Ray Peat Email Advice Depository Discussion/Comment Thread

Dr. B

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Q:
I notice when I wear a cap or any type of headwear I get a great boost in temps/metabolism and feel serotonin lower a lot - I feel a lot more calm.

Does head insulation and increasing temperature for the brain provide a good boost in metabolism ? I was curious why I never see you in headwear or if this was correct

A:

I wear a hat when I’m in a cold place, but generally my thick hair has been enough. Keeping the brain temperature up is extremely important, especially for restful sleep. It’s natural for the forehead to be a little cooler than the rear parts of the brain. In the winter I keep a high-watt bulb over my work area, shining on my head.
this is the comment thread
do humans create more MUFA in lower temperatures and more SFA in higher temperatures?
should we not be using things like fans or air conditioning in the summer? to keep temperatures higher throughout the day?
and should heaters be activated full force in winter? so youre sweating constantly all day?
 

Dr. B

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I posted his whole answer. No explanation. I assume he thinks so because FDR was in fact awesome, and president when Ray was a kid. Probably left a big impression on him.
some claim he was one of the worst or very evil
 
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I think Ray has a positive view of FDR because of his "Good Neighbor Policy" unlike his predecessors, and his genuine desire to help the poor during the Great Depression, along with his getting along quite well with Stalin in WW2 and fighting the Nazis. Even then, he doesn't see FDR as perfect, since he was trying to save capitalism by his reforms, and his early admiration of Mussolini's fascism, rather than trying to implement the kind of socialism that Peat favours.

As for Truman, Peat sees him as Dulles' placeman who benefitted from FDR's assassination, the President who through Operation Paperclip oversaw the Nazification of America's intelligence services, and the initiator of the Cold War against Russia.

So they are probably the two opposing archetypes of Presidents in his mind.
 

Dr. B

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I think Ray has a positive view of FDR because of his "Good Neighbor Policy" unlike his predecessors, and his genuine desire to help the poor during the Great Depression, along with his getting along quite well with Stalin in WW2 and fighting the Nazis. Even then, he doesn't see FDR as perfect, since he was trying to save capitalism by his reforms, and his early admiration of Mussolini's fascism, rather than trying to implement the kind of socialism that Peat favours.

As for Truman, Peat sees him as Dulles' placeman who benefitted from FDR's assassination, the President who through Operation Paperclip oversaw the Nazification of America's intelligence services, and the initiator of the Cold War against Russia.

So they are probably the two opposing archetypes of Presidents in his mind.
what are Rays thoughts on the holocaust, Hitler, nazis etc. i thought he said in a podcast or quote on here that a lot of what we saw about the holocaust/hitler was soviet propoganda.
what kind of socialism does Peat prefer
 
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what are Rays thoughts on the holocaust, Hitler, nazis etc. i thought he said in a podcast or quote on here that a lot of what we saw about the holocaust/hitler was soviet propoganda.
what kind of socialism does Peat prefer
Ray seems to prefer the kind of anarchist-socialism that Kropotkin write about, with more emphasis on mutual aid and cooperation than the top-down Bolshevik model that the Soviet Union implemented. Though he did still support the USSR as an imperfect alternative to Tsarism and imperialism, as well as the Social Darwinism of the Western countries.

As to Hitler and the Nazis, he doesn't like them. He thinks Hitler was supported by the banking institutions in Britain, France and America, who wanted him to save capitalism in Germany and go to war against the Soviet Union. He says Hitler used progressive/socialist language to hoodwink the German people into accepting authoritarian government, misdirecting anti-capitalist feeling by blaming only the Jewish capitalists. Saving capitalism by blaming its faults solely on the Jews.

I've never heard him mention the Holocaust as a historical context, but he probably has somewhere. He did say on one podcast that most of his friends in the 1950s and '60s were Jews, but by the mid-1970s they started to conflate anti-Zionism with anti-Semitism, which upset Peat because he was very critical of Zionism, but wasn't anti-Semitic.
 

Dr. B

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Ray seems to prefer the kind of anarchist-socialism that Kropotkin write about, with more emphasis on mutual aid and cooperation than the top-down Bolshevik model that the Soviet Union implemented. Though he did still support the USSR as an imperfect alternative to Tsarism and imperialism, as well as the Social Darwinism of the Western countries.

As to Hitler and the Nazis, he doesn't like them. He thinks Hitler was supported by the banking institutions in Britain, France and America, who wanted him to save capitalism in Germany and go to war against the Soviet Union. He says Hitler used progressive/socialist language to hoodwink the German people into accepting authoritarian government, misdirecting anti-capitalist feeling by blaming only the Jewish capitalists. Saving capitalism by blaming its faults solely on the Jews.

I've never heard him mention the Holocaust as a historical context, but he probably has somewhere. He did say on one podcast that most of his friends in the 1950s and '60s were Jews, but by the mid-1970s they started to conflate anti-Zionism with anti-Semitism, which upset Peat because he was very critical of Zionism, but wasn't anti-Semitic.
wow when did he mention that anti zionism anti semitism stuff?

and interesting, i thought Hitler actually was against the banking system of the US, Britain, France etc
 
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wow when did he mention that anti zionism anti semitism stuff?

and interesting, i thought Hitler actually was against the banking system of the US, Britain, France etc
Yes, he has an interesting/alternative perspective on these historical matters, it's always illuminating to listen to.

He mentioned the Zionist thing in a Danny Roddy interview: "Thyroid Function & Pulse Rate | Weaponized Culture | Finasteride as an "Insane Decision"", at about 23 minutes into it.
 

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@JamesGatz @Shackles

Q: "Dear Dr. Raymond Peat,
I was not specifically asking if they are safe to wear, but rather, if copper bracelets might actually be beneficial in terms of its electric morphogenesis or simply just absorption through the skin.
Maybe a Brass (5% Zinc) bracelet would be of interest, too?"

A: "A copper bracelet does release enough copper to be absorbed in a nutritionally useful quantity."

Q: "Does the copper differ from "organic copper" found in e.g. milk? Does it matter or can the body produce enzymes to deal with that?"

A:"With very small amounts there’s not much difference."


this is interesting just wearing the bracelet, gives you enough to absorb nutritionally?! then it may be the same for gold and platinum. how does this work, a couple milligrams of copper absorb through the wrists? maybe half a milligram a day?
 

Shackles

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@JamesGatz @Shackles

Q: "Dear Dr. Raymond Peat,
I was not specifically asking if they are safe to wear, but rather, if copper bracelets might actually be beneficial in terms of its electric morphogenesis or simply just absorption through the skin.
Maybe a Brass (5% Zinc) bracelet would be of interest, too?"

A: "A copper bracelet does release enough copper to be absorbed in a nutritionally useful quantity."

Q: "Does the copper differ from "organic copper" found in e.g. milk? Does it matter or can the body produce enzymes to deal with that?"

A:"With very small amounts there’s not much difference."


this is interesting just wearing the bracelet, gives you enough to absorb nutritionally?! then it may be the same for gold and platinum. how does this work, a couple milligrams of copper absorb through the wrists? maybe half a milligram a day?
80-90mg is lost by the bracelet in 30 days
 

Dr. B

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80-90mg is lost by the bracelet in 30 days
that's a massive amount. 1 gram lost per year basically.
so 100 grams of copper will turn to nothing in 100 years? a bracelet worn for 100 years?

@AdoTintor I've heard Dr Peat say OLE is ok

what did he say about olive leaf extract
does it increase histamine due to being a leaf product
 

Mauritio

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@Peater Piper @LeeLemonoil
Q: Do you think the nanotechnology that novavax uses for their vaccine makes it more dangerous?

A: Using a new adjuvant as well as a new way of making antigens, so different from historical methods—considering that we are still discovering hrmful effects of the old vaccines, how long would testing have to be to show its long-range safety?
 

golder

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Q: What would be your go-to medicines/food etc, if you started to develop "Covid" like symptoms like shortness of breath and fever?

RP: Aspirin, antihistamines, and antibiotics (azithromycin has been tested in covid), vitamin D, milk, orange juice,nebulized 4% saline, lidocaine (nebulized or oral), progesterone.


Br J Anaesth. 2020 Oct; 125(4): e391–e394.
A novel role for lidocaine in COVID-19 patients?

Dylan T. Finnerty1,2,3,∗ and Donal J. Buggy1,2,3,4
Editor—Coronavirus disease 2019 (COVID-19) is a novel viral respiratory disease that was declared a global pandemic by the WHO on March 11, 2020. The pathophysiology of the disease remains under investigation; however, a new perspective has emerged that neutrophils may play a central role in the organ damage and mortality associated with COVID-19.1

The most abundant leucocyte in peripheral blood, neutrophils play a crucial role in immune response to infection by killing pathogens (bacteria, fungi, viruses) by means of phagocytosis and oxidative burst. A third mechanism by which neutrophils kill invading organisms was discovered in 2004: formation of neutrophil extracellular traps (NETs).2 NETs are web-like structures of DNA studded with proteins that are extruded from the nucleus of neutrophils and function to trap and kill circulating pathogens. Like much of the immune response, netosis (the process of forming NETs) functions well as long as it is closely regulated. When dysregulation of netosis occurs, collateral damage ensues. Excessive production of NETS has been associated with disease progression in a range of pathological conditions including pre-eclampsia, lupus erythematosis, myocardial infarction, and sepsis.3, 4, 5, 6 Interestingly, the organ systems most commonly damaged by NETS, the pulmonary, cardiovascular, and renal systems, are the same organ systems that are most affected in severe COVID-19.1

NETs and COVID-19

Elevated levels of citrullinated histone H3 (Cit-H3) have been observed in hospitalised patients with COVID-19.7 Cit H3 is a specific biomarker of the presence of NETs. Whether the presence of markers of netosis bears clinical relevance is unknown as no longitudinal cohort studies have been published. However, in numerous disease models elevated Cit H3 is associated with poor outcomes.8, 9, 10 Interestingly, serum from COVID-19 patients triggered NET release from control neutrophils in vitro, suggesting COVID-19 creates a cellular environment in which netosis is more likely to occur.

NETs and acute respiratory distress syndrome

A subgroup of COVID-19 patients develops an acute respiratory distress syndrome (ARDS)-like state that frequently requires ICU-level support. Although there is some disagreement as to whether these patients fit the Berlin definition of ARDS, such discussions are to some degree academic.11 What is clear is that COVID-19 can cause a severe viral pneumonia associated with profound hypoxaemia and need for mechanical ventilation. NETs have been shown to contribute to disease progression in pulmonary infections,12, 13, 14 and animal models suggest that therapies that reduce formation of or lyse NETs reduce lung injury and mortality.15 , 16 Levels of NETs in the plasma and broncho-alveolar lavage fluid correlate with disease severity in patients with pneumonia-induced ARDS.17

NETs and thrombosis

A hypercoagulable state has been described in COVID-19 patients resulting in a high incidence of venous thromboembolic phenomena that contribute to the disease burden.18 NETs activate the contact pathway of the coagulation system while at the same time neutrophil elastase (a component of NETs) degrades natural antithrombotic agents such as antithrombin III and tissue factor pathway inhibitor.19 NETs are a prognostic indicator of venous thromboembolism in cancer patients and partly explain the hypercoagulable state associated with cancer.20 An animal model has shown that aberrant production of NETs causes microvascular thrombi particularly in the lungs.21

NETs and the COVID-19 cytokine storm

A proportion of COVID-19 patients develop a dysregulated release of pro-inflammatory cytokines that is termed a cytokine storm. Onset of this disease state in COVID-19 patients is associated with high mortality, and suppression of these overactivated cytokines is a therapeutic target of current interest. NETs have been shown to induce macrophages to secrete interleukin-1 (IL-1), which in turn induces IL-6.22 , 23 Both these ILs are seen as key players of the cytokine response, and antagonists to these cytokines (tocilizumab and anakinira) are currently being investigated in COVID-19 patients. Decreasing NET formation may help to dampen the upstream signal stimulating the release of these cytokines.

NETs as a therapeutic target

A recombinant DNAase (Dornase Alfa) is currently licensed for use in cystic fibrosis patients where it functions to dissolve NETs present in sputum and hence reduce the associated viscosity.24 Its use has been suggested in COVID-19 patients who may also have thick gelatinous airway secretions.1 Colchicine is currently being trialled in COVID-19 patients with a hypothesis that it may reduce neutrophil recruitment and hence NET formation (ClinicalTrials.gov identifiers: NCT04326790, NCT04328480, NCT04322565, NCT04322682).

Lidocaine as a potential therapy

The local anaesthetic drug lidocaine has been shown to reduce markers of netosis.25 This prospective RCT looked at the influence of anaesthetic interventions on netosis expression in patients undergoing breast cancer surgery. Subjects who received a lidocaine infusion, commencing at induction and continuing for 24 h postoperatively, had lower levels of Cit-H3 detected in plasma compared with well-matched control subjects who did not receive lidocaine. This is the first trial to show that lidocaine can positively influence the development of NETs in patients undergoing surgery. A mechanism for how lidocaine could suppress the formation of NETs has not been described but could be partly explained by its known anti-inflammatory properties.26

The evidence that lidocaine can suppress development of netosis in perioperative patients raises the possibility of repurposing it for use in COVID-19 patients. As evidence mounts that NETs play an important role in the pathological process of COVID-19, an agent that suppresses this could bring potential therapeutic benefits. Although lidocaine would not have a direct effect on the SARS CoV-2 virus, it may help to temper the immunological storm that is triggered in patients with severe disease (Fig. 1 ).

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Fig 1
Proposed mechanism of lidocaine suppression of netosis. Purple cell represents a neutrophil undergoing netosis. G-CSF, granulocyte colony stimulating factor; G-CSF R, granulocyte colony stimulating factor receptor; HMGB-1, high mobility group box-1; TLR-4, Toll-like receptor-4.

Lidocaine infusions have a strong record of safety in clinical medicine. They are frequently used in chronic pain conditions and in gastrointestinal surgery where they have been shown to reduce postoperative opioid requirements and enhance bowel recovery.27 , 28 We hypothesise that lidocaine infusion in COVID-19 patients may decrease the formation of NETs and modulate the severity of disease.

Apart from its primary role as a local anaesthetic agent, lidocaine exhibits cytoprotective properties. Its ability to delay the onset of ischaemia-related potassium efflux may explain its benefit in animal models of brain injury.29 In addition, lidocaine has been shown to exhibit a number of anti-inflammatory properties. The ability of lidocaine to inhibit high mobility group box-1 (HMGB-1),30 and granulocyte colony stimulating factor (G-CSF) merits further research as both HMGB-1 via Toll-like receptor 4 (TLR-4)31 and G-CSF32 are key mediators in the initiation of netosis.33

Triggering of netosis is a complex process that can occur through a variety of mechanisms. The generation of reactive oxygen species (ROS) is a well-described pathway with some evidence suggesting that commonly used anaesthetic drugs such as propofol may suppress ROS and subsequent NET formation in healthy volunteers.34 However, netosis can also occur through ROS-independent pathways such as the HMGB-1 and G-CSF pathways. The primary pathway of netosis in COVID-19 patients is not currently known.

Important limitations should be highlighted with this proposal. The current evidence for lidocaine in suppressing netosis is in the perioperative setting. Here it is the surgical stress response that triggers formation of NETs. The mechanisms by which netosis occurs are not fully understood and possibly differ between patients undergoing surgery and those with viral pneumonia.

The optimum timing and duration of administration of lidocaine with a view to suppressing netosis is unknown. Furthermore, it is not known if this results in longer-term clinical benefits once the infusion is stopped. The work by Galoș and colleagues25 showed that lidocaine can suppress a biomarker of netosis at 24 h after surgery, but whether this translates into meaningful clinical benefits for patients was not answered. However, we do know that higher levels of NETs in the postoperative setting correlate with disease progression in cancer surgery and a higher incidence of venous thromboembolism.35 , 36

References

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Interesting timing. I’ve just had a blood test back and I’ve got extremely low neutrophil count. Any idea on what kind of lidocaine dosage (and any other ideas for that matter), of ways to increase neutrophils and improve the immune response?
 

Miso

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Interesting timing. I’ve just had a blood test back and I’ve got extremely low neutrophil count. Any idea on what kind of lidocaine dosage (and any other ideas for that matter), of ways to increase neutrophils and improve the immune response?

Dosage and safety of nebulized lidocaine​

"Nebulized solutions varying in concentration from 1% to 4% have been studied and used without major side effects on patients [29]. Studies have found that large doses of lidocaine inhalation up to 575 mg are quite safe [29]. Lidocaine has short half-life; using nebulized lidocaine every 4–6 h in a dose of 4% Lidocaine in 2 ml saline will achieve between 320 and 480 mg of a daily dose of lidocaine. Studies have been done to evaluate the plasma level of nebulized lidocaine; 400–525 mg of nebulized lidocaine produced peak levels of 1.1 and 1.4 mcg/ml, respectively, which is far below the 5 mcg/ml level associated with toxicity [32], [33]. Lidocaine has been safely administered to patients with COVID-19 infection to manage cough during intubation and extubation [34], and prevent potential cardiac complications of chloroquine, hydroxychloroquine or azithromycin [35]."

"Common adverse effects are unpleasant taste, throat and mouth irritation, and oropharyngeal numbness [36]. Numbness of the oropharynx with lidocaine use could theoretically predispose patients to micro-aspiration and subsequently secondary bacterial infections; however, earlier studies demonstrated inhibitory actions of lidocaine on various strains of bacteria which suggests a prophylactic rule of lidocaine against bacterial infections [19], [37]."

"The risk of bronchoconstriction is still controversial. Some studies have showed that extensive use of 10% lidocaine infusion may cause reflex bronchoconstriction in asthmatics [38], [39], other studies found no effect on the airways [36], [40] and it appears that route of administration may be important in this adverse outcome (nebulized being safer). If patients suffer from asthma or hyperreactive airway, it may be reasonable to pre-administer a bronchodilator which usually prevents the potential of a bronchospasm induced by lidocaine [39]."
 

Regina

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Dosage and safety of nebulized lidocaine​

"Nebulized solutions varying in concentration from 1% to 4% have been studied and used without major side effects on patients [29]. Studies have found that large doses of lidocaine inhalation up to 575 mg are quite safe [29]. Lidocaine has short half-life; using nebulized lidocaine every 4–6 h in a dose of 4% Lidocaine in 2 ml saline will achieve between 320 and 480 mg of a daily dose of lidocaine. Studies have been done to evaluate the plasma level of nebulized lidocaine; 400–525 mg of nebulized lidocaine produced peak levels of 1.1 and 1.4 mcg/ml, respectively, which is far below the 5 mcg/ml level associated with toxicity [32], [33]. Lidocaine has been safely administered to patients with COVID-19 infection to manage cough during intubation and extubation [34], and prevent potential cardiac complications of chloroquine, hydroxychloroquine or azithromycin [35]."

"Common adverse effects are unpleasant taste, throat and mouth irritation, and oropharyngeal numbness [36]. Numbness of the oropharynx with lidocaine use could theoretically predispose patients to micro-aspiration and subsequently secondary bacterial infections; however, earlier studies demonstrated inhibitory actions of lidocaine on various strains of bacteria which suggests a prophylactic rule of lidocaine against bacterial infections [19], [37]."

"The risk of bronchoconstriction is still controversial. Some studies have showed that extensive use of 10% lidocaine infusion may cause reflex bronchoconstriction in asthmatics [38], [39], other studies found no effect on the airways [36], [40] and it appears that route of administration may be important in this adverse outcome (nebulized being safer). If patients suffer from asthma or hyperreactive airway, it may be reasonable to pre-administer a bronchodilator which usually prevents the potential of a bronchospasm induced by lidocaine [39]."
Thx for posting this.
Whenever Dr Peat mentions lidocaine, I think, "well, how would this be taken?"
 

golder

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Thx for posting this.
Whenever Dr Peat mentions lidocaine, I think, "well, how would this be taken?"
I’ve never actually used a nebuliser. I’ve got some lidocaine powder - forgive the naïveté but is it easy to go from pure powder to nebuliser ready, lol. How does one do it?
 
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