative pulmonary metastases. We investigated whether the additional administration of bosutinib (a known Src inhibitor) influences lidocaine's observed beneficial effect in this in vivo model. Female BALB/c mice (n = 95) were inoculated with 25,000 4T1 cells into the mammary fad pad and after 7 days the resulting tumours were excised under sevoflurane anaesthesia. Experimental animals were randomized to one of four treatments administered intravenously prior to excision: lidocaine, bosutinib, both lidocaine and bosutinib in combination, or saline. Animals were euthanized 14 days post-surgery and lung and liver metastatic colonies were evaluated. Post-mortem serum was analysed for MMP-2 and MMP-9, pro-metastatic enzymes whose expression is influenced by the Src pathway. Lidocaine reduced lung, but not liver metastatic colonies versus sevoflurane alone (p = 0.041), but bosutinib alone had no metastasis-inhibiting effect. When combined with lidocaine, bosutinib reversed the anti-metastatic effect observed with lidocaine on sevoflurane anaesthesia. Only lidocaine alone reduced MMP-2 versus sevoflurane (p = 0.044). Both bosutinib (p = 0.001) and bosutinib/lidocaine combined (p = 0.001) reduced MMP-9 versus sevoflurane, whereas lidocaine alone did not. In a murine surgical breast cancer model, the anti-metastatic effects of lidocaine under sevoflurane anaesthesia are abolished by the Src inhibitor bosutinib, and lidocaine reduces serum MMP-2. These results suggest that lidocaine may act, at least partly, via an inhibitory effect on MMP-2 expression to reduce pulmonary metastasis, but whether this is due to an effect on Src or via another pathway remains unclear.
Keywords: Src; anaesthesia; bosutinib; cancer recurrence; lidocaine; local anaesthetics; metastasis.
Conflict of interest statement
Donal Buggy is a guest editor for the Cancers Special Issue on ‘Perioperative interventions on oncologic outcome’. All other authors have no conflicts of interest to declare.

Cancers (Basel). 2019 May 1;11(5):613.
Effect of Perioperative Lidocaine, Propofol and Steroids on Pulmonary Metastasis in a Murine Model of Breast Cancer Surgery
James Freeman 1 2 , Peter D Crowley 3 , Andrew G Foley 4 , Helen C Gallagher 5 , Masae Iwasaki 6 , Daqing Ma 7 , Donal J Buggy 8 9 10
Addressing the hypothesis that anaesthetic-analgesic technique during cancer surgery might influence recurrence or metastatic spread is a research priority. Propofol, which has anti-inflammatory properties in vitro, is clinically associated with reduced risk of cancer recurrence compared with sevoflurane anaesthesia in retrospective studies. Amide local anaesthetics, such as lidocaine, have cancer inhibiting effects in vitro. Steroids have anti-inflammatory and immunosuppressive effects and are associated with improved recovery after major non-cancer surgery. We compared the effects of propofol, lidocaine and methylprednisolone on postoperative metastasis in a murine model of breast cancer surgery under sevoflurane anaesthesia. 4T1 tumour cells were introduced into the mammary fat-pad of female BALB/c mice and the resulting tumour resected seven days later under general anaesthesia with sevoflurane. Mice (n = 72) were randomized to four treatment groups: Sevoflurane alone (control); Propofol group received 5 mg.kg-1; Lidocaine group received 1.5 mg.kg-1 followed by 2 mg.kg-1.h-1 infusion; Methylprednisolone group received 30 mg.kg-1 methylprednisolone. The primary outcome measure was pulmonary metastasis colony count, as assessed by in-vitro proliferation, two weeks post-operatively. This was achieved by treating the post-mortem lung tissue with collagenase IV, straining and culturing for 14 days prior to colony count. Compared with control, lidocaine and propofol each individually reduced pulmonary metastasis colonies; mean (SD) 846 (±581) vs. 88 (±52) vs. 34 (±44) respectively, (p = 0.0001 and p = 0.0001). Methylprednisolone increased lung metastasis, 2555 (±609) vs. 846 (±581), p = 0.0001. Post-operative hepatic metastatic disease and serum interleukin-6 and vascular endothelial growth factor levels were similar in all groups. In conclusion, in a murine model of breast cancer surgery during sevoflurane anaesthesia, propofol and lidocaine each decreased pulmonary metastasis, while methylprednisolone increased it.
Keywords: anaesthesia inhalation; anaesthesia intravenous propofol; cancer metastasis; cancer recurrence; lidocaine; local anaesthetics; steroid methylprednisolone.
Conflict of interest statement
D.M and D.J.B are Editorial Board members of British Journal of Anaesthesia. All other authors have no competing interests to declare.

Cancers (Basel). 2021 Jan 10;13(2):234.
Lidocaine Suppresses Viability and Migration of Human Breast Cancer Cells: TRPM7 as a Target for Some Breast Cancer Cell Lines
Hengrui Liu, James P Dilger 1 , Jun Lin 1
Free PMC article
Abstract
Background: The local anesthetic lidocaine suppresses some cancer cell lines but the mechanism is unclear. The melastatin-like transient receptor potential 7 (TRPM7) ion channel is aberrantly expressed in some cancers and may play a role in the disease. Hence, we suggested that lidocaine affects the viability and migration of breast cancer cells by regulating TRPM7.
Methods: We measured the effects of lidocaine on TRPM7 function in HEK293 with exogenous TRPM7 expression (HEK-M7) using whole-cell patch-clamp and fura-2AM-based quench assay. We measured the effect of lidocaine on TRPM7 function, cell viability, and migration in TRPM7 expressing human breast cancer cell lines using fura-2AM-based quench, MTT, and wound-healing assays respectively. We compared cell viability and migration of wild type HEK293 cells (WT-HEK) with HEK-M7 and wild type MDA-MB-231 (WT-231) with TRPM7 knockout MDA-MB-231 (KO-231).
Results: Lidocaine (1-3 mM) inhibited the viability and migration of all of these breast cancer cell lines. Functional evidence for TRPM7 was confirmed in the MDA-MB-231, AU565, T47D, and MDA-MB-468 cell lines where lidocaine at 0.3-3 mM suppressed the TRPM7 function. Lidocaine preferentially suppressed viability and migration of HEK-M7 over WT-HEK and WT-231 over KO-231.
Conclusions: Lidocaine differentially reduced the viability and migration of human breast cancer cell lines tested. TRPM7 is one of the potential targets for the effects of lidocaine on viability and migration in MDA-MB-231, AU565, T47D, and MDA-MB-468.
Keywords: HEK293; TRPM7; breast cancer cells; migration; viability.

Oncol Lett. 2016 Aug;12(2):1164-1170.
Lidocaine inhibits the invasion and migration of TRPV6-expressing cancer cells by TRPV6 downregulation
Yuan Jiang 1 , Hui Gou 2 , Jiang Zhu 2 , Si Tian 2 , Lehua Yu 2
Free PMC article
It is well known that local anesthetics have a broad spectrum of pharmacological actions, acting as nerve blocks, and treating pain and cardiac arrhythmias via blocking of the sodium channel. The use of local anesthetics could reduce the possibility of cancer metastasis and recurrence following surgical tumor excision. The purpose of the present study was to investigate the inhibitory effect of lidocaine upon the invasion and migration of transient receptor potential cation channel subfamily V member 6 (TRPV6)-expressing cancer cells. Human breast cancer MDA-MB-231 cells, prostatic cancer PC-3 cells and ovarian cancer ES-2 cells were treated with lidocaine. Cell viability was quantitatively determined by MTT assay. The migration of the cells was evaluated using the wound healing assay, and the invasion of the cells was assessed using a Transwell assay. Calcium (Ca2+) measurements were performed using a Fluo-3 AM fluorescence kit. The expression of TRPV6 mRNA and protein in the cells was determined by quantitative-polymerase chain reaction and western blot analysis, respectively. The results suggested that lidocaine inhibits the cell invasion and migration of MDA-MB-231, PC-3 and ES-2 cells at lower than clinical concentrations. The inhibitory effect of lidocaine on TRPV6-expressing cancer cells was associated with a reduced rate of calcium influx, and could occur partly as a result of the downregulation of TRPV6 expression. The use of appropriate local anesthetics may confer potential benefits in clinical practice for the treatment of patients with TRPV6-expressing cancer.

Acta Anaesthesiol Scand. 2002 Aug;46(7):836-44.
Influence of non-volatile anesthetics on the migration behavior of the human breast cancer cell line MDA-MB-468
V Garib 1 , B Niggemann, K S Zänker, L Brandt, B S Kubens
Background: Anesthetic agents are known to influence functions of the immune system. Anesthetic drugs also support cancer progression by suppressing the activity of immune cells. In breast carcinoma an increase in expression of peripheral-type benzodiazepine receptors (PBR) and the gamma aminobutyl acid (GABA) level has been discovered. Therefore, an investigation of a direct influence of GABA-A agonist propofol, GABA-A and PBR-agonist etomidate, and the local anesthetic drug lidocaine, which can also bind to the GABA-A receptor and PBR, on migration of breast carcinoma cells was performed.
Methods: MDA-MB-468 cells were incubated with anesthetic agents using clinically relevant concentrations (propofol 3, 6, 9 mg/l, etomidate 2, 3, 4 mg/l, and lidocaine 1.25, 2.5, 5 mg/l). Locomotion was investigated in a three-dimensional collagen matrix using time-lapse video microscopy and computer-assisted cell-tracking.
Results: The percentage of migrating cells (57.4+/-1.9) as well as the velocity (0.22+/-0.09 microm/min) and distance migrated (89.4+/-66.8 microm/10 h) increased in the presence of propofol in a dose-dependent manner (up to 74.4+/-7.5, 0.30+/-0.09, 143.8+/-89.1, respectively) compared with the long chain triglyceride (LCT) control. In contrast, no influence of etomidate on the number of migrating cells could be observed. The velocity and distance migrated at 3 and 4 mg/l were found to be statistically significantly enhanced. Treatment with lidocaine caused an increase in the percentage of migrating cells (up to 75.0+/-5.6) in velocity dose dependently (up to 0.33+/-0.06) and in distance migrated (up to 151.5+/-92.9).
Conclusion: These results show that different anesthetic drugs are able to modulate the migratory machinery of human breast carcinoma cells in vitro.

Anticancer Res. 2018 Oct;38(10):5599-5606. doi: 10.21873/anticanres.12894.
Effect of Perioperative Lidocaine and Cisplatin on Metastasis in a Murine Model of Breast Cancer Surgery
James Freeman 1 2 , Peter D Crowley 2 , Andrew G Foley 3 , Helen C Gallagher 2 , Masae Iwasaki 4 , Daqing Ma 4 , Donal J Buggy 5 2 6
Background/aim: Mortality from breast cancer is usually attributable to metastasis. In vitro data suggest that amide local anaesthetics, e.g. lidocaine, inhibit metastasis by multiple mechanisms and recent in vivo data support this. Experimental data also suggest that opioids may inhibit cisplatin chemotherapy. Whether lidocaine would influence cisplatin chemotherapy has not been evaluated.
Materials and methods: 4T1 cells were injected into the mammary gland of immunocompetent female BALB/c mice, with resection of the tumour under sevoflurane anaesthesia one week later. Mice (n=45) were randomized into one of three groups: The cisplatin group received 3 mg.kg-1 cisplatin; cisplatin and lidocaine group received 3 mg.kg-1 cisplatin and lidocaine bolus of 1.5 mg.kg-1 followed by an infusion of 2 mg.kg-1.h-1 The control group received sevoflurane only. All agents were given perioperatively. After 14 postoperative days, post-mortem lung, serum and liver samples were collected. Primary outcome measure was lung metastasis colony count.
Results: During sevoflurane anaesthesia, the addition of lidocaine to cisplatin significantly decreased metastatic lung colony count [(mean±SD) (157±87)] compared to control [846±581, (p=0.001)], and cisplatin alone [580±383, (p=0.018)]. However, liver metastasis colony count was not reduced with the combination of cisplatin and lidocaine (9.3±13.9) when compared to control (74.7±257.3), p=0.78 or to cisplatin alone (110±388.8), p=0.569. Serum VEGF and interleukin-6 concentrations were not significantly different.
Conclusion: In a 4T1 murine model of breast cancer surgery, under sevoflurane anaesthesia, lidocaine enhanced the metastasis-inhibiting action of cisplatin. Clinical evaluation of the hypothesis that co-administration of systemic lidocaine during cisplatin chemotherapy seems warranted.
Keywords: Breast cancer; anaesthesia; chemotherapy; cisplatin; inhalation; metastasis.
Copyright© 2018, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

J Toxicol Sci. 2021;46(7):329-339.
Lidocaine prevents breast cancer growth by targeting neuronatin to inhibit nerve fibers formation
Bingda Li 1 , Hao Xu 2 , Chongwu He 3 , Wenxiong Zou 4 , Yun Tu 5
Free article
Abstract
Lidocaine has been shown to inhibit the invasion and metastasis of breast cancer, but the mechanism still remains unclear. This study explored the relationship between lidocaine and circulating seeding of breast cancer cells from the perspective of nerve fiber formation. The cell lines MDA-MB-231 and 4T1 were subcutaneously inoculated in mice to simulate the tumor self-seeding by circulating cancer cells. Lidocaine was used to treat these mice and tumor growth was observed. Silver staining was performed to observe the distribution of nerve fibers in tumor-bearing tissues, and immunohistochemical analysis was performed to observe the expression levels of nerve-related proteins. The results showed that lidocaine treatment effectively inhibited tumor growth and nerve fiber formation, and down-regulated the expression levels of protein gene product 9.5, neurofilament, nerve growth factor (NGF), and neuronatin (Nnat). Overexpression NGF and Nnat both could reverse the therapeutic effects of lidocaine. These results suggest that the effect of lidocaine on inhibiting breast cancer invasion and metastasis may be achieved by targeting Nnat, regulating the production of NGFs in cancer cells, and subsequently inhibiting the formation of nerve fibers.

Br J Anaesth. 2012 Aug;109(2):200-7.
Lidocaine time- and dose-dependently demethylates deoxyribonucleic acid in breast cancer cell lines in vitro
P Lirk 1 , R Berger, M W Hollmann, H Fiegl
Erratum in
Br J Anaesth. 2013 Jan;110(1):165
Abstract
Background: Anaesthetic management of cancer surgery may influence tumour recurrence. The modulation of gene expression by methylation of deoxyribonucleic acid (DNA) (epigenetics) is increasingly recognized as a major hallmark of cancer. Next to direct effects of local anaesthetics upon tumour cells, the ester-type local anaesthetic, procaine, has been shown to affect methylation status in several tumour cell lines, promoting the reactivation of tumour suppressor genes. We sought to determine whether the prototype amide-type local anaesthetic, lidocaine, influences the survival and epigenetic status of oestrogen receptor (ER)-positive and -negative breast cancer cell lines in vitro.
Methods: Breast cancer cell lines BT-20 (ER-negative) and MCF-7 (ER-positive) were incubated with lidocaine and procaine as the reference substance. We performed cell count and determined apoptosis using TUNEL stain. Further, we assessed global methylation status, and methylation of three known tumour suppressor genes (RASSF1A, MYOD1, and GSTP1) using the MethyLight assay and real-time quantitative polymerase chain reaction, respectively.
Results: Baseline methylation was 100-fold higher in BT-20 cells. Here, we observed a dose-dependent decrease in DNA methylation in response to lidocaine (1, 0.01, and 0.01 mM) after 72 h (P<0.001, <0.001, and 0.004, respectively). The corresponding changes were smaller in MCF-7 cells. Global methylation status was profoundly influenced, but the methylation and mRNA expression status of three tumour suppressor genes was unchanged.
Conclusions: Our findings suggest that demethylating tumour-suppressive effects of anaesthetic interventions may only be detectable in specific types of cancer due to differential methylation profiles. In conclusion, at clinically relevant concentrations, lidocaine demethylates DNA of breast cancer cell lines in vitro.
Cited by 31 articles

Anticancer Res. 2021 Jun;41(6):2835-2840. .
The Effect of Lidocaine and Bosutinib on 4T1 Murine Breast Cancer Cell Behaviour In Vitro
Thomas P Wall 1 2 , Peter D Crowley 3 , Donal J Buggy 4 2 5
Background/aim: Systemic lidocaine has recently emerged as a promising agent possessing numerous potentially anti-neoplastic effects. In vitro studies suggest that lidocaine may prevent metastasis by acting on the tyrosine kinase enzyme Src. Intravenous lidocaine has been reported to reduce pulmonary metastasis in vivo in a murine breast cancer model, however the beneficial effect is abolished by the Src inhibitor bosutinib. In this study we examined whether lidocaine and/or bosutinib affects 4T1 breast cancer cell activity in vitro and whether any drug interactions similar to that seen in murine models occur.
Materials and methods: 4T1 murine breast cancer cells were exposed to lidocaine and/or bosutinib. Cell viability after 1 h of exposure was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell migration after 24 h of exposure was measured using the Oris™ migration assay.
Results: Lidocaine and bosutinib alone or combined inhibited 4T1 cell viability and migration, but only at supratherapeutic concentrations. Bosutinib did not modulate lidocaine's effect on viability or migration at any concentration tested.
Conclusion: Although lidocaine may inhibit 4T1 metastasis in vivo, a direct effect on 4T1 cells is not detectable in vitro at non-toxic concentrations and unlike murine model testing, no unusual interaction with bosutinib was detected. Lidocaine's anti-metastatic properties are likely to be complex and multifactorial and difficult to replicate outside of a biological host.
Keywords: Lidocaine; Src; bosutinib; cancer; local anesthetics; metastasis.
Copyright © 2021 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Br J Anaesth. 2018 Jul;121(1):76-85.
Effect of perioperative lidocaine on metastasis after sevoflurane or ketamine-xylazine anaesthesia for breast tumour resection in a murine model
M Z Johnson 1 , P D Crowley 2 , A G Foley 3 , C Xue 2 , C Connolly 4 , H C Gallagher 5 , D J Buggy 6
Free article
Abstract
Background: Breast cancer accounts for 7% of female cancer deaths, usually attributable to metastasis. While surgery is a mainstay of treatment, perioperative interventions may influence risk of metastasis during breast tumour resection. Amide local anaesthetics influence cancer cell biology via numerous mechanisms in vitro, but in vivo data is lacking. We aimed to test the hypothesis that perioperative lidocaine reduces pulmonary metastasis after inhalation and i.v. anaesthesia in the 4T1 murine breast cancer model.
Methods: 4T1 Cancer cells were injected into the mammary fat-pad of immunocompetent BALB/c female mice. After 7 days, the resultant tumour was excised under either sevoflurane or ketamine/xylazine anaesthesia with or without perioperative i.v. lidocaine (1.5 mg kg-1 bolus followed by 25 min infusion 2 mg kg-1 h-1). Fourteen days post-surgery, posthumous lung and liver specimens were examined for metastasis. Pro-inflammatory and pro-metastatic cytokines were profiled in post-mortem serum from a small number of the mice.
Results: Primary tumour diameter was similar between groups. Lidocaine reduced lung metastatic colony count vs sevoflurane alone; median (inter-quartile range) 0 (0-2) compared with 22.5 (0-481), P=0.02 and reduced the proportion of animals with pulmonary metastasis (28.5% compared with 52.5%, P=0.04). In mice receiving ketamine-xylazine, lidocaine did not decrease the overall colony count: 60 (26-123) compared with 23.5 (0-225), P=0.43, but increased the proportion of animals with pulmonary metastasis (100% compared with 50%, P<0.01). Post-mortem serum analysis demonstrated reduced pro-inflammatory and angiogenic cytokine expression in animals without metastasis which received lidocaine with sevoflurane.
Conclusions: In this 4T1 murine model of breast cancer, lidocaine decreased pulmonary metastasis when combined with sevoflurane anaesthesia, perhaps via anti-inflammatory and anti-angiogenic effects. It had no such effect in mice given ketamine anaesthesia.

Br J Anaesth. 2014 Jul;113 Suppl 1:i39-i48.
Potent inhibition by ropivacaine of metastatic colon cancer SW620 cell invasion and NaV1.5 channel function
D T Baptista-Hon 1 , F M Robertson 1 , G B Robertson 1 , S J Owen 1 , G W Rogers 1 , E L Lydon 1 , N H Lee 2 , T G Hales 3
Free article
Background: Metastatic breast and colon cancer cells express neonatal and adult splice variants of NaV1.5 voltage-activated Na(+) channels (VASCs). Block of VASCs inhibits cell invasion. Local anaesthetics used during surgical tumour excision inhibit VASC activity on nociceptive neurones providing regional anaesthesia. Inhibition of VASCs on circulating metastatic cancer cells may also be beneficial during the perioperative period. However, ropivacaine, frequently used to provide analgesia during tumour resection, has not been tested on colon cancer cell VASC function or invasion.
Methods: We used reverse transcription-polymerase chain reaction and sequencing to identify NaV1.5 variants in the SW620 metastatic colon cancer cell line. Recombinant adult and neonatal NaV1.5 variants were expressed in human embryonic kidney cells. Voltage-clamp recordings and invasion assays were used to examine the effects of ropivacaine on recombinant NaV1.5 channels and the metastatic potential of SW620 cells, respectively.
Results: SW620 cells expressed adult and neonatal NaV1.5 variants, which had similar steady-state inactivation profiles, but distinctive activation curves with the neonatal variant having a V1/2 of activation 7.8 mV more depolarized than the adult variant. Ropivacaine caused a concentration-dependent block of both NaV1.5 variants, with IC50 values of 2.5 and 3.9 µM, respectively. However, the reduction in available steady-state current was selective for neonatal NaV1.5 channels. Ropivacaine inhibited SW620 invasion, with a potency similar to that of inhibition of NaV1.5 channels (3.8 µM).
Conclusions: Ropivacaine is a potent inhibitor of both NaV1.5 channel activity and metastatic colon cancer cell invasion, which may be beneficial during surgical colon cancer excision.

On Jul 7, 2021, at 6:20 PM, melissa jacobs <[email protected]> wrote:
Thanks Dr. Peat. Yes, makes sense that the increased T3 probably stopped the menstruation; but I wanted to do all i could to counteract the radiation since I reacted to it so badly. Interesting about the humic, ive been trying a bottle and not sure if it is really doing anything so maybe will finish the bottle and then stop and see if there were any effects by comparing with and without it.

I have taken the lidocaine powder (I think about 25 mg per dose) the last few weeks on three separate occasions, per your prior suggestion to me for the hypersensitivity. Each time I take it, it has a very invigorating energizing effect on me- almost feels like a stimulant or drug like feeling but a good feeling-not quite what i would expect as i thought it was more of a relaxant. Need to try it more to see if it helps with the chemical hypersensitivity.

Does 25 mg for a dose seem right? Would it be appropriate to take daily for a period of time to see if it has an effect cumulatively on the hypersensitivities?
On Wed, Jul 7, 2021 at 6:32 PM Ray Peat <[email protected]> wrote:

Small amounts of the humic stuff are safe, but I doubt that they are effective. Too much T3 can reduce estrogen to the point that it stops menstruation, and taking progesterone a day or two before ovulation can cause it to happen a little prematurely, but they help to repair radiation damage. Drinking extra orange juice is protective against radiation after-effects.

On Jul 6, 2021, at 5:07 PM, melissa wrote:
Thanks Dr. Peat- will probably get it extracted. Unfortunately, in order to get the evaluation, I had to have the whole roster of x-rays and had a pronounced reaction that is only now starting to dissipate over a week later despite all of the mitigation measures immediately before and after and ongoing-aspirin, thyroid, progesterone, methylene blue and red light. Also, much to my dismay, my period did not come as expected- almost one week late now. My cycles were a bit different the last three months- no alarming blood clots- but off. Hard to know with my history; but i wonder if i am being affected by these injected people- hard to completely avoid them- they are everywhere. Also wondering if the x-ray session could have anything to do with this. I have been loading up on progesterone to see if that will bring it on. I also increased thyroid after the x-ray and wondering if the increase in T3 might have suppressed menstruation. So many variables. All thoughts are appreciated.

I am heading down to San Antonio, Texas in a couple of weeks for a summit with America's Frontline Doctors, the group I am working with on the civil legal efforts and both of my colleagues on the criminal initiative will be there as well. I am considering a move to Texas in September and am pursuing other opportunities there in various areas as well. Meanwhile, citizen groups in Colorado are about to mass file the criminal complaints here and I have been approached regarding my representation on a large civil lawsuit here. Perhaps I will practice in multiple states, including NY remotely where I am barred currently. The information I get on a daily basis is increasingly alarming and inciting further urgency on the legal efforts.

Lastly, i wanted to know your thoughts on this product: Restore Gut Health & Microbiome - Intelligence of Nature

Take 5 ml (a teaspoon) three times a day (before meals if you can).
Sensitive usage: 3-5 drops twice daily increasing slowly as tolerated. Visit our FAQs for more details.
Purified water, Terrahydrite (Aqueous humic substances),
and less than 1% mineral amino acid complexes.
On Thu, Jul 1, 2021 at 9:12 AM Ray Peat <[email protected]> wrote:

If a heavy course of antibiotics couldn’t clear it up, and they won’t re-do the root treatment, than pulling it could be a solution.

On Jun 30, 2021, at 8:33 PM, melissa wrote:
Thanks Dr Peat. The tooth itself has no pain- only sensations and clicking above it in my sinus and cheek area. I was told by and endodontist And this dentist that re treat not possible on this situation so seems only option is to extract. But do you think the fact that the tooth itself has no pain and only the symptoms I described above it that this contraindicated extracting it?

On Jun 30, 2021, at 3:36 PM, Ray Peat <[email protected]> wrote:

If it causes steady pain, then either doing a new root treatment or pulling it would seem best.
If there’s a problem in the bone that the body’s restorative-immune system hasn’t been able to take care of, dental implants would be more likely than usual to cause problems, and implants in the upper jaw are riskier anyway, because of the porous nature of the bone and the closeness to sinuses.

On Jun 29, 2021, at 9:19 PM, melissa jacobs <[email protected]> wrote:
Me too- I will keep you posted on the legal actions. The lead of the activist group here mentioned that her network in Oregon is interested in the criminal complaint initiative.

Thank you for all of this information- yes I am a bit suspicious of the cavitation diagnosis. Probably will hold off on the cavitation work. However, I think the extraction of the root canaled tooth seems to make sense. I have had a lot of symptoms above it and the image of That area looked distinct. Just 2 Questions To you in bold below:

Do you think that sounds reasonable To extract that one back upper left root canal tooth and hold off on the cavitation work? Do you think since it is the very back tooth, it would be ok to leave it alone after extraction and forego an impant?

Thanks so much for the info on the chlorine dioxide- will study up. My gut reaction to it was again suspicion ; but it has been coming up much In the context of Covid and so many are touting it as a miracle for everything under the sun - so wanted to ask you about it.

Talk soon with more updates! Melissa

On Jun 29, 2021, at 9:51 PM, Ray Peat <[email protected]> wrote:

I’m really glad to hear about the acceleration of the legal actions.

When I hear about “biological dentists” and their cavitations, I think of the “Lyme disease doctors.” I think it’s an extention of the old “focal infection” scam, opening new profit opportunities. If some of the jaw bone is removed, the healing is very slow, with prolonged more intense pain. The older a person is, the slower and less certain the bone regeneration is.
Dental Cavitations: Definition, Facts, & Myths - Ask the Dentist “But some patients are misdiagnosed with a dental cavitation. The dentist might see an area of “demineralization” in the jawbone that is not pathologic. If this demineralized area is treated as a true dental cavitation, it could lead to unnecessary surgery and significant expense.
Since “cavitation” is not a recognized dental term or condition, there is much confusion revolving around its diagnosis and treatment. In my opinion, misdiagnosis is an error that may be understandable. Yet, overdiagnosis of dental cavitations is fraud in my opinion and could lead to unnecessary treatment, high cost, and pain."

Chronic intestinal problems are a possible cause of jaw/facial neuralgia, and I think disinfection of the bowel should be worked on before any dentistry. The potential long-range effects of chlorine, including mutations and cancer, are risks of using chlorine antiseptic products. Here are some articles relating to chlorine dioxide.

Proc Natl Acad Sci U S A. 1986 Mar;83(5):1485-9.
Relationship of drinking water disinfectants to plasma cholesterol and thyroid
hormone levels in experimental studies.
Revis NW, McCauley P, Bull R, Holdsworth G.
The effects of drinking water containing 2 or 15 ppm chlorine (pH 6.5 and 8.5),
chlorine dioxide, and monochloramine on thyroid function and plasma cholesterol
were studied because previous investigators have reported cardiovascular
abnormalities in experimental animals exposed to chlorinated water. Plasma
thyroxine (T4) levels, as compared to controls, were significantly decreased in
pigeons fed a normal or high-cholesterol diet and drinking water containing these
drinking water disinfectants at a concentration of 15 ppm (the exception was
chlorine at pH 6.5) for 3 months. In most of the treatment groups, T4 levels were
significantly lower following the exposure to drinking water containing the 2 ppm
dose. Increases in plasma cholesterol were frequently observed in the groups with
lower T4 levels. This association was most evident in pigeons fed the
high-cholesterol diet and exposed to these disinfectants at a dose of 15 ppm. For
example, after 3 months of exposure to deionized water or water containing 15 ppm
monochloramine, plasma cholesterol was 1266 +/- 172 and 2049 +/- 212 mg/dl,
respectively, a difference of 783 mg/dl. The factor(s) associated with the effect
of these disinfectants on plasma T4 and cholesterol is not known. We suggest
however that these effects are probably mediated by products formed when these
disinfectants react with organic matter in the upper gastrointestinal tract.

Environ Health Perspect. 1996 May;104(5):516-20.
Association between drinking water disinfection and somatic parameters at birth.
Kanitz S, Franco Y, Patrone V, Caltabellotta M, Raffo E, Riggi C, Timitilli D,
Ravera G.
Institute of Hygiene and Preventive Medicine, University of Genoa, Italy.
We conducted an epidemiological study in Liguria, Italy, on the association
between somatic parameters at birth and drinking water disinfection with chlorine
dioxide and/or sodium hypochlorite. Over 2 years (1988-1989), 676 births at two
public hospitals, one in Genoa (548 cases) and another in Chiavari (128 cases)
were examined and data regarding both mother and child were obtained from
hospital records. Results indicate a higher frequency of small body length (< or
= 49.5 cm) and small cranial circumference (< or = 35 cm) in infants born to
mothers who drank water treated with chlorine compounds. In particular, the
statistical analysis (by simultaneous variance analysis and Scheffé test)
indicated that there may be an association between infants with smaller body
length and mothers who drank water treated with chlorine dioxide [adjusted odds
radio (OR) = 2.0; 95% CI = 1.2-3.3] or sodium hypoclorite (adjusted OR = 2.3; 95%
CI = 1.3-4.2) and between infants with smaller cranial circumference and mothers
who drank water treated with chlorine dioxide (adjusted OR = 2.2; 95% CI =
1.4-3.9) or sodium hypochlorite (adjusted OR = 3.5; 95% CI = 2.1-8.5). The
presence of neonatal jaundice is almost twice as likely (adjusted OR = 1.7; 95%
CI = 1.1-3.1) in infants whose mothers drank water treated with chlorine dioxide.

Water Res. 2008 Sep;42(15):4075-82. Epub 2008 Jun 26.
Evaluation of chlorite and chlorate genotoxicity using plant bioassays and in
vitro DNA damage tests.
Feretti D, Zerbini I, Ceretti E, Villarini M, Zani C, Moretti M, Fatigoni C,
Orizio G, Donato F, Monarca S.
Department of Experimental and Applied Medicine, Hygiene Section, University of
Brescia, Viale Europa 11, 25123 Brescia, Italy. [email protected]
In the last few years chlorine dioxide has been increasingly used for
disinfecting drinking water in many countries. Although it does not react with
humic substances, chlorine dioxide added to water is reduced primarily to
chlorite and chlorate ions, compounds that are under investigation for their
potential adverse effects on human health. The aim of this research was to study
the genotoxicity of chlorite and chlorate and their mixtures. The end-points
included two plant tests (chromosomal aberration test in Allium cepa and
micronucleus assay in Tradescantia, carried out at different times of exposure)
and two genotoxicity tests in human HepG2 cells (comet assay and
cytokinesis-blocked micronucleus test). Preliminary toxicity tests were carried
out for both plant and HepG2 assays. The results showed that chlorite and
chlorate are able to induce chromosomal damage to plant systems, particularly
chromosomal aberrations in A. cepa root tip cells, even at concentrations lower
than the limit established by Italian normative law and WHO guidelines. In HepG2
cells increased DNA damage was only observed for chlorate at the lowest
concentration. No increase in micronuclei frequency was detected in any of the
samples tested in human HepG2 cells.

Environ Res. 2002 Jun;89(2):124-30.
Chlorination byproducts and nitrate in drinking water and risk for congenital
cardiac defects.
Cedergren MI, Selbing AJ, Löfman O, Källen BA.
Division of Obstetrics and Gynaecology, Department of Health and Environment,
Faculty of Health Sciences, Linköping University, Linköping SE-581 85, Sweden.
Drinking water disinfection byproducts have been associated with an increased
risk for congenital defects including cardiac defects. Using Swedish health
registers linked to information on municipal drinking water composition,
individual data on drinking water characteristics were obtained for 58,669 women.
Among the infants born, 753 had a cardiac defect. The risk for a cardiac defect
was determined for ground water versus surface water, for different chlorination
procedures, and for trihalomethane and nitrate concentrations. Ground water was
associated with an increased risk for cardiac defect when crude rates were
analyzed but after suitable adjustments this excess rate was found to be
determined by chlorination procedures including chlorine dioxide. Chlorine
dioxide appears itself as an independent risk factor for cardiac defects
(adjusted odds ratio 1.61 (95%CI 1.00-2.59)). The risk for cardiac defects
increased with increasing trihalomethane concentrations (P=0.0005). There was an
indicated but statistically nonsignificant excess risk associated with nitrate
concentration. The individual risk for congenital cardiac defect caused by
chlorine dioxide and trihalomethanes is small but as a large population is
exposed to public drinking water, the attributable risk for cardiac defects may
not be negligible.

J Water Health. 2004 Dec;2(4):233-47.
Chlorination by-products (CBPs) in drinking water and adverse pregnancy outcomes
in Italy.
Aggazzotti G, Righi E, Fantuzzi G, Biasotti B, Ravera G, Kanitz S, Barbone F,
Sansebastiano G, Battaglia MA, Leoni V, Fabiani L, Triassi M, Sciacca S;
Collaborative Group for the Study of Chlorinated Drinking Waters and Pregnancy.
Dipartimento di Scienze Igienistiche, Microbiologiche e Biostatistiche,
Università degli Studi di Modena e Reggio Emilia, Via Campi 287. 41100 Modena,
Italy. [email protected]
Chlorination by-products (CBPs) in drinking water have been associated with an
increased risk of adverse pregnancy outcomes, including small for gestational age
at term (term-SGA) and preterm delivery. Epidemiological evidence is weakened by
a generally inaccurate exposure assessment, often at an ecological level. A case
control study with incident cases was performed in nine Italian towns between
October 1999 and September 2000. A total of 1,194 subjects were enrolled: 343
preterm births (26th-37th not completed week of pregnancy), 239 term-SGA (from
37th completed week, and weight less than the lowest 10th percentile) and 612
controls. Exposure was assessed both by applying a questionnaire on mothers'
personal habits during pregnancy and by water sampling directly at mothers'
homes. Levels of trihalomethanes (THMs) were low (median: 1.10 microg l(-1)),
while chlorite and chlorate concentrations were relatively high (median: 216.5
microg l(-1) for chlorites and 76.5 microg l(-1) for chlorates). Preterm birth
showed no association with CBPs, while term-SGA, when chlorite levels > or =200
microg l(-1) combined with low and high levels of inhalation exposure are
considered, suggested a dose-response relationship (adjusted-Odds Ratios (ORs):
1.52, 95%CI: 0.91-2.54 and 1.70, 95%CI: 0.97-3.0, respectively). A weak
association with high exposure levels of either THMs (> or =30 microg l(-1)), or
chlorite or chlorate (> or =200 microg l(-1)) was also found (adjusted-OR: 1.38,
95%CI: 0.92-2.07). Chlorine dioxide treatment is widespread in Italy; therefore,
chlorite levels should be regularly and carefully monitored and their potential
effects on pregnancy further evaluated and better understood.

Ann Ig. 2004 Sep-Oct;16(5):639-46.
[Trihalomethanes and chlorites in finished drinking water in Sardinia (Italy) and
possible health effects]
[Article in Italian]
Contu A, Carlini M, Meloni P, Puddu D, Schintu M.
Dipartimento di Sanità Pubblica, Università degli Studi di Cagliari.
[email protected]
A five years monitoring was carried out in central and southern Sardinia (Italy)
to assess the levels of two disinfection by-products (DBPs)--total
thrialomethanes (TTHMs) and chlorites--in drinking water Between 1997 and 2002,
about 1900 drinking water samples were analysed for both of them. The results
showed that TTHMs exceeded very often the maximum admissible concentration.
Chlorite concentration was found rising in all the distribution networks since
the utilization of chlorine dioxide as disinfectant in 1999, exceeding the
maximum contaminant level goals suggested by the World Health Organization. These
results are relevant for epidemiological studies on health effects from DBPs
exposure.

Mutat Res. 2004 Dec 12;564(2):179-93.
In vitro potential genotoxic effects of surface drinking water treated with
chlorine and alternative disinfectants.
Guzzella L, Monarca S, Zani C, Feretti D, Zerbini I, Buschini A, Poli P, Rossi C,
Richardson SD.
Water Research Institute-National Research Council (IRSA-CNR), via della Mornera
25, Brugherio 20047, Milan, Italy. [email protected]
A battery of in vitro short-term tests revealing different genetic end-points was
set up in order to study surface-water genotoxicity after disinfection with
different biocides: sodium hypochlorite (NaClO), chlorine dioxide (ClO(2)) and
peracetic acid (PAA). The surface water both before and after disinfection was
concentrated by adsorption on C(18) silica cartridges and the concentrates
containing non-volatile organics were divided into different portions for
chemical analyses and biological assays. The following in vitro tests were
conducted on the water concentrates dissolved in DMSO: the Salmonella
mutagenicity assay with S. typhimurium strains TA98 and TA100; the SOS Chromotest
with Escherichia coli, the Microtox and Mutatox assays with Vibrio fischeri; and
gene conversion, point mutation and mitochondrial DNA mutability assays with D7
diploid Saccharomices cerevisiae strain. The results show that the SOS Chromotest
and the yeast assays are highly sensitive in detecting genotoxicity. The
surface-water extracts were very often toxic to most of the test organisms
considered, partially masking their potential mutagenic activity. Therefore, the
assays with E. coli and with S. cerevisiae are more likely to show a mutagenic
effect because these organisms are generally less sensitive to most toxic
compounds. Among the tested disinfectants, NaClO and ClO(2) increased water
genotoxicity, whereas PAA was able to slightly reduce raw water activity.
However, because the organic compounds in the lake water varied with the season
of the year, the disinfection processes, at times, both increased and decreased
the raw water activity.

Ann Ig. 2003 Sep-Oct;15(5):649-62.
[Exposure to water disinfection by-products and adverse pregnancy outcomes:
results of a case-control study carried out in Modena (Italy)]
[Article in Italian]
Righi E, Fantuzzi G, Montanari M, Bargellini A, Predieri G, Aggazzotti G.
Dipartimento di Scienze Igienistiche, Microbiologiche e Biostatistiche,
Università degli Studi di Modena e Reggio Emilia, Italy. [email protected]
Chlorination By Products (CBPs) in drinking water have been associated with an
increased risk of adverse pregnancy outcomes, such as small term birth (STB) and
preterm delivery. Up to date epidemiological evidence is weakened by a generally
inaccurate exposure assessment, often at an ecological level: in this study the
exposure is evaluated at the individual level. A case control study with incident
cases was performed in Modena between October 1999-September 2000. 332 subjects
were enrolled: 93 preterm births (26th-37th week of pregnancy), 73 STB (from 38th
week, and weight less than the lowest 10th percentile) and 166 controls. Exposure
was assessed both by applying a questionnaire on personal habits and by personal
water sampling directly at subjects' home. THMs were analysed in all samples,
chlorite and chlorate in water samples treated with chlorine dioxide. Subjects
usually drinking tap water were few (5.2%): most of them were living in areas
supplied by water treated with chlorine dioxide (87%). Levels of THMs were low
(mean: 0.73 microgram/l), while chlorite and chlorate concentrations were
relatively high (mean: 217.8 microgram/l for chlorites and 95.2 microgram/l for
chlorates). Preterm birth did not show any significant association with CBPs,
while STB appeared significantly associated, after adjusting for many potential
confounders, with CBPs induced by chlorine dioxide treatment, especially with
levels of chlorate higher than 200 microgram/l (OR: 4.7; 95%CI: 1.15-19.72). The
association between STB and chlorate must be investigated further as the number
of water utilities applying chlorine dioxide as disinfection treatment is
increasing.

Environ Mol Mutagen. 2003;41(5):353-9.
Genotoxicity of surface water treated with different disinfectants using in situ
plant tests.
Monarca S, Rizzoni M, Gustavino B, Zani C, Alberti A, Feretti D, Zerbini I.
Department of Hygiene and Public Health, University of Perugia, Italy.
[email protected]
Disinfection of surface drinking water, in particular water chlorination, results
in many by-products with potential genotoxic and/or carcinogenic activity. In the
present study, we evaluated the genotoxicity of surface water after treatment
with different disinfectants by means of in situ plant genotoxicity assays
(micronucleus and chromosomal aberration tests) which can detect both clastogenic
and aneugenic effects. The study was carried out at a pilot plant using lake
water after sedimentation and filtration. This water supplied four stainless
steel basins: three basins were disinfected with sodium hypochlorite, chlorine
dioxide, and peracetic acid and the fourth basin containing untreated lake water
was used as a control. Plants were exposed in situ in the basins. The study was
carried out using water collected in different seasons over a period of about 1
year in order to assess the treatments in different physical and chemical lake
water conditions. The micronucleus test in root cells of Vicia faba (Vicia
faba/MCN test) revealed genotoxicity in many samples of disinfected water. The
micronucleus test in Tradescantia pollen cells and the chromosome aberration test
in root cells of Allium cepa showed genotoxic effects only in some disinfected
samples, but also revealed genotoxicity in raw water. The results of the study
indicated that the Vicia faba/MCN test was the most sensitive plant assay for
disinfected water and that peracetic acid disinfection produced similar or lower
genotoxicity than sodium hypochlorite or chlorine dioxide treatment. Copyright
2003 Wiley-Liss, Inc.

Med Pr. 1993;44(5):439-45.
[Safety conditions for working with stabilized chlorine dioxide used for
disinfection]
[Article in Polish]
Adamiak-Ziemba J.
Zakładu Informacji Naukowej, Instytutu Medycyny Pracy, Lodzi.
Disinfectants called by producers stabilized chlorine dioxide (ClO2) are most
often composed of sodium carbonate aqueous solution and ClO2. Stability is due to
sodium chlorate which is produced under these conditions. Solutions of active
ClO2 obtained through acidification of the preparation with citric acid and an
appropriate water dilution are used in disinfection. Then, free ClO2 becomes an
active disinfecting factor--a gas of strong irritative properties. During a
disinfecting process the gas is liberated from the solution due to pulverization
and dryness of disinfected objects. The study indicated that the safety of work
with disinfectants requires mechanical ventilation of working premises. The
transformation of stabile ClO2 into an active form should be induced by adding an
appropriate volume of the stabilising preparation to citric acid solution. Such a
procedure assures that a maximum of gaseous ClO2 will be retained in water.

Sci Total Environ. 1985 Dec;47:229-56.
Evaluation of different treatment processes with respect to mutagenic activity in
drinking water.
Kool HJ, Hrubec J, van Kreijl CF, Piet GJ.
Treatment processes which are applied in The Netherlands during the preparation
of drinking water have been evaluated with regard to introduction and removal of
organic mutagens as well as halogenated organics. It appeared that the most
efficient processes in reducing mutagenic activity were activated carbon
filtration and artificial dune recharge. In general these processes were also the
most efficient in removing halogenated organics. Using low doses of chlorine
dioxide (less than 1 mg C1O2/l) for safety disinfection of drinking water, no
change or substantial less mutagenic activity than by chlorination (1 mg Cl/l)
was found. This counts too for the formation of halogenated organics. Transport
chlorination of stored river Meuse water was able to introduce or activate
mutagenic nitro organics which have not been found previously. Ozone treatment
under field conditions showed mostly a tendency to decrease the activity of
organic mutagens. It was also shown that dependent on the water quality and
treatment conditions a slight increase of mutagenic activity occurred, but this
activity would be reduced by increasing the ozone dose. It seems possible to
optimize the ozone treatment conditions regarding the level of ozone dose and the
contact time to avoid an increase of mutagenic activity. Furthermore it was shown
that when a mutagenic raw water source was used a proper combination of treatment
processes is able to produce drinking water in which no mutagenic activity could
be detected under the test conditions. Finally it is stated that before
far-reaching decisions with respect to use mutagenicity data for a selection of
water sources or treatment processes will be made, more information on the
relation mutagenic activity from drinking water and effects on human health
should become available.

Med Hypotheses. 1978 Sep-Oct;4(5):481-96.
Potential health effects of chlorine dioxide as a disinfectant in potable water
supplies.
Moore GS, Calabrese EJ, DiNardi SR, Tuthill RW.
Chlorination of potable water supplies high in organics may yield carcinogenic
compounds such as trihalomethanes. Chlorine dioxide has been proposed as an
alternative disinfectant to chlorine. However, chlorine dioxide is a strong
oxidant that forms significant amounts of chlorite when added to potable water
supplies, and chlorite is similar to nitrite in its molecular structure and may
be similar in its mechanism of methemoglobin production. Nitrites and chlorites
are thought to act synergistically to produce MetHb. Neonates and persons with
G-*-PD deficiency are likely to be unusually susceptible to MetHb formation from
these compounds because their red cells lack the metabolic machinery to
adequately protect against oxidant stress. Since male blacks represent the
largest population in the U.S. to be G-6PD deficient, Black male neonates may
represent the group at highest risk to the use of chlorine dioxide as a
disinfectant in the nations water supplies.

AMA Arch Ind Health. 1957 Aug;16(2):169-76.
Health hazards from chlorine dioxide.
GLOEMME J, LUNDGREN KD.

Toxicol Lett. 1986 Dec;34(2-3):141-7.
Iodination of nutrients in the presence of chlorine based disinfectants used in
drinking water treatment.
Bercz JP, Bawa R.
Under conditions simulating the gastrointestinal tract chlorine dioxide (ClO2),
HOCl, and NH2Cl caused covalent organification of iodide to nutrient
biochemicals. The extent of binding seemed to be proportional to the
electromotive force (EMF) and stoichiometry of the redox couple between iodide
and the oxidant. Almost half of 71 nutrients examined were found to bind reactive
iodine. Iodide was found to inhibit the quinoidal chromogen formation from
tyrosine and ClO2, demonstrating the preferential generation of reactive iodine
in complex organic mixtures. These findings indicate that ingestion of residual
disinfectants via drinking water may pose a health risk in terms of in vivo
generation of iodinated organics. Structure, formation, and biological activity
of these compounds are under study.

On Jun 29, 2021, at 6:58 PM, melissa wrote:
Thanks Dr. Peat. I really really minimize my dental x-rays to the greatest degree possible and take aspirin, progesterone, methylene blue and thyroid right before and right after any x-ray and I carry my portable 250 watt red light in the brooder lamp with me to the dentist and apply it directly after for up to an hour immediately. Unfortunately, almost all dentists, even the biological dentists, cannot seem to work without them. Per the images, i have both an infected root canal, cavitations, and a crown that is improper. It seems the only solution is to extract the root canaled tooth and clean out the cavitations. I know that you think it best not to disturb root canaled teeth but I have been having chronic issues above where it was done for five years now and issues in my both sides of my face for even longer that seem to suggest infection.

On a positive legal note, we are gaining steam with the criminal justice initiative I sent you and will have massive filings in counties all over Colorado presently per connections with large citizen groups here. I am pursuing many opportunities at present, one of which is to step up and file a massive lawsuit in Colorado'; although I am also pursuing opportunities in Texas. I will go wherever I am most needed and the criminal initiative may become a full-time job as well. Also, America's Frontline Doctors has filed a lawsuit pertaining to Covid-recovered plaintiffs. More is happening every day and i truly feel we will have a revolution soon. I heard back from Reiner Fuellmich and he will discuss our criminal initiative and i am trying to arrange to appear on one of his sessions. I continue to work with lawyers all over the country on the civil rights violations with university and employment mandates etc. More to unfold.....

Any thoughts on chlorine dioxide? Seems to me the new rage.
On Tue, Jun 29, 2021 at 7:19 PM Ray Peat <[email protected]> wrote:

A study in Seattle found that pregnant women, with shielding, who had “bite wing” images made (panoramic), had babies that were smaller than normal at birth. There’s good evidence that x-ray scatter from teeth is associated with cancer of brain, eye, tonsils, tongue, and thyroid.

On Jun 28, 2021, at 1:39 PM, melissa wrote:
Hi Dr. Peat. I have been pretty immersed in legal efforts and have some news to report and trying to get my remaining health issues ironed out so that I can be my best when I fight in the world. i am still having issues that seem to be above a root canal and trying to get to bottom of it. I found a biological dentist but she does a lot of x rays per below to properly treat. I know where you stand with dental x-rays but does the below technology and proposal make any difference?


We're so sorry to hear that! We can take the 2D x-rays (FMX) with the protective vest with the thyroid collar tight and in place. However, for the 3D x-ray (CBCT) we can't use the vest or collar, it causes scatter so we wouldn't be able to evaluate from the imaging. The machine for CBCT that we have is the Planmeca Ultra Low Dose and only scans the jaw to the top of the head, it does not interfere with the thyroid or require a vest and/or collar to be worn for protection.

Can we take the CBCT without a vest and collar, but use it for the FMX?

...

 

[Advocate2021]

​	May 17, 2019, 6:09 PM
to Ray

wish they came with remote controls so you could never get near them but you have to be near it to answer it or turn it on or text on it before you can move away. I think we are better off without them.

On Fri, May 17, 2019 at 5:59 PM Ray Peat <[email protected]> wrote:

I don’t get near them.

On May 17, 2019, at 4:52 PM, melissa wrote:
yes I got one but thought the phone is still radiating even if not directly to the head. Do you use a cell phone and think they are OK if used properly? The meter readings are so high with them, just seems eliminating them is best.
On Fri, May 17, 2019 at 5:49 PM Ray Peat <[email protected]> wrote:

There are earpieces that are connected by an air tube, so that the field isn’t transmitted by wire from the phone to your head.

On May 17, 2019, at 4:46 PM, melissa wrote:
thanks. i always keep it on airplane mode but as soon as it must be turned on for calling or texting, feels terrible. if the cases don't work wondering what could be used as an effective shield? Although in order to get it off airplane to use it requires exposure before shielding.
On Fri, May 17, 2019 at 5:36 PM Ray Peat <[email protected]> wrote:

Mine were a calcium compound. If you switch your phone to airplane mode it won’t create the harmful radiation.

On May 16, 2019, at 7:50 PM, melissa wrote:
thanks Dr. Peat. I am going to find a doctor here so I can get blood tests and see where all is at. Almost everyone I speak to here in the health field says root canals are related to ill health, cancer etc. and thinks I should have it removed when i explain my symptoms arise on the same side it was done. Amazing if that whole philosophy arose from complete fallacy.

1-Does it perhaps relate to how the root canal is done and what material is used? What material and method are yours?

2- For the cell phone, you mean only use it for calls and go over to it to answer and then step away and place a shield between myself and the phone? what kind of shield and where would one find such a thing?


On Thu, May 16, 2019 at 1:26 PM Ray Peat <[email protected]> wrote:

I wouldn’t risk sudden exposure to the sun if you haven’t had a blood test for vitamin D, and then it should still be gradually increasing exposure over several days, to watch your response.

The claims I have seen about phone cases just don’t make sense—if it blocks the radiation, the phone can’t work. For use in the house, you could leave your phone in a position that lets it communicate with a tower, and put a shield between it and yourself; in that arrangement, it needn’t be very far away from you.

On May 15, 2019, at 10:17 PM, melissa wrote:
1-Well I have been taking vitamin D for 15 years currently at 3,000 IU's per day for maintenance and cheese and greek yogurt are staples in my diet but I am very fair with freckles. You are saying to try going in the sun with no sunscreen, even at high altitude where I am at in Colorado?

2- do you have any opinion on the cell phone cases being of any value?

On Wed, May 15, 2019 at 11:10 PM Ray Peat <[email protected]> wrote:

I have seen great increases in resistance to sun damage in people who get enough calcium and vitamin D; people who always got severe sunburn in a few minutes can now spend hours in the sun without burning, and with moderate tanning. The light-sensitive substances in the skin don’t undergo the chemical changes that cause the damage, protecting DNA.

On May 15, 2019, at 9:43 PM, melissa wrote:
thanks Dr. Peat.

1- Is there a safer effective sunscreen than zinc oxide now?

2-Also do you think cell phones should be eliminated or do you think there is any validity to using with a protection case such as the below. I have seen a lot of info supporting that these cases are not reliable and can even make matter worse. I am inclined to give up my cell phone completely as it causes symptoms even when used 20 feet away on speaker phone.

Cell Phone EMF Radiation Protection Cases : DefenderShield
On Wed, May 15, 2019 at 5:47 PM Ray Peat <[email protected]> wrote:

Fine particles can sensitize cells to the fields.

On May 15, 2019, at 1:10 PM, melissa wrote:
thanks. another thought I had is wearing zinc oxide as a sunscreen-might this intensify electric sensitivity since zinc is a metal? I noticed a heightened reaction after taking a dose of argentyn silver for a urinary infection--thinking maybe the silver ions were radiated by the wireless exposures?
On Wed, May 15, 2019 at 12:52 PM Ray Peat <[email protected]> wrote:

1. I don’t know of any portable shielding that works.
2. Allergens affecting the intestine are often the source of unexpected sensitivities. Also, too much washing can disturb the skin’s natural metabolism and electrical field.
3. An electrical field can be neutralized by grounding. If the house wiring doesn’t have a ground connection, a wire can be connected to a water pipe for grounding.

On May 15, 2019, at 10:15 AM, melissa wrote:

Resending this as internet was not stable when I sent this last night:

Thanks so much Dr. Peat-- so you do not subscribe to root canals being such a nemesis--it is odd that the one i had is on the left side and I seem to get strange symptoms, including severe facial clicking, on that side. While I continue with thyroid, progesterone pregnenolone, etc, I continue to experience severe hypersensitivity and imbalance. I have been focusing on GI health and have been doing a program by microbiome labs to heal the gi tract which seems to be yielding results despite persistence of the other issues.

I've done all I can at home to address the EMF sensitivity-- no wifi, all wired connections, an emf meter etc, but it has become impossible to avoid EMF's out in the world- they are everywhere.

1-Do you believe that there are any stones/crystals like shungite or orgonite that can help with the sensitivity or do you think this is complete hogwash or or there is anything else one can wear/do that can help since avoidance is not possible outside the home?

2- Have you had any new insights or info come to light regarding extreme and persistent chemical/electrical/toxin hypersensitivity despite addressing the obvious factors (thyroid, hormones, intestinal health, nutrition, etc)? After all of these years, I am truly at a loss as to what I can try next.

3-Also, with wired connections (via a modem) for laptop using a wired keyboard and mouse and keeping laptop far away from body and on airplane mode, the electric radiation measurement via EMF meter on the wired keyboard and mouse increase beyond what they were when using WIFI even though RF is eliminated with the wired set-up. Is there anything more that can be done to minimize the electrical emissions from the wired keyboard and mouse via this configuration? Thanks!!!!!


On Tue, May 14, 2019 at 10:58 PM Ray Peat <[email protected]> wrote:

100 years ago, debilitated people often had infections that would linger for years or decades—osteomyelitis, TB, for example, and when something couldn’t easily be diagnosed, it was popular to blame it on a “focal infection.” That idea has persisted on the fringes of dentistry, which, as a whole, is even less scientific than general medicine. If a tooth root is infected, pus gathers near the base of the root, forming a painful abscess, which can usually be cured with an antibiotic and a change of diet. If the immune system senses continuing infection, the collection of white blood cells will be renewed, and expanding, can eventually cause the tooth to simply fall out. A dead tooth can remain in place for 70 or 80 years, without causing a problem, when the adjoining tissue is healthy, that is, when the person’s general health is such that invading bacteria will be destroyed. The adjoining tissue is the first to react to signs of danger.

On May 14, 2019, at 7:15 PM, melissa wrote:
Hi,I know it has been quite some time since we have corresponded--hope you are well. I remember you mentioning you have gotten root canals and I ended up needing one a little less than three years ago. Since I experienced more issues following same and have now developed extreme electric sensitivity, I am wondering what you think of the below philosophy regarding root canals. I have some other questions to ask you regarding EMF's and new technologies but very curious about this root canal information. thanks!!

How Flavonoids Can Contribute to a Sharp Mind

 

[windinthepines]

[2014]

Me:

If I'm vitamin A deficient enough to get dandruff and acne, could that cause anxiety too?

RP:

Since it's needed to make pregnenolone and progesterone, I think it could.

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

Me:

I'm curious about different types of thought, visual, verbal, etc. When you personally try to remember a person's name, does the name come up automatically, or do you "look" in your mind's eye to see the person's name written somewhere in text?

RP:

When I have known a person for years, their name sometimes becomes
closely associated with their personality, but for me, names of people
usually come up very indirectly, with a cluster of associations. I have,
for a very long time if not always, tried to avoid using the same words
for describing a situation that I have described before, and the same
deliberate separation between language and reality seems to apply to
people's names.

Me:

That's extremely interesting. Recently I started taking some more Cynoplus each day, and noticed a few changes: I felt no anxiety, and my thoughts were different. With more cynoplus (3/4 of a pill, along with the cynomel I was already taking), I had rich visual thoughts, but found that it was harder and took longer to think of a specific person's name, like a scientist, or author, or celebrity, even when I could clearly visualize their face. To think of their name, I would have to first see their face, and then think of something related to them, at which point I might see their name as if it were printed on a page, or below a youtube video. On less thyroid, I can think of names more easily, but I usually can't picture their face. Earlier, I noticed that taking thyroid for me was associated with a move from more verbal to visual thinking in general, but it was never this strong. I couldn't tell if these changes were good or not, because with more cynoplus I also didn't enjoy my favorite music at all, because it just sounded like a bunch of distinct and detailed sounds, and I seemed to fell less happy overall.

RP:

I think that as oxidative energy decreases, and stress hormones including adrenaline rise, thinking tends to become more verbal or symbolic--at noon in a hilly landscape, valleys and peaks are parts of a continuous whole, but at sunset only the peaks are lighted--those are like the words that get their meaning from the whole, but when the (image) valleys are darkened, the (word) peaks seem to have meaning autonomously. One summer as a project for a psychology course I asked people about the way they dreamed. In my dormitory, there was a group of teachers from Nepal, as well as the usual US teachers meeting their certification requirements. There were 2 or 3 people from the upper castes, Brahman and Kshatriya, and two Vaishyas. The Brahmans described colorful and meaningful dreams as regular events, the Kshatriyas said they prayed for them and had them occasionally when they were fortunate; the Vaishya dreams were more like the common Americans' dreams, often in monochrome, not always pleasant. One US teacher said his dreams were like listening to stories, and he didn't seem to understand the idea of colored dreams. I suspect that the effects of social power, and the degree of chronically perceived threat in the background of their life, affect the whole organism so deeply that even the color and texture of consciousness is affected.

Me:

Your dream survey reminded me of the Herman Hesse Book Siddhartha, in which I believe a Brahman becomes enlightened. When I was a teenager I noticed that I had gradually lost my ability to visualize well. When I was in college, I had a period with those verbal dreams; it was like I was listening to a conversation between a few people. Now, I only have a sense of having dreamt. Is it important to remember dreams? William Burroughs wrote about language as an actual virus, and I think Ginsberg had an essay defending pot use, saying that it allowed people to think without language, an effect I don't think I've found myself. I used to work at an upscale grocery store (Whole Foods) with high prices, and saw that most of the shoppers there looked healthier than those at the regular price grocery store. I thought the food was making them healthier, but after a summer of eating most of my meals from their salad bar, my eczema/psoriasis had gotten much worse. Now when I read the labels in Whole Foods, I can't see how most of their products are better than anywhere else, but the people still look better. [...]

RP:

It's the class history of the customers that accounts for their health, how easy life was for their grandparents and parents. Walmart customers are likely to be sick and obese, and the logic of the system requires the company to pay its employees so little that they need food stamps to live. The USDA has diets for the different social classes; doctors in Los Angeles tell Mexican mothers that they should wean their babies to beans when they're six months old.

Me:

As someone increases their thyroid hormone dose, and if adrenalin and cortisol are lowered, could mood also lower? On a lower dose of thyroid, I often feel euphoric, and initially thought that it was because I was getting a higher ratio of T3 to T4.

RP:

If the liver isn't keeping up, T4 can accumulate.

Me:

How would I tell if T4 is accumulating?

RP:

At an extreme, it has an antithyroid effect, slowing metabolism, dulling consciousness.

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

Me:

A 59 year old woman is on an SSRI and a benzodiazapine. She has been having recurring kidney stones over the last few years. Some time ago, the doctors found a non-cancerous mass on one kidney. Then they recently surgically removed a kidney stone from the ureter of the kidney without the mass; in the surgery process they took a biopsy and found early-stage cancer. They are waiting 2 weeks to see take another biopsy, to see if the injury from the stone and removal caused a false positive on the biopsy. I sent her your article on aspirin, and thought maybe taking some until the next biopsy might be helpful. If the biopsy is positive again, they plan to remove the kidney. Is there anything you might recommend for such a situation? Thanks.

RP:

Besides aspirin, Benadryl and progesterone would help to normalize the
tissue.

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

Me:

I had written to you about suggestions for a woman who had cancer in the kidney. I don't know if she used any of the aspirin, benadryl, or progesterone, but the second round of tests showed that there was actually no cancer, just inflammation from the kidney stones, and now they want to focus on preventing the recurring kidney stones. For kidney stone prevention, would it be good to focus on calcium regulation, like getting more calcium in the diet, and taking vitamins K and D? I think the doctors have been recommending increasing water intake, but I can't see how that would help, and the stones haven't abated. Thanks.

RP:

Do you know about her regular diet? Keeping the urine acidic is usually
helpful, and getting her vitamin D around the middle of the range, and
with vitamin B6, is important, preferably with PTH at the low end of the
normal range.

Curr Opin Nephrol Hypertens. 2013 Jul;22(4):383-9.
Vitamin D and kidney stone disease.
Tang J(1), Chonchol MB.
(1)Division of Renal Disease and Hypertension, University of Colorado
School of Medicine, Aurora, Colorado 80045, USA.
PURPOSE OF REVIEW: Vitamin D is important in maintaining calcium
homeostasis, but its role in kidney stone disease and its effect on stone formation are
still not clear.
RECENT FINDINGS: Kidney stone formers tend to experience enhanced intestinal
calcium absorption, increased urinary calcium excretion, and excessive bone
mineral loss. Although direct actions of active vitamin D have been
implicated in
all these processes, the effect of nutritional vitamin D (vitamin D2 or
vitamin
D3) use on calcium balance among stone formers is still not clear. In
addition, the safety of nutritional vitamin D use in the stone forming population
is also not established, considering the potential effect of its use on raising
urinary calcium. However, most of the observational studies do not support a
significant association between higher nutritional vitamin D store and increased risk of
stone formation. Short-term nutritional vitamin D repletion in stone
formers with vitamin D deficiency also does not appear to increase urinary calcium
excretion.
SUMMARY: The effect of nutritional vitamin D use in stone formers is
still not
clear. As vitamin D deficiency is highly prevalent among stone formers,
future
prospective studies are needed to establish the biological effect, as
well as the
safety and efficacy of nutritional vitamin D therapy in this unique patient
population.

Nephron Clin Pract. 2012;122(3-4):134-8.
Vitamin D status in patients with recurrent kidney stones.
Pipili C(1), Oreopoulos DG.
(1)Kidney Stone Clinic, University Health Network, Toronto, Ont., Canada.
[email protected]
Comment in
J Urol. 2014 Mar;191(3):679.
Data regarding the prevalence of 25-hydroxyvitamin D (25(OH)D)
insufficiency in patients with nephrolithiasis, and the effects of vitamin D
supplementation on parathyroid hormone (PTH) are few and conflicting. In this article, we
examined the prevalence of vitamin D insufficiency and deficiency in 236
recurrent kidney stone formers and the correlation of vitamin D levels with other
parameters of stone formation. The prevalent stone composition was calcium oxalate
(80.4%) and uric acid (16.45%). One third of stone formers had vitamin D
insufficiency and a
quarter of them high PTH levels (PTH >7.5 pmol/l) with normal serum
(total and
ionized) calcium values. Predictor of high PTH was low 25(OH)D level (r
= 0.989, r(2) = 0.977, p < 0.001). Stone formers with hypercalciuria had higher
25(OH)D
values (72.26 ± 4.21 vs. 59.29 ± 1.76, p = 0.0013) compared to stone
formers with
urine calcium within normal ranges. Further studies are needed in order
to better
define the consequences of vitamin D insufficiency and to evaluate the
impact of
the therapeutic interventions in this cohort.
Copyright © 2013 S. Karger AG, Basel.

Clin Nephrol. 2012 May;77(5):352-7.
Normocalcemic hyperparathyroidism in patients with recurrent kidney
stones: a
disease entity or vitamin D deficiency?
Pipili C(1), Sekecioglu N, Oreopoulos DG.
(1)Kidney Stone Clinic, Toronto Western Hospital, Division of
Nephrology, University Health Network and University of Toronto, Toronto, Canada.
[email protected]
This retrospective data analysis was undertaken to examine the biochemical
differences between renal stone formers with normocalcemic
hyperparathyroidism
(NHPT) and those with normal parathyroid hormone (PTH) levels. Our goal
was to ascertain whether 25-hydroxyvitamin D (25(OH)D) status related to PTH
levels in this patient cohort. Our findings among 74 patients with NHPT indicate
that stone formers with NHPT had significantly lower 25(OH)D levels compared to 192
controls (p = 0.0001) and that 25(OH)D is positively correlated with
1,25-dihydroxyvitamin
D values (R = 0.736, p = 0.015). Sequential measurements (after 3 - 5
years), among 11 patients with NHPT who did not receive vitamin D (VitD)
preparations,
showed a significant increase in urinary calcium (3.43 ± 1.96 vs. 5.72 ±
3.95, p = 0.0426) without a significant change in PTH levels. VitD
supplementation, to 3 patients resulted in significant PTH decrease (11.8 ± 1.8 vs. 9.8 ± 1.3, p =
0.003). Prospective studies are needed to confirm the role of vitamin
supplementation in renal stone formers with NHPT.

Me:

Thanks, I will tell her about vitamin D, and show her those studies. For her diet, I think she generally has a low appetite, but has a little yogurt, some cereal, regular US lunch sandwiches, and maybe some meat and potatoes, with wine. How would she keep the urine acidic?

RP:

I think stopping the cereal and sandwiches, replacing them with milk, eggs, cheese, and some sea food, liver, etc., would be helpful, but she's probably hypothyroid, and is likely to have alkaline urine unless her metabolic rate and appetite increase. Do you know whether her creatinine was high, GFR low?

 

[windinthepines]

[2014]

Me:

Do you think the electric universe theory and thunderbolts.info is on the right track? Does it mean anything for us on the personal biological level?

RP:

I think it's right. The same simple application of realistic physics that led to that view of cosmology has biological implications, e.g., R.O. Becker, Yuri Holodov, Solco Tromp, Madeleine Barnothy, Michele Gauquelin, et al.

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

Me:

Hi, Because you've written very interesting things about languages, I thought I might ask you your thoughts on learning a foreign language, and about continuing to learn one after many common words are already known. For example, how did you learn to read French after you had memorized many common words. Did you just continue to read, gradually gaining understanding?

I came across a linguist named Stephen Krashen, who has what he calls his 'input hypothesis.' In some ways, he seems like an antidote to Chomsky's grammar ideas. For example, he says that it's possible to learn languages after adolescence. Krashen says that you can learn a language just by exposure, by reading or listening, and that gradually you'll understand, and eventually produce correct speech of your own. There are a lot of examples on the web of people using his ideas. For example, a US man listened constantly to Japanese on his headphones for one year, and then moved to Japan and was able to work and communicate.

I found a method online that is an extreme extrapolation of Krashen's ideas. The gist of it is that you listen to an audiobook in your unknown language, while simultaneously reading the same book in print in your known language. The idea is to make the 'input' as 'comprehensible' as possible. When I tried it, it seems to be more effective the more hours a day I do it, and the creator claimed that this was due to the memory curve, and that it is best to do it for as many hours as possible for as many days as possible.

I was wondering if you see associating one language with another as useful, considering what you've said about images being behind the words, although despite the method I'm using I don't actually feel as if I'm associating the two languages with one another. I'm trying to understand how the new language is being learned, and how the memories are forming. I'm also trying to notice whether my current metabolic state (high adrenaline, whether I'm thinking more in pictures or words, what my dreams are like) has anything to do with the learning process.

RP:

As kids, we hear language spoken in situations that we understand. For a
new language, listening to the telling of a familiar story has the same
function. It could be listening to a standard fairy tale, or listening
to the day's news in the new language after learning about the situation
in the old language. When I started reading French, I found that there
were enough familiar cognate words to reveal most of the meaning, and
that, reading very quickly, the context would reveal the meaning of some
of the unfamiliar words; some of the grammatical words were functioning
in reading before I was able to define them when I saw them separately.
With Russian, I started with publications in science journals, and the
large number of cognates in those had the same function, making the
meaning of a paragraph clear before I knew all the individual words
independently.

Me:

That's interesting. Reading and listening is mostly what I'm doing, but while I can understand some conversations, I can't talk much. Did you learn French after Spanish--were the French words cognates to English, Spanish, or both? I'm in Mexico City, where I've met some French people who seem to speak Spanish easily. I was studying audiobooks before I came here, but they were from Spain, and when I got here I found I understood almost nothing at all here with the different accent.

RP:

When I first went to Mexico I hadn't studied Spanish, but I first learned a few phrases for getting around, and would listen to people at the boarding house at supper. After I had learned some Spanish, I saw that the grammar was similar to French, and because I had a good English vocabulary from reading, I saw that the French vocabulary was very close to English--modern English was the result of the French invasion. Although I've never had an opportunity to speak French (when I visited in Paris, it was immediately after the student rebellion, and it wasn't a friendly atmosphere) it's probably easier for me to read than Spanish, because there are so many regional variations in Spanish.

 

[dannyroddy]

Some of these are my questions to him, and some aren't.

[LATEX BEDS SAFE?]

"Some people are allergic to it, but it can make a very good foam mattress. In recent years, most of the latex mattresses are designed to be stiff and firm, but that isn’t intrinsic to the latex." — RP (2021)

[IS A FIRM MATTRESS DESIRABLE?]

"Common bed spring technology in the 19th century resulted in a hammock-like sag as the springs aged. The inner-spring mattress people showed how much better it was if the bed didn’t sag in the middle, and for about a generation Simmons and other companies made very soft innerspring mattresses that allowed the hips and shoulder to sink, letting the back stay straight.

The idea of mattress firmness blended with ideas of duty, toughness, exercise, and health, until the most expensive mattresses felt like a futon on concrete." — RP (2021)

[THE PURPOSE OF THE VDR?]

"I think the VDR and 1,25-OH are very analogous to the estrogen system. Rodents are supposedly more sensitive to vitamin D than people, but the standard rat poison concentration in human food would probably eventually kill some people." — RP (2021)

[DOES ALLEN DULLES' INVOLVEMENT WITH THE PROTOCOLS OF THE ELDERS OF ZION PROVE THAT IT IS AUTHENTIC?]

"Wikipedia emphasizes the plagiarism in the Protocols, from fictional works, but neither plagiarism nor forgery affects its importance. A novelist who said things like that in the 1860s was obviously onto something, since there are prominant people now in Israel who are saying similar, and worse, things. People who just speak honestly about what they observe are called prophets---it can take others a very long time to recognize that such things happen." — RP (2021)

["RELATIONSHIP" WITH ANALOG MACHINES?]

"Yes, that’s the property that makes it possible for us to relate to them in a natural way. Norbert Wiener wrote about it." — RP (2021)

[DOCTOR RECOMMENDS PROSTATECTOMY]

"The language “intermediate probability for malignancy” and equivocal presence of clinically significant cancer, means that they haven’t understood the concept of “watchful waiting” that was responsible for reducing mortality from prostate cancer in the late 1990s.

What they prescribe tamsulosin for is probably usually just weakness of the bladder contraction muscle, the detrusor, that’s common with overweight and low testosterone. His TSH is likely to be high, a supplement of thyroid and vitamin D would probably help." — RP (2021)

[MEANING OF EMPATHIC REACTION TO SELF-DESTRUCTIVE NPC?]

"I think it’s kind of a political judgment—if you want to optimize your efforts, supporting the efforts of others to do good things, and defending yourself against the energy-consuming processes of destructive people, is more effective than focussing on the suppression of evil." — RP (2021)

[BITCOIN]

"When you mine gold, you have something that exists separately from what anyone might think about it. Bank lending counts ownership of debt as assests, if the debtors fail, the system fails, but at least some real value is there, as something mortgaged; it isn’t all pure fiat money. Bitcoin mining is a way of creating belief, nothing more." — RP (2021)

 

[Roni123@]

Ray about atraction and high carb

 

[windinthepines]

[2014]

Me:

[A woman has a stress reaction when taking thyroid. Took iodine in the past.]

Peat:

Overdoses of iodine can damage the thyroid, but other things in her diet
might be a problem. Being in Mexico City, she might benefit from lots of
good orange juice.

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

[2015]

Me:

I've been interested in methylene blue since your newsletter and KMUD interview. Do you think the purity of some methylene blue could be a problem? I bought some that is used for fish and aquariums. I have read online that a lot of methylene blue is contaminated with heavy metals, but I don't know what to think, because the people making these claims were trying to sell their own methylene blue, which they claimed was free of heavy metals.

Peat:

I suspect it all might be made at the same factory, but I haven't seen
the analysis. The seller could tell you the metal content.

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

Me:

It's probably too early to really tell, but for the few weeks I've been taking methylene blue, I haven't had my normal insomnia ("circadian rhythm disorder"). I've been looking for information on nitric oxide and insomnia but haven't found anything good. My digestion is also better. Is there some reason methylene blue might help insomnia?

Peat:

Yes, it restores mitochondrial energy production, and lowers nitric
oxide. High nitric oxide seems to be involved in insomnia

How much of it are you taking? Are you buying a prepared solution?

Me:

My dose is about 15mg a day in the morning. Is that a good dose? I saw that some studies were using higher amounts. I bought a 2.3% solution sold for fish, but I might eventually look for another source because the company won't send me any type of analysis. I've had a couple things fix my insomnia for a few weeks, only to have the problem return, so I'll have to wait and see. One of the things that worked temporarily for my insomnia in the past was bromocriptine, and I had been wondering whether there was some connection between the growth hormone I had used years before and the insomnia, and now I'm wondering if there's a relationship for me between growth hormone (or prolactin), nitric oxide, and insomnia, but I don't know enough to really figure it out.

Peat:

I think the amount needed might decrease with time; I know someone who's getting very good results with one mg. per day.

Hypothyroidism is likely to be behind the insomnia, high prolactin, and inappropriate nitric oxide.

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

Me:

Do you think people can feel spacey and sleepy when increasing a thyroid supplement dose, if the thyroid is lowering stress hormones and the pulse is decreasing?

Peat:

Yes, it sometimes does that during the first week or two of using it.

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

Me:

Hi, do you know what kind of things would cause someone to have trouble reading facial expressions? Thanks.

Peat:

That can happen after a person has a stroke in a certain area, but I think there’s a great natural variation, some of it a matter of character and attitude.

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

Me:

Hi, I was wondering what it could mean that my pulse is 92 when sitting, but immediately rises to 120 when I get up and walk around just a little. Thanks.

Peat

That’s fairly common, slightly low blood sugar, or slightly high thyroid, can cause it.

Me:

So the pulse should stay around 90 when walking? Also, should your pulse go above 90 after coffee, or does coffee bring your pulse to 90?

Peat:

No, it’s normal for the pulse to be faster when you move. With fast walking, mine’s usually 130 or more.

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

Me:

I was wondering if you ever give classes, seminars, or anything like that.

Peat:

Not very often, but occasionally.

 

[windinthepines]

[2015]

[Amount of DHT safe for men]

I think it would be in the range of one or two milligrams per day.

[Woman with hypothyroid symptoms but good diet and reaction to bad thyroid supplements]

Has she used pregnenolone or progesterone for the depression? Extremely hypothyroid people, with high stress hormones, often feel anxiety with small increases of T3, but that can be overcome using food and the stabilizing supplements. A selenium deficiency is sometimes involved in hypothyroidism, so she should have sea food (low fat, no salmon) regularly. Low fat cheese, and at least one egg per day, for a total of 100 grams of protein/day, will often correct a thyroid problem. Well cooked white button mushrooms are a good alternative to potatoes.

[Follow-up info provided]

Things that reduce stress should be used at the same time as the T3. Sugar and aspirin, sometimes Periactin, can reduce the stress hormones. T4 is probably preferred by most doctors because it doesn’t have those immediate effects, and she might find that that’s easier (although it takes weeks to adjust to the right dose). The problem is that it has to be metabolized to work, and depressed women often have so much adrenalin, cortisol, and serotonin circulating that the liver changes it to reverse T3.

[Cynoplus not available. Alternatives?]

ERFA seems to work, and in Mexico Proloid-S and Novotiral are still available—but if people in the US start buying enough of those to affect the US industry I expect them to disappear too.

[Proloid-S availability]

I haven’t seen it online, but a friend in a small town says it’s in the local store.

[How long synethetic thyroid lasts]

I have some Cytomel that’s 25 years old, and some Cynomel that’s 17 years old, and they still work.

[Do you keep them in the refrigerator?]

No.

 

[windinthepines]

[2015]

[Hypothyroid woman can't tolerate very small amounts of thyroid supplement]

Do you know what form of magnesium she uses? Does she drink any milk or orange juice? Has her vitamin D ever been measured? Has she occasionally checked her waking and midday temperature and pulse rate?

[Other ideas?]

Has she tried bag breathing? How much calcium does she average? Did she try 1 mcg doses of Cytomel? What happened with beta blockers, pregnenolone, progesterone? Did she see temperature increase with progesterone? Cyproheptadine and acetazolamide can calm over-excitable nerves.

[Hunger and blood sugar. Why always hungry?]

Hypothyroid people waste glucose by failing to oxidize it completely, and that typically causes fluctuations of blood glucose and increased appetite. Keeping glucose stable with the right amount of thyroid prevents inappropriate hunger. A supplement of pantothenic acid sometimes helps, with oxidation and prevention of hyperinsulinemia.

[Could a low vitamin D level lead to a bad response to thyroid supplementation?]

I’ve known of other deficiencies causing a poor response to thyroid, that seems possible. Were there changes in her pulse rate or temperature?

[Boil leaves for calcium, magnesium, and protein instead of drinking milk?]

The leaf water is good for magnesium and calcium, but has very little protein. About 3 cups of greens would provide enough of the minerals. If you don’t eat the leaves, it takes more, since not all the calcium is released into the water. Do you eat cheese?

[Using beta blockers to tolerate small amounts of thyroid?]

I think it’s best for anxious people to use the anxiety to motivate a thorough study of the issues. Hypoglycemia can be a factor in anxiety, and when low thyroid and high estrogen are involved, a beta blocker has the possibility of lowering blood sugar.

 

[des yeux]

Last email from Ray, Oct 17 2022:

Me: [Where do you think Reich went wrong in his thinking? Do you think his Contact with Space was full of errors where he mistook cause for effect? What about Puharich, where did he wrong? Was it related to his work with Uri Geller and Arigo the surgeon of the rusty knife?]

Ray: Even people with good insights can get confused in. the complexity, and in trying to promote their special views.

 

[windinthepines]

[2015]

[Woman can't tolerate thyroid supplement]

Has she had blood tests? Sometimes extremely low cholesterol slows adaptation to normal thyroid. Has she tried other brands? Are her hands and feet usually cold?

[Woman can't tolerate thyroid supplement]

More calcium and vitamin D might help—calcium has a sedative, stabilizing effect.

Vitamin D3 Cured my Anxiety, Depression, and Panic Disorder ...

anxietyforum.net › Forum › Mood Disorders › Depression Forum
Sep 2, 2012 - 10 posts - ‎7 authors
Hello: I suffered from depression, anxiety, and panic disorder for a few decades. ... "Unfortunately, This exciting new knowledge about vitamin D hasn't reached ... Calcium is a mineral that you need, while taking vitamin D3.
Anxiety and Vitamin D deficiency - Anxiety Forum

anxietyforum.net › Forum › Community Board › News
Jan 6, 2013 - 10 posts - ‎4 authors
I was recently diagnosed with vitamin D deficiency. ... Due to Vitamin D3 deficiency, I had anxiety, depression, and panic disorder for a long ...
Could Vitamin D Deficiency Cause Anxiety and Panic Attacks

www.easy-immune-health.com/could-vitamin-d-deficiency-cause-anxiet...
(Texas). Anxiety and Panic Attacks- Vitamin D Deficiency Symptoms? ..... I take 10,000 IU Vitamin D3 and 1200 IU of Calcium that I buy at Walmart. I also use a ...
Decreased vitamin D levels linked to panic, depression ...

www.lifeextension.com/newsletter/2013/2/...vitamin-d...panic.../page-01
Feb 12, 2013 - Decreased vitamin D levels linked to panic, depression ... reduced vitamin D levels and an increased risk of panic disorder and depression.

[Anxiety]

Large amounts of calcium have a sedative, anti-inflammatory effect, and the casein and other nutrients have anti-stress actions. Inflammation increases parathyroid hormone, and a large intake of calcium is a safe way to lower that.

[2016]

[Stopping thyroid supplement in hot season]

Yes, I think it’s better to become hypothyroid during the high temperature.

[Thyroid brands]

I tried some T3-Pro and it seemed o.k., and Novotiral can be helpful, despite its lower T3 content.

[Can't breath out of alternating nostrils]

I think the alternation argues against infection; reflexes from different parts of the intestine can cause very focused inflammation in different places.

[Alcohol as antioxidant]

I think about that much, a few milliliters, can have an antioxidant effect. Years ago I was having dinner at a friend’s house and ate something that I’m normally extremely allergic to, but I had some tequila with the meal, and had no reaction at all. That was what led me to investigate the antioxidant effect.

 

[windinthepines]

[2016]

[Possible Cushing's disease]

Has she tried progesterone or pregnenolone? I think pituitary surgery for Cushing’s has been obsolete for 30 years. Both progesterone and pregnenolone make thyroid easier to use, while lowering ACTH. Aspirin, cabergoline, bromocriptine, and cyproheptadine all lower ACTH.

1. Expert Opin Emerg Drugs. 2009 Dec;14(4):661-71.
Drugs in the medical treatment of Cushing's syndrome.
Schteingart DE(1).
Author information:
(1)Department of Internal Medicine, University of Michigan, Ann Arbor, MI, 48109,
USA. [email protected]
Cushing's syndrome is a complex endocrine condition with potential serious
complications if untreated or inadequately treated. Transsphenoidal surgery with
resection of a pituitary adenoma is successful in 75 - 80% of patients, but
approximately 20 - 25% show persistence of Cushing's, and a similar proportion
may experience recurrence within 2 - 4 years post-op. When surgery fails, medical
treatment can temporarily suppress excessive cortisol production and ameliorate
its clinical manifestations while more definitive therapy becomes effective. We
describe pharmacological approaches to the treatment of Cushing's syndrome. Drugs
used to suppress cortisol secretion are mostly inhibitors of steroidogenesis.
Ketoconazole, fluconazole aminoglutethimide, metyrapone, mitotane and etomidate
are in that category. Ketoconazole is in current use while other drugs, although
mostly available in the past, continue to have a potential role either alone or
in combination. Drugs that suppress adrenocorticotropic hormone (ACTH) secretion
are less popular as standard treatment and include cyproheptadine, valproic acid,
cabergoline, somatostatin analogs, PPAR-gamma agonists, vasopressin antagonists.
Some of these drugs have been tested in limited clinical trials but there is
potential therapeutic benefit in analogs with better specificity for the class of
receptors present in ACTH-secreting tumors. A third category of drugs is
glucocorticoid receptor antagonists. Mifepristone is currently being tested in
clinical trials in patients with persistent or recurrent Cushing's disease and in
patients with metastatic adrenal cortical carcinoma or ectopic ACTH syndrome not
amenable to surgery. We also review replacement therapy after surgery and
non-specific drugs to treat complications in patients with severe hypercortisol.
The review provides a complete survey of the drugs used in the medical treatment
of Cushing's, and new advances in the development of pituitary-active drugs as
well as receptor blockers of glucocorticoid action. It also provides avenues for
exploration of new drugs active on somatostatin, dopamine and vasopressin
receptors. There are effective pharmacological agents capable of chronically
reversing biochemical and clinical manifestations of hypercortisolemia in
Cushing's syndrome but new drugs are needed with action at the pituitary level.



2. J Endocrinol Invest. 1996 Apr;19(4):242-7.
Cyproheptadine treatment in Cushing's disease.
Tanakol R(1), Alagöl F, Azizlerli H, Sandalci O, Terzioğlu T, Berker F.
Author information:
(1)University of Istanbul, Istanbul Faculty of Medicine, Department of Medicine,
Turkey.
Cyproheptadine, a nonselective 5-hydroxytryptamine receptor blocking agent,
reduces ACTH and beta-endorphin secretion from the ACTH-producing tumors. A
35-year-old female suffering from Cushing's disease due to microadenoma of the
pituitary gland has been followed since the age of 15. Subtotal adrenalectomy
followed by total adrenalectomy, pituitary irradiation, and transsphenoidal
hypophysectomy, combined with second radiotherapy of the pituitary, were
unsuccessful in achieving remission of the disease. Remission was achieved with
cyproheptadine up to a dosage of 24 mg/day. Every attempt to discontinue
cyproheptadine treatment was accompanied by recurrence of the disease. This is
the first case of Cushing's disease in which cyproheptadine treatment has been
the only efficacious therapy for a period of 11 yr. Cyproheptadine may be an
alternative long-term therapy for Cushing's disease when other methods of
treatment fail.


3. Nihon Naika Gakkai Zasshi. 1994 Sep 10;83(9):1627-32.
[Non-invasive therapy of Cushing's syndrome].
[Article in Japanese]
Miura K.




4. J Clin Endocrinol Metab. 1996 Feb;81(2):652-5.
Cortisol secretory patterns in Cushing's disease and response to cyproheptadine
treatment.
van Waveren Hogervorst CO(1), Koppeschaar HP, Zelissen PM, Lips CJ, Garcia BM.
(1)Department of Endocrinology, University Hospital, Utrecht, The Netherlands.
To investigate whether cortisol secretory patterns are associated with a response
to cyproheptadine treatment in Cushing's disease, we studied two patients with a
hyperpulsatile pattern and one patient with a hypopulsatile pattern before and
during chronic cyproheptadine therapy (24 mg daily). In the two patients with a
hyperpulsatile cortisol secretory pattern, pituitary magnetic resonance imaging
with gadolinium did not reveal a pituitary adenoma, whereas in the patient with a
hypopulsatile cortisol secretory pattern, a microadenoma was identified. Plasma
cortisol levels were measured every 30 min for 24 h. In the two patients with a
hyperpulsatile cortisol secretory pattern, chronic treatment with cyproheptadine
resulted in sustained clinical and biochemical improvement and normalization of
the median of absolute and relative increments in cortisol spikes. In the patient
with a hypopulsatile cortisol secretory pattern, only a reduction of cortisol
spikes was noticed during treatment. These results suggest that patients with
Cushing's disease who are characterized by a hyperpulsatile cortisol secretory
pattern and in whom no pituitary lesion can be identified by magnetic resonance
imaging, cyproheptadine treatment may be useful.


5. G Ital Cardiol. 1994 May;24(5):533-8.
[Arterial hypertension in Cushing's disease: the 24-hour pressure profile without
and during treatment with beta-blockers or cyproheptadine].
[Article in Italian]
Prattichizzo FA(1).

Author information:
(1)I Unità Operativa Medicina Generale, Ospedale Degli Infermi di San Miniato,
PI.

Studying a patient with Cushing's disease by 24-hour indirect blood pressure
monitoring, we confirmed that the normal nocturnal fall in blood pressure was
absent, although the usual decrease in heart rate persisted. Thereafter we found
a hypervariability in blood pressure and heart rate, which was reversed by
treatment with betablockers and/or cyproheptadine. The therapy restored also the
normal nocturnal fall in blood pressure. The low-dose cyproheptadine therapy
normalized urinary free cortisol levels and restored a 24-hour blood pressure
profile better than the low-dose beta-blocker therapy.




6. Rev Clin Esp. 1991 Jan;188(1):37-40.

[Clinical remission in Cushing's disease through treatment with sodium valproate
and bromocriptine].

[Article in Spanish]

García Rojas JF(1), Mangas Rojas A, Barba Chacón A, García Osle M, Zamora Madaria
E.

Author information:
(1)Departamento de Medicina Interna, Universidad de Cádiz.

A patient suffering Cushing disease is presented in whom the administration of
ciproheptadine, bromocriptine and sodium valproate in a single dose did not
manage to control the clinical-biologic manifestations of the process. Combined
treatment with 1.200 mg/day of sodium valproate and 15 mg/day of bromocriptine
induced a complete clinical-biological remission, being arterial pressure the
last parameter to normalize. The patient who has always refused to undergo
surgery has stayed with this treatment for three years, maintaining remission and
without appearance of side effects. On two occasions (after one and a half years
and after two and half years) the transitory interruption of treatment induced in
a few weeks an increase in plasma cortisol levels which again normalized after
treatment was re-established. There were no clinical-biological data,
pharmacological tests which permitted the prediction of these therapeutic results
and therefore, the therapeutic response obtained is not indicative of any
specific etiological subtype of Cushing disease.




7. Neuroendocrinology. 2010;92 Suppl 1:44-9. doi: 10.1159/000314315. Epub 2010 Sep
10.

Hypertension in Cushing's syndrome: from pathogenesis to treatment.

Cicala MV(1), Mantero F.

Author information:
(1)Division of Endocrinology, University of Padua, Padua, Italy.

Hypertension is one of the most distinguishing features of endogenous Cushing's
syndrome (CS), as it is present in about 80% of adult patients whereas in
children its prevalence is about 47%. Hypertension in CS is significantly
correlated with the duration of hypercortisolism and results from the interplay
between several pathophysiological mechanisms regulating plasma volume,
peripheral vascular resistance and cardiac output, all of which are increased in
this state. Glucocorticoids cause hypertension through several mechanisms: their
intrinsic mineralocorticoid activity; through activation of the renin-angiotensin
system; by enhancement of vasoactive substances, and by causing suppression of
the vasodilatory systems. In addition, glucocorticoids may exert some
hypertensive effects on cardiovascular regulation through the CNS via both
glucocorticoid and mineralocorticoid receptors. Hypertension in CS usually
resolves with surgical removal of the tumor, but some patients require
pharmacological antihypertensive treatment both pre- and postoperatively.
Thiazides and furosemide should be avoided, while adrenergic blockade and calcium
channel antagonists are usually ineffective. Mineralocorticoid receptor
antagonists, Ang II blockers and ACE inhibitors are good anti-hypertensive
options; PPAR-γ agonists may help in many aspects of the insulin resistance
syndrome. The relatively selective glucocorticoid receptor antagonist
Mifepristone (RU 486) could reduce blood pressure in patients with CS.
Neuromodulatory agents such as the serotonin inhibitors cyproheptadine and
ritanserin, valproid acid, dopamine agonists, somatostatin analogs may
occasionally be effective, as well as drugs acting directly at the adrenal
levels, such as Ketoconazole and aminoglutetimide or even opDDD. Treating
hypertension in CS remains a difficult task and a big challenge, in order to
decrease the morbidity and mortality associated with the disease.
Copyright © 2010 S. Karger AG, Basel.


8. J Endocrinol Invest. 2006 Apr;29(4):358-62.

Long-term quiescence of ectopic Cushing's syndrome caused by pulmonary
neuroendocrine tumor (typical carcinoid) and tumorlets: spontaneous remission or
therapeutic effect of bromocriptine?

Francia G(1), Davì MV, Montresor E, Colato C, Ferdeghini M, Lo Cascio V.

Author information:
(1)Biomedical and Surgery Science Department, University of Verona, 37134 Verona,
Italy. [email protected]

In 1990, a 55-yr-old woman was admitted to the Medical Department of our hospital
for severe hypercortisolism complicated by secondary diabetes mellitus and
serious hypokalemia. Although inferior petrosal sinus sampling did not show any
significant difference between central and peripheral ACTH concentration,
suggesting an ectopic source of ACTH secretion, diagnostic imaging was negative
and Cushing's disease due to hyperplasia of the pituitary intermediate lobe was
suspected. Medical treatment with bromocriptine and cyproheptadine led to a rapid
and stabile normalization of adrenal function, so that after two months
cyproheptadine was stopped and bromocriptine was tapered to a smaller dose. An
attempt to discontinue medical treatment, carried out 3 yr later, was followed by
a quick increase of ACTH and cortisol levels, which were normalized by the
resumption of the bromocriptine. Adrenal function remained normal until 1994 when
hypercortisolism relapsed despite the treatment. Chest radiography and computed
tomography (CT) scan detected a 6 mm nodule in the middle lobe of the lung which
proved to be a neuroendocrine tumor, with immunohistochemical positivity for
ACTH. Nests of neuroendocrine cells (tumorlets) were also demonstrated in the
surrounding lung tissue. After the lobectomy, the patient recovered completely
from Cushing's syndrome and no symptoms and/or signs of recurrence have been
observed over the subsequent follow-up period. Although cyclical spontaneous
Cushing's syndrome could not be excluded, there was strong evidence that medical
treatment with bromocriptine might have played a key role in long-lasting
remission. To our knowledge, this is the second case described in literature of
Cushing's syndrome caused by neuroendocrine lung tumor responsive to
bromocriptine.



9. Prog Neuropsychopharmacol Biol Psychiatry. 2002 May;26(4):763-70.
Residual symptoms in depression an emerging therapeutic concept.
Sonino N(1), Fava GA.

Author information:
(1)Department of Medical and Surgical Sciences, Division of Endocrinology,
University of Padova, Italy. [email protected]

Corrected and republished in
Prog Neuropsychopharmacol Biol Psychiatry. 2002 Jun;26(5):1011-8.

Cushing's syndrome is due to chronic glucocorticoid excess that may have various
etiologies. The most common endogenous form is pituitary-dependent bilateral
adrenal hyperplasia, which is termed Cushing's disease. Major depression occurs
in more than half of the cases. The presence of depressive symptoms connotes
severity of clinical presentation and, in patients with hypothalamic-pituitary
forms, entails prognostic value. Medical treatment may be used while awaiting
more definitive solutions for the illness by surgery. The inhibitors of steroid
production (e.g., ketoconazole, metyrapone and aminoglutethimide), rather than
antidepressant drugs, are generally successful in lifting depression as well as
other disabling symptoms. Since central serotonergic regulation could have a role
in the course of Cushing's disease, serotonin antagonists (e.g., cyproheptadine,
ritanserin and ketanserin) have been employed. Findings related to the
pharmacological response of depression in Cushing's disease were found to have
implications for the pathophysiology of depression and the potential involvement
of the hypothalamic-pituitary-adrenal axis (HPA axis) in resistance and tolerance
to antidepressant drugs. The use of serotonergic drugs in Cushing's disease may
yield important insights in the understanding of serotonergic regulation both in
Cushing's disease and in the HPA axis in nonendocrine major depression.




10. Clin Endocrinol (Oxf). 1990 Feb;32(2):193-201.

The effect of cyproheptadine and/or bromocriptine on plasma ACTH levels in
patients cured of Cushing's disease by bilateral adrenalectomy.

Whitehead HM(1), Beacom R, Sheridan B, Atkinson AB.

Author information:
(1)Sir George E. Clark Metabolic Unit, Royal Victoria Hospital, Belfast, UK.

Cyproheptadine and bromocriptine have been reported to be therapeutic in
suppressing ACTH levels in Cushing's disease and Nelson's syndrome. However,
there have been only scattered reports of their effect in suppressing raised ACTH
levels found in patients cured of Cushing's disease by bilateral adrenalectomy.
In order to assess whether these agents could prove beneficial in such patients
we studied 12 patients previously treated with bilateral adrenalectomy alone for
Cushing's disease before and after 3 weeks of cyproheptadine and/or bromocroptine
therapy. All had raised plasma ACTH values but no patient had evidence of a
pituitary macroadenoma. Plasma ACTH and cortisol were sampled 2-hourly for 24 h.
Neither drug regime led to any change in plasma levels of cortisol for 24 h after
a 20 mg dose of oral hydrocortisone. Plasma ACTH (mean +/- SEM) showed a small
but significant overall reduction (523 +/- 45 vs 392 +/- 34 ng/l; P less than
0.05) while on bromocriptine alone (5 mg given at 0800 and 1800 h, n = 5). When
each time point was analysed individually this reduction was significant at only
five out of 13 time points. At 0400 h plasma ACTH (mean +/- SEM) was 758.4 +/-
298.1 vs 380.2 +/- 166.6; 0600 h, 795 +/- 288.7 vs 477.8 +/- 191.7; 1200 h, 266.8
+/- 106.2 vs 187.0 +/- 80.3; 1400 h, 470.0 +/- 239.0 vs 302.0 +/- 135.9; 1600 h,
548.6 +/- 262.5 vs 394.2 +/- 178.5 ng/l (P less than 0.05). There was no
significant change in plasma ACTH during treatment with the combination of
bromocriptine and cyproheptadine.(ABSTRACT TRUNCATED AT 250 WORDS)



11. Minerva Endocrinol. 1990 Jan-Mar;15(1):17-21.

[Medical treatment of Cushing syndrome].

[Article in Italian]

Mantero F(1), Sonino N.

Author information:
(1)Istituto di Semeiotica Medica, Università di Padova.

Cushing's syndrome is a serious endocrine condition for which no treatment has
been proven fully satisfactory at least for its pituitary dependent form
(Cushing's disease). Indeed, despite some advances in pharmacology
(cyproheptadine, bromocriptine, lisuride) and in surgical and radiation
procedures at pituitary level, a definitive cure is often delayed. The inhibitors
of steroids synthesis (ketoconazole, aminoglutethimide, metyrapone, mitotane) are
still very valuable tools in its management as a palliative treatment.




12. Endocrinol Metab Clin North Am. 1989 Jun;18(2):311-38.

Cushing's syndrome.

Schteingart DE(1).

Author information:
(1)Division of Endocrinology and Metabolism, University of Michigan Medical
School, Ann Arbor.

The clinical characteristics and current concepts of pathophysiology of Cushing's
syndrome have been reviewed. The specific type of pituitary or ectopic
ACTH-dependent and ACTH-independent Cushing's syndrome and the underlying
pathology can be determined biochemically and with the aid of anatomic
localization procedures. Several approaches are available for treating pituitary
ACTH-dependent Cushing's syndrome, but transsphenoidal pituitary microsurgery is
the ideal type, with remission of the disease being observed in 80 to 90% of
cases. When successful, pituitary microsurgery is followed by preservation of
normal pituitary function and restoration of normal
hypothalamic-pituitary-adrenal function within 6 to 12 months postoperatively.
Medical therapy of Cushing's disease includes drugs that inhibit CRH-ACTH
secretion, such as cyproheptadine and bromocriptine, and agents that inhibit
cortisol synthesis, such as aminoglutethimide, metyrapone, ketoconazole, and
mitotane, or that block the action of cortisol at the glucocorticoid receptor
level, such as RU-485. With the exception of mitotane, which has adrenalytic
effects, the action of the other pharmacologic agents is promptly reversed when
treatment is discontinued. Thus, drug therapy is effective only as temporary
treatment for Cushing's syndrome when surgical approaches are contraindicated or
when attempts are made to improve the patient's clinical and metabolic status in
preparation for surgery. Mitotane is effective in extending survival of patients
with adrenal carcinoma, particularly when it is administered early as adjuvant
therapy or when it is combined with repeated debulking resection of recurrent
tumor. The toxicity associated with mitotane administration limits the use of
larger and probably more effective doses in these patients. The synthesis of more
specific cytochrome P-450 enzyme inhibitors and of mitotane analogues with more
limited toxicity may ultimately provide more effective tools in the pharmacologic
management of Cushing's syndrome.



13. J Endocrinol Invest. 1989 Mar;12(3):197-200.

Cyproheptadine may act at the pituitary in Cushing's disease: evidence from CRF
stimulation.

Tucci JR(1), Nowakowski KJ, Jackson IM.

Author information:
(1)Roger Williams General Hospital, Division of Endocrinology and Metabolism,
Providence, Rhode Island 02908.

Cyproheptadine has been reported to effect remissions in up to 50% of patients
with Cushing's disease presumably at a hypothalamic level. Endocrine studies
including CRF testing were performed in a 37-year-old woman with Cushing's
disease. Cyproheptadine therapy resulted in a clinical and chemical remission.
During therapy, basal plasma and urinary steroid levels were normal as were
responses to dexamethasone, metyrapone, and insulin induced hypoglycemia. CRF
administration in the untreated patient resulted in a markedly exaggerated
increase in plasma ACTH and cortisol levels, while with cyproheptadine therapy
responses were considerably blunted but still greater than normal. These
observations are the first to provide evidence supporting a pituitary effect of
cyproheptadine in Cushing's disease in vivo and raise questions regarding the
assumption of hypothalamic dysfunction in those patients with Cushing's disease
responding to cyproheptadine.


14. J Clin Endocrinol Metab. 1989 Feb;68(2):495-8.

Bromocriptine-responsive Cushing's disease associated with anterior pituitary
corticotroph hyperplasia or normal pituitary gland.

Croughs RJ(1), Koppeschaar HP, van't Verlaat JW, McNicol AM.

Author information:
(1)Department of Endocrinology, University Hospital Utrecht, The Netherlands.

Cushing's disease may originate from either the anterior pituitary lobe or the
neurointermediate lobe, a major characteristic of the latter group being
bromocriptine responsiveness. This study of two patients with Cushing's disease
demonstrates that bromocriptine responsiveness also may be associated with
anterior pituitary corticotroph hyperplasia or a normal pituitary gland. The two
patients were a 14-yr-old boy (patient 1) and a 29-yr-old woman (patient 2);
their cortisol production rates were 121 and 234 mumol/24 h (normal values, less
than 80 mumol/24 h), respectively. A single oral dose of 2.5 mg bromocriptine
resulted in a gradual decrease in plasma cortisol from 680 to 130 nmol/L after 6
h in patient 1 and from 640 to 170 nmol/L after 4 h in patient 2. Both patients
then received medical treatment for a period of 2 yr. Whereas sodium valproate
was ineffective, bromocriptine (5 mg/day) abruptly decreased the cortisol
production rate to 60 mumol/24 h in patient 1 and to 138 mumol/24 h in patient 2,
and both patients had a partial clinical remission. Despite an increase in
bromocriptine dosage to 30 mg daily and 24 mg/day cyproheptadine, the clinical
and biochemical remission was not sustained in patient 1, and no further
improvement occurred in patient 2. Total hypophysectomy then was performed in
both patients. Sections of the pituitary from patient 1 showed diffuse anterior
pituitary corticotroph hyperplasia, with early nodule formation in some areas.
The sections from patient 2 showed normal numbers and distribution of
corticotrophs. We conclude that the heterogeneous nature of Cushing's disease
cannot be explained on the basis simply of anterior vs. intermediate lobe origin
of the disease.


15. Exp Clin Endocrinol. 1985 Jun;85(3):341-50.

Effect of the antiserotonin drug, cyproheptadine, on plasma beta-endorphin and
beta-lipotropin in patients with Itsenko-Cushing's disease.

Slavnov VN, Valueva GV, Luchitsky EV.

In the present paper evidences are provided for the changes occurring in blood
opioid neuropeptides in patients with Itsenko-Cushing's disease), who were
treated with an antiserotonin drug, cyproheptadine (peritol). An increase in the
plasma contents of beta-endorphin and beta-lipotrophin in the above patients has
been found to be one of the factors conditioning an enhanced activity of the
hypothalamic-pituitary-adrenal system. Treatment of the patients suffering from
Itsenko-Cushing's disease with cyproheptadine (peritol) resulted in a decrease of
the plasma beta-endorphin and beta-lipotropin, as well as a display in 60% of
cases of clinical and laboratory remission. Absence of the clinical remission in
some patients treated with peritol indicated a need for intervention in the
metabolism of other monoamines involved in the modulation of the action of opioid
neuropeptides on the activity of the hypothalamic-pituitary system.


16. Ter Arkh. 1984;56(9):119-22.

[Dynamics of beta-lipotropin and beta-endorphin levels in Itsenko-Cushing disease
patients being treated with the antiserotonin preparation cyproheptadine
(peritol) and chloditan].

[Article in Russian]

Slavnov VN, Valueva GV, Luchitskiĭ EV.

The authors provide the data on the changes in the blood content of opioid
neuropeptides in patients with Icenko-Cushing's disease treated with an
antiserotonin drug peritol. The high content of beta-endorphine and
beta-lipotropin in the patients' blood was one of the factors determining
activation of the hypothalamus-pituitary-adrenal system. The treatment of
patients with Icenko-Cushing's disease by peritol led to a decrease in the blood
content of beta-endorphine and beta-lipotropin, promoting a clinical and
laboratory remission in 60% of patients. Some patients treated with peritol did
not develop a clinical remission. This indicates the necessity of acting on the
metabolism of other monoamines involved in the modulation of the action of
neuropeptides on the hypothalamus-pituitary system.



17. Acta Endocrinol (Copenh). 1983 Oct;104(2):160-3.

Sodium valproate and cyproheptadine may independently induce a remission in the
same patient with Cushing's disease.

Koppeschaar HP, Croughs RJ, Thijssen JH, Schwarz F.

A patient with Cushing's disease was unsuccessfully treated by pituitary surgery
and external pituitary irradiation. One year later sodium valproate treatment
induced a remission and finally hypocorticism developed. After drug withdrawal
hypercoticism recurred. Treatment with cyproheptadine again induced hypocorticism
necessitating corticosteroid substitution therapy. Biochemical characteristics of
this patient included responsiveness to bromocriptine and cyproheptadine in acute
tests. The study demonstrates that sodium valproate and cyproheptadine may both
be effective independently in the treatment of the same patient with Cushing's
disease. It is proposed that the disease is due to an ACTH producing tumour of
pituitary intermediate lobe origin.



18. J Clin Endocrinol Metab. 1983 Jun;56(6):1094-9.

Effects of cyproheptadine, reserpine, and synthetic corticotropin-releasing
factor on pituitary glands from patients with Cushing's disease.

Suda T, Tozawa F, Mouri T, Sasaki A, Shibasaki T, Demura H, Shizume K.

Direct effects of cyproheptadine, reserpine, synthetic ovine
corticotropin-releasing factor (CRF), dexamethasone, and lysine-8-vasopressin
(LVP) on the secretion of immunoreactive ACTH and beta-endorphin from the adenoma
and the nonadenomatous tissue of patients with Cushing's disease were examined
using a superfusion system. Cyproheptadine and reserpine (10(-9)-10(-7) M of
each) suppressed immunoreactive ACTH and beta-endorphin secretion from both
tissues. CRF (10(10)-10(7) M) stimulated the secretion of both peptides from the
nonadenomatous tissue, but only a high dose of CRF could stimulate the secretion
of these peptides from some adenomas. Such CRF-induced secretion was partially
suppressed by dexamethasone. LVP (10(-9)-10(-7) M) stimulated peptide secretion
from both types of tissue. These results suggest direct inhibitory effects of
cyproheptadine and reserpine on the secretion of these peptides from the
pituitary of patients with Cushing's disease, a different stimulatory mechanism
of LVP from that of CRF in these tissues, and low sensitivity of the adenoma to
CRF.

19. Farmakol Toksikol. 1983 Mar-Apr;46(2):50-3.
[Potential use of the antiserotonin preparation cyproheptadine (peritol) in
Itsenko-Cushing disease].
[Article in Russian]
Valueva GV, Luchitskiĭ EV, Iakovlev AA.
Experiments on male rats have shown that the inhibitory effect of peritol on the
hypothalamohypophyseal-adrenal system (HHAS) is determined both by its influence
on the regulatory mechanisms of the CNS and direct action on secretion and,
possibly, synthesis of steroids. The degree of the antiserotonin and the
HHAS-inhibiting effects depends on the frequency of drug administrations rather
than on its dose. The experimental studies made it possible to successfully apply
peritol to the treatment of inpatients suffering from Icenko-Cushing's disease.
Almost 60% of the inpatients manifested a remission, which was confirmed by the
reduced blood content of ACTH, hydrocortisone and aldosterone.


20. Acta Endocrinol (Copenh). 1983 Mar;102(3):436-8.
Prolonged remission of a case of Cushing's disease following cessation of
cyproheptadine therapy.
Wiesen M, Ross F, Krieger DT.

 

[windinthepines]

[2016]

[vision changes: darkening and slight loss of periphery, poor night vision, and general darkening of the whole vision field.]

Have you noticed whether your pupils are smaller than normal? An excessively activated parasympathetic nervous system can cause effects like that, by reducing the amount of light entering the eye. Histamine and some drugs can cause it.

[vision changes...]

Nicotine constricts the pupils. When a person starts taking thyroid there is sometimes a mobilization of stored fat (similar to being on a low calorie diet), and the shrinking fat cells will release stored toxins (such as drugs or organophosphate insecticide) that can shrink the pupils.
The coated tongue and itching suggest that there’s a digestive problem—the stimulating effect of some fibrous food (raw carrot, cooked mushrooms or oat bran) might help. If you alternate eyes, do you notice a difference in brightness (or color) between them?

[vision changes... chemical exposure]

It’s possible that irritating foods could chronically increase histamine, but I think you should investigate what your room might have been treated with. There have been some awful insecticides in wide use in Mexico. I think No-Pest-Strips are sold there. In 1979, buses, restrooms, and cheap motels were washed with a product called PinoSol with insecticide. After I had been exposed to its peculiar fumes in various places, one night I woke up and smelled that on my breath as I exhaled. During the daytime, when I started getting hungry before a meal I would smell it. I kept smelling it for a few weeks after returning to the US, and as soon as the smell disappeared, I became hyperthyroid, and that lasted for a few weeks. Apparently, the substance had been blocking thyroid secretion as long as it was in my tissues.

[Consistent 'smile energy' in chest from... a piece of T3... eating large servings of carrot salad each day, and also taking small amounts of an anti serotonin drug every few days.]

I’ve found that keeping the intestine free of inflammation and active is essential for the effect. What city are you in? Do the pharmacies there have Proloid-S?

[Proloid-S]

My friends in Coeneo got some, but it might have just been old stock.

[2017]

[Absorbing chromium from tanned leather]

I haven’t seen the studies, but it seems likely, if there’s moisture.

[Strategy for clothing, shoes, mattresses, things that could contain harmful substances... concern about pesticides and radiation from cancer treatment.]

I think it’s best to thoroughly wash clothes, both new and used, before wearing them. Traces of radioactive isotopes would be removed by washing.