Show starts at 2:37.
The last caller (starting at 56:55) asked about vaccines, febrile seizures and Tylenol: "is this a vaccine problem, or a Tylenol problem?"
RP: "Tylenol has very serious side effects. For example, Prenatal use of Tylenol is well-associated with the increased risk of autism. It's a matter of toxic effects. Any inflammation during gestation, or poisoning by something such as Tylenol, will increase birth defects and neurological defects such as autism." [...] "They warn people not to use aspirin before getting vaccinated, because aspirin actually defends against the harmful effects of vaccines. But Tylenol is poisonous enough that it doesn't protect very well against the inflammatory damage."
Question for you all: what are your experiences with Tylenol? After the show I messaged my Canadian friend to caution her again about Tylenol, and said that if she had to take something Ibuprofen would probably be safer. She wrote back to say she'd taken some Tylenol earlier that day, and had gotten dizzy, but didn't connect the dizziness to the pills until I'd messaged. Someone else told me today that she'd taken Aleve when her knees were at their worst, before the replacements. Is Aleve any better than ibuprofen?
After this show I emailed Dr. Peat about Tylenol. He didn't answer my specific questions, but I think he figured out what I was actually asking. This was his response:
The last caller (starting at 56:55) asked about vaccines, febrile seizures and Tylenol: "is this a vaccine problem, or a Tylenol problem?"
RP: "Tylenol has very serious side effects. For example, Prenatal use of Tylenol is well-associated with the increased risk of autism. It's a matter of toxic effects. Any inflammation during gestation, or poisoning by something such as Tylenol, will increase birth defects and neurological defects such as autism." [...] "They warn people not to use aspirin before getting vaccinated, because aspirin actually defends against the harmful effects of vaccines. But Tylenol is poisonous enough that it doesn't protect very well against the inflammatory damage."
Question for you all: what are your experiences with Tylenol? After the show I messaged my Canadian friend to caution her again about Tylenol, and said that if she had to take something Ibuprofen would probably be safer. She wrote back to say she'd taken some Tylenol earlier that day, and had gotten dizzy, but didn't connect the dizziness to the pills until I'd messaged. Someone else told me today that she'd taken Aleve when her knees were at their worst, before the replacements. Is Aleve any better than ibuprofen?
After this show I emailed Dr. Peat about Tylenol. He didn't answer my specific questions, but I think he figured out what I was actually asking. This was his response:
Tylenol damages the electron transport chain in mitochondria, producing reactive oxygen species. Increased concentration of PUFA can amplify the damage caused by ROS.
Drug Discov Ther. 2021 Nov 21;15(5):278-280.
Does immunosuppressive property of non-steroidal anti-inflammatory drugs (NSAIDs) reduce COVID-19 vaccine-induced systemic side effects?
Itsuro Kazama 1 , Momono Senzaki 1
Free article
Abstract
To help stop the coronavirus disease 2019 (COVID-19) pandemic, vaccines are currently the most critical tool. However, the COVID-19 mRNA vaccines frequently cause systemic side effects shortly after the injection, such as fever, headache and generalized fatigue. In our survey, after receiving the second dose of the COVID-19 vaccine, 80% developed fever, 62% headache and 69% generalized fatigue. Among people who required antipyretics, the average durations of fever and headache were significantly shorter in those who took non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin, loxoprofen and ibuprofen, than those who took acetaminophen. In our patch-clamp studies, NSAIDs effectively suppressed the delayed rectifier K+-channel (Kv1.3) currents in T-lymphocytes and thus exerted immunosuppressive effects. Because of this pharmacological property, the use of NSAIDs should be more effective in reducing the vaccine-induced systemic side effects that are caused primarily by the enhanced cellular immunity.
Altern Med Rev. 2009 Dec;14(4):364-72.
Did acetaminophen provoke the autism epidemic?
Peter Good
Schultz et al (2008) raised the question whether regression into autism is triggered, not by the measles-mumps-rubella (MMR) vaccine, but by acetaminophen (Tylenol) given for its fever and pain. Considerable evidence supports this contention, most notably the exponential rise in the incidence of autism since 1980, when acetaminophen began to replace aspirin for infants and young children. The impetus for this shift - a Centers for Disease Control and Prevention warning that aspirin was associated with Reye's syndrome - has since been compellingly debunked. If aspirin is not to be feared as a cause of Reyes syndrome, and acetaminophen is to be feared as a cause of autism, can the autism epidemic be reversed by replacing acetaminophen with aspirin or other remedies?
Planta Med 1989; 55(5): 417-419
© Georg Thieme Verlag Stuttgart · New York
Silybin Dihemisuccinate Protects Against Glutathione Depletion and Lipid Peroxidation Induced by Acetaminophen on Rat Liver
Rolando Campos, Argelia Garrido, Ricardo Guerra, Alfonso Valenzuela
Laboratorio de Bioquímica Farmacológica, Instituto de Nutrición y Tecnología de los Alimentas. Universidad de Chile, Casilla 15138, Santiago 11, Chile
Abstract
Acetaminophen hepatotoxicity is characterized by glutathione depletion, cellular necrosis, and, in some instances, by the induction of lipid peroxidation. Silybin dihemisuccinate, a soluble form of the flavonoid silymarin, protects rats against liver glutathione depletion and lipid peroxidation induced by acute acetaminophen intoxication. Other biochemical parameters such as serum transaminases did not show the drastic increase observed under acetaminophen intoxication when animals were treated with the flavonoid. Preliminary results suggest that silybin dihemisuccinate may be another antidote against acetaminophen hepatotoxicity.
React Oxyg Species (Apex). 2018 May; 5(15): 145–158.
Oxidant Stress and Lipid Peroxidation in Acetaminophen Hepatotoxicity
Hartmut Jaeschke and Anup Ramachandran
Abstract
Acetaminophen (APAP) overdose is the most frequent cause of liver injury and acute liver failure in many western countries. The mechanism of APAP-induced hepatocyte necrosis has been investigated extensively. The formation of a reactive metabolite and its binding to cellular proteins was initially thought to be responsible for cell death. A competing hypothesis was introduced that questioned the relevance of protein binding and instead suggested that P450-derived oxidant stress and lipid peroxidation causes APAP-induced liver injury. However, work over the last 15 years has reconciled some of these apparent contradictory hypotheses. This review summarizes the present state of knowledge on the role of reactive oxygen species (ROS) in APAP hepatotoxicity. Detailed investigations into the sources and relevance of the oxidant stress have clearly shown the critical role of the electron transport chain of mitochondria as main source of the oxidant stress. Other potential sources of ROS such as cytochrome P450 enzymes or NADPH oxidase on phagocytes are of limited relevance. The mitochondria-derived superoxide and peroxynitrite formation is initiated by the binding of the reactive metabolite to mitochondrial proteins and the amplification by mitogen activated protein kinases. The consequences of this oxidant stress are the opening of the mitochondrial membrane permeability transition pore with cessation of ATP synthesis, nuclear DNA fragmentation and ultimately cell necrosis. Lipid peroxidation is not a relevant mechanism of cell death but can be a marker of ROS formation. These mechanistic insights suggest that targeting mitochondrial oxidant stress is a promising therapeutic option for APAP hepatotoxicity.