Ray Peat Email Advice Depository

[UG Krishnamurti]

​	Sat, Oct 16, 2021, 2:18 AM

Q: Hello Dr. Peat

What is a good daily dose of Methylene blue?

Much love

RP: People have told me that half a milligram stopped their depression.

 

[UG Krishnamurti]

​	Fri, Oct 15, 2021, 8:31 PM

Q: Hi Dr. Ray

I think you've said something like "If the cell accumulates too much calcium it will be hard to stimulate it".

Would you say then that If someone's bowel - or particularly ileocolic valve - is calcified do to a lot of tissue damage from crohn's disease and inflammation - would you say that if the organism is trying to stimulate it in any way ( by person's trying to increase metabolism by supplementing thyroid or using something like cascara sagrada) will actually make things worse and make the tissue release blood and cause more tissue damage?

Much love Dr Peat

RP: I think those things, and progesterone, would help.

 

[UG Krishnamurti]

​	Oct 13, 2021, 6:27 PM

Q: Hello Dr. Peat

What do you think of the "Innate immune system" and it's suppression and activation? Does it even exist and can you actually activate it or suppress it?

I hear a lot of doctors using angiotensin II receptor blockers like losartan and olmesartan just to name a few using it to improve innate immune response.

What is your take on it?

Much love

RP: Those do help; also quinine.

Q: Thank you Dr. Peat

I've been exposed to a lot of biotoxins and mycotoxins during my lifetime and I always fall back on their symptoms as soon as my immune system goes down.
Clogged nose, balanitis (white coating and inflammation of glans), intestine/digestion problems, skin issues, histamine, liver/kidney problems, fatigue, mood swings etc. They always seem to linger though, never fully disappear.
Progesterone unfortunately doesn't help [12-24mg a day] or VIT K also...

Things like Doxycycline, Thyroid [cynomel, cynoplus], VIT D make me bleed out of my intestine - probably by somehow modulating immune response - I have no idea how.
But since I have Crohn's disease there must have been some bug involved right?

I'm so confused about these immunosuppressive and immunostimulating ideas. How would one know the difference? For some VIT D is immunosuppressive as well as progesterone for example.
I've had extremely bad exacerbation of all of my symptoms and even some old childhood ones reappeared after using high doses of VIT D3 [In olive oil, topically and orally]. Is this because VIT D is immunosuppressive or immunostimulant?

RP: The receptor blockers have many important protective effects.
Do you eat any preparted (canned or packaged) foods?

Q: I don't recall eating any canned or packaged food - so no citric acid or any other bad stuff.

 

[UG Krishnamurti]

Q: Hello Dr. Peat

For the past month I've been using:

K2 [MK-4]: 45mg
Whole VIT E [Whole E 2oz]: 1.5g
Progesterone [12-24mg]
And 1/4 Cynomel for the past 6 days.

All orally.

My temp after dinner is between 36.9- 37.1 celsius and my heart rate ranges from 87 BPM - 95 BPM. I feel warm. Much more than ever before.

I have been using these to try to remedy my damaged skin from using high doses of VIT D.
It didn't help with that.
I can feel some little improvements in some other areas.

But I did have some heart, circulation weirdness. One night I felt like my heart [or the area around my heart] was getting calcified and more "stiff". I also have some kind of weird pressure in my head [Similar as when I used Cynomel and Cynoplus for a month or when I used high doses of VIT D]. It's definitely the blood thinning effect.

Do you think the blood thinning effect of these supplements could cause some problems?

What dosing would you recommend now that I am trying to lower it. And should I even take a break from some of them?

Much love Dr Peat.

RP: What are the exact ingredients of the vitamin E product, including any substance besides vitamin E?

Q: I use Whole VIT E from "Health Natura" [Link of the product]

RP: According to the information on that website, the tocopherols account for 55% of the volume. The other materials could be responsible for some of the symptoms

Q: I just checked again.
Tocopherols account for 76% total Tocopherols and another ingredient is MCT oil.

RP: The 45% of nontocopherol material is probably the problem, likely to include rancid soy PUFA.

 

[UG Krishnamurti]

​	Wed, Oct 27, 2021, 8:53 PM

Q: Hello Dr. Peat

Do you think that if you use some antibacterial, antifungal or antiviral compounds like Methylene Blue, VIT D3 or Doxycycline - symptoms can actually get worse if a particular person has a higher toxic load?
And what would specifically aid the process of removing that toxic load?

I'm using 400mcg of MB 2x a day along with progesterone, 1/4 of cynomel, K2 and I have some symptoms of sciatica, diarrhea, intestinal discomfort, hardening of the scalp and skin problems. I have a lot of symptoms that suggest I have a lot of parasites along with fungal and bacterial overgrowth.

Thanks Dr. Peat

RP: Doxycycline has some intrinsic toxicity. A good diet and good liver function keeps the detoxifying systems working.

 

[UG Krishnamurti]

​	Fri, Oct 29, 2021, 2:18 AM

Q: Hello Dr. Peat

One quick question:
If I had iron overload in my tissues. Intestines for example. Would ingesting something like Methylene Blue cause the oxidation of that iron and cause more problems?

STUDY: Cellular and Molecular Actions of Methylene Blue in the Nervous System
"MB also directly inhibits both constitutive and inducible forms of nitric oxide synthase (NOS) by oxidation of ferrous iron bound to the enzyme (Mayer et al., 1993; Volke et al., 1999). It inactivates nitric oxide (NO) by generation of superoxide anions."

RP: I think it can produce harmful free radicals. There are chelators that help to remove excess iron, but just drinking coffee helps.

 

[UG Krishnamurti]

Q: Hello Dr. Peat

I got severe symptoms of pulmonary edema/myocarditis after using 45mg K2 MK-4 for around 2 months. [I was also using T3 and VIT E with it. I stopped VIT E and T3 and used only K for 10 + days and symptoms worsened].

Progesterone helps relieve my chest tightness but doesn't resolve it.

I haven't seen a single bad study on VIT K but it seems that all the side effects will happens to me.

Do you know why this happens and what can I do to improve this condition?

Much love

RP: The solvents used in vitamin K can be very harmful.

Q: Hello Dr. Peat

I was using K2 MK-4 dissolved in MCT oil topically on my skin for the last 20 days.
My symptoms were stiffness of the intestine and colon, stiffness of blood vessels, [I felt if I move to quickly my aorta/blood vessel would "crack"], extreme chest tightening, hyperventilating, extreme pulsating kidney pain, symptoms of blood clotting [blood "spots" on my skin], body soreness/pain after waking up [progesterone made it much tolerable].

I think the K2 increased my clotting time, which also messed up with my calcium homeostasis somehow?
Could you see any mechanism that could lead to this?

Q: I also forgot to mention that after just 2 days of applying K2 on my belly, it resolved my eczema/red face and hard coated scalp, before it caused me all these severe bad reactions.

RP: Cooked greens, milk, cheese, and eggs are very good sources of K. The solvents used to extract vitamin K, for example from natto, often cause problems. The present vitamin K culture is the creation of marketing campaigns, and is causing a lot of harm.

Int J Vitam Nutr Res. 1971;41(2):180-8.
The relationship between the storage forms of vitamin K and dietary phylloquinone
in the dog.
Duello TJ, Matschiner JT.

J Nutr. 1998 Feb;128(2):220-3.
Conversion of dietary phylloquinone to tissue menaquinone-4 in rats is not
dependent on gut bacteria.
Davidson RT, Foley AL, Engelke JA, Suttie JW.
Department of Nutritional Sciences, College of Agricultural and Life Sciences,
University of Wisconsin-Madison, Madison, WI 53706, USA.
The ability of male rats to accumulate menaquinone-4 (MK-4) in tissues when fed a
vitamin K-deficient diet supplemented with intraperitoneal phylloquinone (K) as
the sole source of vitamin K for 14 d was assessed. In both conventionally housed
controls and gnotobiotic rats, supplementation with the equivalent of 1500 microg
vitamin K/kg diet increased (P < 0.001) tissue MK-4 concentrations above those of
controls fed a vitamin K-deficient diet. MK-4 concentrations were approximately 5
ng/g (11 pmol/g) in liver, 14 ng/g in heart, 17 ng/g in kidney, 50 ng/g in brain
and 250 ng/g in mandibular salivary glands of gnotobiotic rats. MK-4
concentrations in conventionally housed rats were higher than in gnotobiotic rats
in heart (P < 0.01), brain (P < 0.01) and kidney (P < 0.05) but lower in salivary
gland (P < 0.05). Cultures of a kidney-derived cell line (293) converted K to the
expoxide of MK-4 in a manner that was dependent on both time of incubation and
concentration of vitamin K in the media. A liver-derived cell line (H-35) was
less active in carrying out this conversion. These data offer conclusive proof
that the tissue-specific formation of MK-4 from K is a metabolic transformation
that does not require bacterial transformation to menadione as an intermediate in
the process.

Calif Med. 1970 Apr;112(4):65-7.
Don't use the wrong vitamin K.
Udall JA.
The emergency use of vitamin K is essentially limited to the reversal of
drug-induced hypoprothrombinemia. In patients with adequate liver function,
phytonadione acts promptly and predictably in this capacity whereas the
derivatives of menadione counteract coumarin drugs only slightly or not at all.
It is dangerous to rely on menadione analogues, and these drugs should be removed
from emergency room drug stores.

Biomed Res Int. 2015;2015:296721.
Vitamin K1 exerts antiproliferative effects and induces apoptosis in three
differently graded human colon cancer cell lines.
Orlando A(1), Linsalata M(1), Tutino V(2), D'Attoma B(1), Notarnicola M(2), Russo
F(1).
(1)Laboratory of Nutritional Pathophysiology, National Institute for Digestive
Diseases IRCCS "Saverio de Bellis", Castellana Grotte, 70013 Bari, Italy.
(2)Laboratory of Nutritional Biochemistry, National Institute for Digestive
Diseases IRCCS "Saverio de Bellis", Castellana Grotte, 70013 Bari, Italy.
Vitamin K1 has been demonstrated as having anticancer potentiality mainly in
liver cancer cells. Beyond the reported mechanisms of cancer inhibition (cell
cycle arrest and induction of apoptosis), a possible control by vitamin K1 on
molecules affecting cell growth could be hypothesized. In the literature, few (if
any) data are available on its antitumor effects on colon cancer cells.
Therefore, the aims of the study were to investigate in three differently graded
human colon cancer cell lines (Caco-2, HT-29, and SW480) the effects of
increasing concentrations of vitamin K1 (from 10 μM to 200 μM) administered up to
72 h on (1) cell proliferation, (2) apoptosis with the possible involvement of
the MAPK pathway, and (3) polyamine biosynthesis. Vitamin K1 treatment caused a
significant antiproliferative effect and induced apoptosis in all the cell lines,
with the involvement of the MAPK pathway. A concomitant and significant decrease
in the polyamine biosynthesis occurred. This is the first study demonstrating a
significant polyamine decrease in addition to the antiproliferative and
proapoptotic effects following vitamin K1 administration to colon cancer cell
lines. Therapeutically, combinations of vitamin K1 with polyamine inhibitors
and/or analogues may represent a suitable option for chemoprevention and/or
treatment in future strategies for colorectal cancer management.

Scand J Gastroenterol. 2014 Jun;49(6):715-21.
Vitamin K1 attenuates bile duct ligation-induced liver fibrosis in rats.
Jiao K(1), Sun Q, Chen B, Li S, Lu J.
(1)Department of Laboratory Animal Science, School of Basic Medical Science,
Capital Medical University , Beijing, 100069 , China.
Vitamin K1 is used as a liver protection drug for cholestasis-induced liver
fibrosis in China, but the mechanism of vitamin K1's action in liver fibrosis is
unclear. In this study, a model of liver fibrosis was achieved via bile duct
ligation in rats. The rats were then injected with vitamin K1, and the levels of
serum aspartate aminotransferase, alanine transaminase, total bilirubin and the
fibrotic grade score, collagen content, the expressions of α-smooth muscle actin
(SMA) and cytokeratin 19 (CK19) were measured on day 28 after ligation. The
levels of the biochemical parameters, fibrotic score and collagen content were
significantly reduced by treatment with vitamin K1 in bile duct-ligated rats. In
addition, α-SMA and CK19 expression was significantly reduced by vitamin K1
treatment in bile duct-ligated rats. These results suggested that vitamin K1 may
attenuate liver fibrosis by inhibiting hepatic stellate cell activation in bile
duct-ligated rats.

 

[UG Krishnamurti]

Q: Hello Dr. Peat

What would you recommend to a 31 year old who developed atherosclerosis and aortic calcification.

VIT K2 MK-4 and D3 [taken separately - both topically and orally] not only helped with the problem but led to worsening of the problem. I've never had any aortic/heart problems in my life until supplementing D3 and K2 only a few months ago.

Thank you

RP: What tests were done in relation to the diagnoses?

Q: I've done none of the tests that confirm that. I thought it would be easier just to ask instead of telling the whole story.

I can feel the stiffening of my blood vessels, arteries and intestine. Extreme chest/heart pressure and blood pressure problems. Inability to breathe deeply. Feeling of lightheadedness. Kidney problems/kidney pain and pulsating inflammation.

My grandma died of aortic calcification and my mom's doctor just confirmed stiffening of the arteries for her.

I could feel the blood pressure problems are directly related to inability of the proper blood flow because everything is stiffened/calcified. Whenever I eat some higher calcium food [milk, ice cream, cheese] I could feel the worsening of my symptoms.

With VIT K and D3 I've also used VIT E 750mg - 1.5g for almost 2 months which could also be the reason I've experienced this.
But I've removed VIT E and used only K2 for the next 10 days and felt worsening of the symptomes.

To be honest dr Peat I've never been dramatic but I really feel like I could die in every moment. I really feel that bad.

Also I have some superficial thrombophlebitis appearing in the last 10 days which I also never had before in my life. Which indicates some blood clotting happening.

RP: I think it’s imp0rtant to have some tests, at least vitamin D, PTH, and TSH.

Q: I will also get some ultrasound of the heart. I don't know if ultrasound would be useful for checking on aorta and blood vessels Dr Peat?

Also what you recommend to me based on my symptomes.

Would CO2 baths and magnesium bicarbonate for example be useful?
I already use progesterone [9-18mg a day] and I can't use aspirin because of the increase in my tinnitus.

RP: CO2 does help, and magnesium bicarbonate probably does too.

Q: Just one more question regarding this issue

In your book "generative energy" you mention something about sodium thiosulfate but I forgot what specifically.
I've heard it mentioned in several studies as well as a good option. Would you still think it's safe to use?

Also would you say lidocaine cream would be useful since you mentioned it has some calcium regulatory effect while also being anti inflammatory?

RP: Thiosulphate’s main value is as a fungicide. Lidocaine lotions have some systemic effects on calcium.

 

[UG Krishnamurti]

​	Nov 13, 2021, 7:58 PM

Q: Hello Dr. Peat

Over the years you've said so many fascinating things about IODIDE and bad things about IODINE that made me wonder if they are the same substances?

What should I eat or buy as a supplement in order to increase my IODIDE?

Much love

RP: Very large doses of potassium iodide used to be used for certain inflammations or infections, but its effects haven’t been understood. The small amount of iodide added to salt has been reported in more than 70 studies to damage the thyroid gland, even increasing thyroid cancer.

1. Food Chem Toxicol. 2000 Sep;38(9):773-81.
Studies on the carcinogenicity of potassium iodide in F344 rats.
Takegawa K(1), Mitsumori K, Onodera H, Shimo T, Kitaura K, Yasuhara K, Hirose M,
Takahashi M.
(1)Division of Pathology, National Institute of Health Sciences, 1-18-1 Kamiyoga,
Setagaya-ku, 158-8501, Tokyo, Japan.
A chronic toxicity and carcinogenicity study, in which male and female F344/DuCrj
rats were given potassium iodide (KI) in the drinking water at concentrations of
0, 10, 100 or 1000 ppm for 104 weeks, and a two-stage carcinogenicity study of
application at 0 or 1000 ppm for 83 weeks following a single injection of
N-bis(2-hydroxypropyl)nitrosamine (DHPN), were conducted. In the former, squamous
cell carcinomas were induced in the salivary glands of the 1000 ppm group, but no
tumors were observed in the thyroid. In the two-stage carcinogenicity study,
thyroidal weights and the incidence of thyroid tumors derived from the follicular
epithelium were significantly increased in the DHPN+KI as compared with the DHPN
alone group. The results of our studies suggest that excess KI has a thyroid
tumor-promoting effect, but KI per se does not induce thyroid tumors in rats. In
the salivary gland, KI was suggested to have carcinogenic potential via an
epigenetic mechanism, only active at a high dose.

3. Jpn J Cancer Res. 1998 Feb;89(2):105-9.
Induction of squamous cell carcinomas in the salivary glands of rats by potassium
iodide.
Takegawa K(1), Mitsumori K, Onodera H, Yasuhara K, Kitaura K, Shimo T, Takahashi
M.
(1)Division of Pathology, National Institute of Health Sciences, Tokyo.
In a 2-year carcinogenicity study of potassium iodide (KI) in F344/DuCrj rats,
squamous cell carcinomas (SCCs) were observed in the salivary glands of 4/40
males and 3/40 females receiving 1000 ppm KI in the drinking water. Ductular
proliferation with lobular atrophy was observed at high incidence in the
submandibular glands of the high-dose animals, and squamous metaplasia was
frequently evident within the proliferative ductules and the larger interlobular
ducts. A transition from metaplasia to SCC was apparent. The results suggest that
squamous metaplasia in proliferative ductules, occurring secondarily to lobular
impairment induced by KI, may develop into SCCs via a non-genotoxic,
proliferation-dependent mechanism.

2. Endocrinology. 2000 Feb;141(2):598-605.
Iodide excess induces apoptosis in thyroid cells through a p53-independent
mechanism involving oxidative stress.
Vitale M(1), Di Matola T, D'Ascoli F, Salzano S, Bogazzi F, Fenzi G, Martino E,
Rossi G.
(1)Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università
Federico II, Naples, Italy. [email protected]
Thyroid toxicity of iodide excess has been demonstrated in animals fed with an
iodide-rich diet; in vitro iodide is cytotoxic, inhibits cell growth, and induces
morphological changes in thyroid cells of some species. In this study, we
investigated the effect of iodide excess in an immortalized thyroid cell line
(TAD-2) in primary cultures of human thyroid cells and in cells of nonthyroid
origin. Iodide displayed a dose-dependent cytotoxicity in both TAD-2 and primary
thyroid cells, although at different concentrations, whereas it had no effect on
cells of nonthyroid origin. Thyroid cells treated with iodide excess underwent
apoptosis, as evidenced by morphological changes, plasma membrane
phosphatidylserine exposure, and DNA fragmentation. Apoptosis was unaffected by
protein synthesis inhibition, whereas inhibition of peroxidase enzymatic activity
by propylthiouracil completely blocked iodide cytotoxicity. During KI treatment,
reactive oxygen species were produced, and lipid peroxide levels increased
markedly. Inhibition of endogenous p53 activity did not affect the sensitivity of
TAD-2 cells to iodide, and Western blot analysis demonstrated that p53, Bcl-2,
Bcl-XL, and Bax protein expression did not change when cells were treated with
iodide. These data indicate that excess molecular iodide, generated by oxidation
of ionic iodine by endogenous peroxidases, induces apoptosis in thyroid cells
through a mechanism involving generation of free radicals. This type of apoptosis
is p53 independent, does not require protein synthesis, and is not induced by
modulation of Bcl-2, Bcl-XL, or Bax protein expression.

4. Toxicol Pathol. 1994 Jan-Feb;22(1):23-8.
Effects of a six-week exposure to excess iodide on thyroid glands of growing and
nongrowing male Fischer-344 rats.
Kanno J(1), Nemoto T, Kasuga T, Hayashi Y.
(1)Department of Pathology, Faculty of Medicine, Tokyo Medical and Dental
University, Japan.
A 6-wk exposure to excess iodide intake (EII) via drinking water (260 mg
potassium iodide/L) demonstrated different effects on growing (4-wk old) and
nongrowing (45-wk old) male Fischer-344 rats. In growing rats, EII induced a
significant increase in thyroid weight, pituitary weight, serum
thyroid-stimulating hormone (TSH), and thyroxine (T4). The labeling index (LI) of
thyroid follicular cells was slightly increased, although not statistically
significant. Histologically, an increase in follicular cell height, an increase
in colloid accumulation, and evidence of colloid absorption were noted. The
effect of bovine TSH (bTSH) and protirelin tartrate (TRH-t) on LI was
significantly augmented by EII. In nongrowing rats, EII induced a significant
increase in thyroid weight and serum T4 but no increase in pituitary weight,
serum TSH, and the LI of follicular cells. Histologically, an increase in colloid
accumulation was found in small follicles. EII did not augment the effect of bTSH
and TRH-t on the LI of follicular cells. This study suggests that growing rats
are still susceptible to acute hypothyroidism even after 6 wk of continuous
exposure to excess iodide, whereas nongrowing rats are refractory within an
equivalent treatment period.

5. Food Chem Toxicol. 1984 Dec;22(12):963-70.
Developmental toxicity and psychotoxicity of potassium iodide in rats: a case for
the inclusion of behaviour in toxicological assessment.
Vorhees CV, Butcher RE, Brunner RL.
Potassium iodide (KI) was fed to male and female rats before and during breeding,
to females only during gestation and lactation, and to their offspring after
weaning (day 21 after birth) through to day 90, at levels of 0, 0.025, 0.05 or
0.1% (w/w) of the diet. Dams in a fifth group (positive controls) were given 4
mg/kg ip of the anti-mitotic/cytotoxic drug 5-azacytidine on day 17 of gestation.
All offspring were reared by their natural dams and were evaluated blind with
respect to treatment in a battery of standardized behavioural tests between 3 and
90 days of age. KI produced no significant reductions in parental body weight or
food consumption, though it significantly reduced litter size and increased
offspring mortality at the highest dose, and decreased weight gain at the two
highest doses throughout the first 90 days after birth. Functionally, KI delayed
auditory startle at the two highest doses, delayed olfactory orientation to the
home-cage scent at the middle dose and decreased female running-wheel activity at
all dose levels. In rats killed on day 90 after birth KI reduced brain and body
weight at a dose of 0.1% of the diet, and reduced body but not brain weight at a
dose of 0.05% of the diet. No significant effect was found on absolute or
relative thyroid weight at 90 days of age. Several additional behavioural effects
were observed in the low-dose KI group, but because these effects were not
dose-dependent, they were not regarded as reliable. 5-Azacytidine produced
evidence of substantially greater developmental toxicity than KI. It was
concluded that KI produced evidence of developmental toxicity consistent with a
picture of impaired thyroid function. The inclusion of tests of functional
development added useful evidence to the overall picture of KI developmental
toxicity.

6. J Allergy Clin Immunol. 1980 Sep;66(3):177-8.
A time to abandon the use of iodides in the management of pulmonary diseases.
Hendeles L, Weinberger M.

7. Endocrinol Jpn. 1975 Oct;22(5):389-97.
The effect of iodide administration on hog thyroid gland and the composition of
thyroglobulin and 27-S iodoprotein.
Tarutani O, Kondo T, Horiguchi-Sho K.
The effect of excess iodide on hog thyroid gland has been examined with regard to
the change in the chemical composition of thyroglobulin and in the accumulation
of 27-S iodoprotein by the in vivo treatment of hogs with iodide for various
lengths of time. The iodine content of thyroglobulin was either unchanged by
short term administration of excess iodide, or somewhat lowered. However, the
iodine content as well as the total amount of thyroglobulin increased in the
glands enlarged by prolonged treatment with iodide. The iodine highest reached
1.17% of the protein on an average. On the other hand, 27-S iodoprotein decreased
and finally disappeared after the chronic treatment. Monoiodotyrosine and
diiodotyrosine increased in parallel with the increase in the iodine content
(0.15 to 1.17%) caused by the iodide treatment, while thyroxine increased but
reached a plateau at the level of three residues per mole of thyroglobulin, and
no change was observed even in the proteins with the higher iodine content than
0.75%. Proteolytic activity measured by amino acid release from the thyroid
protein was depressed by the chronic treatment. On the other hand, the amount of
iodocompound released by the autoproteolysis, which may reflect hormone
secretion, increased, possibly because of the marked increase in the iodine
content of thyroglobulin.

8. Am J Vet Res. 1973 Jan;34(1):65-70.
Experimentally induced iodide toxicosis in lambs.
McCauley EH, Linn JG, Goodrich RD.

9. Toxicol Appl Pharmacol. 1966 Mar;8(2):185-92.
The toxicology of potassium and sodium iodates. 3. Acute and subacute oral
toxicity of potassium iodate in dogs.
Webster SH, Stohlman EF, Highman B.

10. Clin Toxicol (Phila). 2013 Jul;51(6):521. doi: 10.3109/15563650.2013.804549. Epub
2013 May 23.
Regional centers: added value to poison center surveillance.
Durigon M, Kosatsky T.
Comment on
Clin Toxicol (Phila). 2013 Jan;51(1):41-6.

11. Environ Toxicol Pharmacol. 2014 Jul;38(1):332-40. doi:
10.1016/j.etap.2014.06.008. Epub 2014 Jun 27.
The effects and underlying mechanism of excessive iodide on excessive
fluoride-induced thyroid cytotoxicity.
Liu H(1), Zeng Q(2), Cui Y(2), Yu L(3), Zhao L(2), Hou C(2), Zhang S(4), Zhang
L(2), Fu G(2), Liu Y(3), Jiang C(4), Chen X(4), Wang A(5).
(1)Tianjin Centers for Disease Control and Prevention, 6 Huayue Road, Hedong
District, Tianjin 300011, PR China; School of Public Health, Tianjin Medical
University, 22 Qi Xiang Tai Road, Heping District, Tianjin 300070, PR China.
Electronic address: [email protected].
(2)Tianjin Centers for Disease Control and Prevention, 6 Huayue Road, Hedong
District, Tianjin 300011, PR China.
(3)School of Public Health, Tianjin Medical University, 22 Qi Xiang Tai Road,
Heping District, Tianjin 300070, PR China.
(4)Department of Environmental Health and MOE Key Lab of Environment and Health,
School of Public Health, Tongji Medical College, Huazhong University of Science
and Technology, 13 Hangkong Road, Hubei, Wuhan 430030, PR China.
(5)Department of Environmental Health and MOE Key Lab of Environment and Health,
School of Public Health, Tongji Medical College, Huazhong University of Science
and Technology, 13 Hangkong Road, Hubei, Wuhan 430030, PR China. Electronic
address: [email protected].
In many regions, excessive fluoride and excessive iodide coexist in groundwater,
which may lead to biphasic hazards to human thyroid. To explore fluoride-induced
thyroid cytotoxicity and the mechanism underlying the effects of excessive iodide
on fluoride-induced cytotoxicity, a thyroid cell line (Nthy-ori 3-1) was exposed
to excessive fluoride and/or excessive iodide. Cell viability, lactate
dehydrogenase (LDH) leakage, reactive oxygen species (ROS) formation, apoptosis,
and the expression levels of inositol-requiring enzyme 1 (IRE1) pathway-related
molecules were detected. Fluoride and/or iodide decreased cell viability and
increased LDH leakage and apoptosis. ROS, the expression levels of
glucose-regulated protein 78 (GRP78), IRE1, C/EBP homologous protein (CHOP), and
spliced X-box-binding protein-1 (sXBP-1) were enhanced by fluoride or the
combination of the two elements. Collectively, excessive fluoride and excessive
iodide have detrimental influences on human thyroid cells. Furthermore, an
antagonistic interaction between fluoride and excessive iodide exists, and
cytotoxicity may be related to IRE1 pathway-induced apoptosis.
Copyright © 2014. Published by Elsevier B.V.

12. Chemosphere. 2015 Feb;120:299-304. doi: 10.1016/j.chemosphere.2014.07.011. Epub
2014 Aug 24.
Toxicity of tetramethylammonium hydroxide to aquatic organisms and its
synergistic action with potassium iodide.
Mori IC(1), Arias-Barreiro CR(2), Koutsaftis A(2), Ogo A(2), Kawano T(3),
Yoshizuka K(3), Inayat-Hussain SH(4), Aoyama I(2).
(1)Institute of Plant Science and Resources, Okayama University, Kurashiki
710-0046, Japan. Electronic address: [email protected].
(2)Institute of Plant Science and Resources, Okayama University, Kurashiki
710-0046, Japan.
(3)School of International Environmental Science, The University of Kitakyushu,
Kitakyushu 808-0135, Japan.
(4)Faculty of Health Sciences, Univerisiti Kebangsaan Malaysia, Kuala Lumpur,
Malaysia.
The aquatic ecotoxicity of chemicals involved in the manufacturing process of
thin film transistor liquid crystal displays was assessed with a battery of four
selected acute toxicity bioassays. We focused on tetramethylammonium hydroxide
(TMAH, CAS No. 75-59-2), a widely utilized etchant. The toxicity of TMAH was low
when tested in the 72 h-algal growth inhibition test (Pseudokirchneriellia
subcapitata, EC50=360 mg L(-1)) and the Microtox® test (Vibrio fischeri, IC50=6.4
g L(-1)). In contrast, the 24h-microcrustacean immobilization and the 96 h-fish
mortality tests showed relatively higher toxicity (Daphnia magna, EC50=32 mg
L(-1) and Oryzias latipes, LC50=154 mg L(-1)). Isobologram and mixture toxicity
index analyses revealed apparent synergism of the mixture of TMAH and potassium
iodide when examined with the D. magna immobilization test. The synergistic
action was unique to iodide over other halide salts i.e. fluoride, chloride and
bromide. Quaternary ammonium ions with longer alkyl chains such as
tetraethylammonium and tetrabutylammonium were more toxic than TMAH in the D.
magna immobilization test.
Copyright © 2014 Elsevier Ltd. All rights reserved.

13. J Invest Dermatol. 1981 May;76(5):381-3.
Sterile cutaneous pustules: a manifestation of primary irritancy? Identification
of contact pustulogens.
Wahlberg JE, Maibach HI.
An animal model (the rabbit) was used to define which of 8 chemicals caused
pustule formation on topical application. Large occlusive chambers (diameter 12
mm), petrolatum as the vehicle and wrapping contributed to efficient occlusion
and pustulation. Sodium lauryl sulfate and mecuric chloride gave reproducible
results and clear dose-responses indicating that this pustulation is an
expression of primary irritancy. Ammonium fluoride pustulation was not
reproducible; croton oil pustules were more difficult to evaluate due to
simultaneous erythema and edema. Sodium arsentate, nickel sulfate and potassium
iodide pustules developed at sites where the skin barriers had been damaged by a
stab injury. Benzalkonium chloride caused yellow staining and edema but not
pustules. Because of lack of epidemiologic data, we do not know how frequently
similar findings occur in man.

Q: If I understand correctly you've changed your mind based on this new data?

"Among the factors that probably have a role in preventing cataracts: Thyroid, progesterone, pregnenolone, vitamin E, iodide, pyruvate. Increasing the carbon dioxide lowers the cell’s pH, and tends to resist swelling. Palmitic acid (a saturated fat that can be synthesized by our tissues) is normally oxidized by the lens. Calcium blockers experimentally prevent cataracts, suggesting that magnesium and thyroid (which also act to exclude calcium from cells) would have the same effect."

"The sea cucumber has been used to study the physical properties of connective tissue, and it has been found that certain salts tend to soften the connective tissues, but that iodide doesn't. The well-established use of iodide to resolve granulomas, even when it doesn't eliminate the infectious agent, might suggest that it is protecting against something which is disrupting the connective tissue structure. The only publications I have seen that presented clear evidence of the disappearance of arteriosclerosis involved treatment with iodides. In the retina, blood vessels can be seen to return to their normal appearance following a course of iodide treatment. Besides its possible direct effects on the mucins, iodide might help to eliminate calcium from the walls of blood vessels, since calcium iodide is very soluble."

"Besides its possible direct effects on the mucins, iodide might help to eliminate calcium from the walls of blood vessels, since calcium iodide is very soluble."

"Endotoxin, produced by bacteria, mainly in the intestine, disrupts energy production, and promotes maladaptive inflammation. The wide spectrum of benefit that iodide has, especially in diseases with an inflammatory component, suggests first that it protects tissue by blocking free radical damage, but it also suggests the possibility that it might specifically protect against endotoxin."

"One of the best-known free radical scavenging substances that has been widely used as a drug is iodide. It has been used to treat asthma, parasites, syphilis, cancer, Graves’ disease, periodontal disease, and arteriosclerosis. Diseases that produce tissue overgrowth associated with inflammation--granulomas--have been treated with iodides, and although the iodide doesn’t necessarily kill the germ, it does help to break down and remove the granuloma. Leprosy and syphilis were among the diseases involving granulomas* that were treated in this way. In the case of tuberculosis, it has been suggested that iodides combine with unsaturated fatty acids which inhibit proteolytic enzymes, and thus allow for the removal of the abnormal tissue."

Do you think supplementing thyroid while using iodide would prevent the damaging effect?

Ever since I stopped eating iodized salt (for 3 months now) and moving to pickled salt I think I've experienced more symptoms of calcification and hardening of the arteries and blood vessels than before. Would you say that it could be because of removing iodine?

Is iodide the same as Iodine or is it different and what would be the safest way to consume it if one decides to use it?

Thank you.

RP: The treatments generally involve local injection of large amounts into the tumor. Iodine is the oxidized form, iodide is the ionized form that appears in the presense of cysteine, vitamin C, and other reductants.

Q: I'm very interested in it's uses in atherosclerosis

You've said" The only publications I have seen that presented clear evidence of the disappearance of arteriosclerosis involved treatment with iodides."

Is there any way that you can remember how it was used and what was the doses for that specific problem?
Also, would you say that increasing thyroid hormone while using potassium iodide would reduce the possible damaging effect?

Much love

RP: Correcting elevated TSH lowers cholesterol and reduces vascular deterioration.

Hypothyroidism and Atherosclerosis
Anne R. Cappola, Paul W. Ladenson
The Journal of Clinical Endocrinology & Metabolism, Volume 88, Issue 6, 1 June 2003, Pages 2438–2444,
Cardiovascular Endocrinology: Special Features
“There was edema of the skin… much serous effusion in the pericardium… the heart was large… the arteries were everywhere thickened, the larger ones atheromatous.” (1)
[Dr. William Smith Greenfield, 1878]
This autopsy finding of diffuse atherosclerosis in a 58-yr-old woman was published as an appendix to William Ord’s classical description of the syndrome of myxedema. Soon thereafter, the hypothesis of a causal relationship between hypothyroidism and atherosclerosis was first raised in 1883 by E. Theodor Kocher (2), who noted that arteriosclerosis commonly occurred after thyroid extirpation. Since the time of the first associations between these two common disorders, hypothyroidism and atherosclerosis have subsequently been linked by a body of clinical case reports, epidemiological studies, and biochemical observations. The hypothesis of a relationship has subsequently been tested in case-control and cohort studies. Important associations have been identified among hypercholesterolemia, hypertension, and certain newer risk factors for atherosclerosis in individuals with overt hypothyroidism and, in some cases, subclinical hypothyroidism. There have also been clinical observations and trials describing the consequences of treating hypothyroidism in patients with ischemic heart disease and of revascularizing patients with ischemic heart disease who are hypothyroid. These studies are the subject of this commentary.

 

[UG Krishnamurti]

​	Nov 15, 2021, 9:53 PM

Q: Hello Dr. Peat

About 2 years ago I went to a practitioner who was doing something called "Live blood analysis" under a microscope.

He drew my blood and saw lots of parasites in my blood as well as red blood cells "clumped" together.
I could even clearly see the parasites on the screen.
He then drew my girlfriends blood and the cells were not clumping and there were no parasites.

I think pathogenic activity is really behind most of my problems and just improving the metabolism didn't get to the "root problem".

What do you think those results mean and what do you think is the best way to improve the body dealing with these pathogens?

Much love

RP: “Live blood analysis” isn’t based on science.

 

[UG Krishnamurti]

​	Nov 17, 2021, 4:29 AM

Q: Hello Dr. Peat

What would be good blood work to assess the state of my liver health and iron overload?
Also what markers are the most reliable to reveal if there is a higher pathogenic/toxic/bacterial load and/or infectious problems?

Much love

RP: The liver enzymes, ALT and AST, are good indicators of continuing liver damage. Also, serum vitamin D and TSH are important.

Q: Are there any other important markers for iron overload and also how should one interpret them to see if they have some higher tissue accumulation?

Thank you for helping out Dr Peat

RP: I don’t think any of the “markers” is very reliable; restriction of iron in the diet is safe and protective.

 

[UG Krishnamurti]

​	Thu, Nov 18, 2021, 2:08 AM

Q: Hello Dr. Peat

What would be the most important thing to do/have in order to be able to break out of the cycle of "learned helplessness" and inescapable stress which has been happening since childhood.

It's obvious that the "stress reaction" is gaining new momentum each time it is being experienced over the years.

It seems that the mind and thought are of the least importance in these "repetitive" situations; the memory of the "event" is stored somewhere in cells and always has to play out in the same way no matter how "well" a thought can rationalise the situation.

Much love

RP: I think the only storage of an event is in the interpretation (made by the whole organism), and so a slight insight is enough to break the pattern.

 

[UG Krishnamurti]

​	Sat, Nov 20, 2021, 6:32 PM

Q: Hello Dr. Peat

Do you think potato chips in palm oil are safe 2-3x a month?
The same question goes for some sardines in olive oil?

Much love

RP: Sardines in olive oil are safe enough to have about that often; palm oil has a lot of PUFA, probably isn’t so safe.

 

[UG Krishnamurti]

​	Wed, Nov 24, 2021, 1:55 AM

Q: Hello Dr. Peat

What would you say that I shouldn't be supplementing or eating if my VIT D is low and I cannot bring it back up by supplementation?

Would things like thyroid, some hormones or vitamins be out of the picture until I find a way to get my VIT D up?

Much love

RP: Good nutrition and thyroid function will help to normalize your vitamin D.

 

[UG Krishnamurti]

​	Fri, Nov 26, 2021, 1:17 AM

Q: Hello Dr. Peat

How much was the Hepatitis B vaccine I received in my 20's (7-8 years ago) responsible for my declining health and what would be the best things to try to restore some sort of equilibrium and balance in the organism (If even possible)?

Much love

RP: I don’t think it would be possible to identify any continuing effects from the particular vaccine.

 

[UG Krishnamurti]

​	Sun, Nov 28, 2021, 10:03 PM

Q: Hello Dr. Peat

Once you've said "During the night, plants emit CO2, so they are helpful."

Since I'm totally clueless - before I go into investigation - I would like to ask you what plants you think would be the best/safest for emitting higher CO2 in one's home?

Much love

RP: The bigger the better.

 

[UG Krishnamurti]

​	Sun, Nov 28, 2021, 11:47 PM

Q: Hello Dr. Peat

I was wondering if a sauna would be useful for someone who doesn't sweat much because of the lack of activity in order to improve detoxification and maybe lower PUFAs/Iron in the tissues?

How long would you recommend and what temperatures would be optimal if one would load his body with glucose and minerals before and after using the sauna?

Much love

RP: It depends on your body temperature. If it is 36 C before, it’s o,k, to increase it to 37.5, keeping your blood sugar up.

 

[UG Krishnamurti]

​	Sat, Dec 11, 2021, 3:45 AM

Q: Hello Dr. Peat

What do you think of making tea [black tea for example] in this way:

Cooking the green leafy vegetables and straining the water in a cup and adding a tea bag and honey to a cup to make a tea with vegetable water. On top of that adding maybe like 0,3l of milk?

RP: It would be o.k.

 

[UG Krishnamurti]

​	Sun, Dec 26, 2021, 2:26 AM

Q: Hello Dr. Peat

If LDH is low on a blood test, does that mean that lactic acid is low?

Are there any side effects of low LDH?

My LDH: 107 [LOW]: 125 - 220

RP: As far as I know, low LDH is usually good.

 

[UG Krishnamurti]

​	Sun, Dec 26, 2021, 9:57 PM

Q: Hello Dr. Peat

I was thinking of using heads of European sprat fish to make a fish head supp for additional thyroid. They are quite small.

Do you think that's a good fish to make a fish head soup from?
Would 250g of fish head be enough to have a decent thyroid effect?

RP: They have a high fat content that could antagonize thyroid function. Supplementing thyroid would be safer and more reliable.