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Posted on 09/16/2026 7:13:44 PM PDT by doc maverick
“A rare and potentially deadly brain disorder has been recorded in people taking weight loss drugs, a new study warns. Wernicke encephalopathy is a neurological condition that causes severe confusion and disorientation, which continue to worsen without treatment…. A rare and potentially deadly brain disorder has been recorded in people taking weight loss drugs, a new study warns. Wernicke encephalopathy is a neurological condition that causes severe confusion and disorientation, which continue to worsen without treatment.”
(Excerpt) Read more at dailymail.com ...
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Are they using those drugs in China?
I don’t care. I’ll be a good looking corpse.
“Wernicke encephalopathy is a neurological condition that causes severe confusion and disorientation”
Now we know the root cause of Democrat Socialists and so many Democrats.
Weight problem? Take a pill.
Sleep problem? Take a pill.
Mental problem? Take a pill.
I think I see the problem......
I’m not surprised either. I’ve seen a number of people who take these drugs. And, yes, the vast majority of them have gotten very thin. Especially considering that most were obese at the start. However, being thin does not mean looking healthy. Almost to a person, they don’t look healthy to me.
There have only been a handful of cases overall, and at least some of them may have been caused by a vitamin B1 deficiency, not by the drug itself.
Why is it so many articles have repetitive text in them. Hard enough for me to read it the first time, then I have reread to see if I missed something and they were not repetitive.
Fasting, eating only one meal a day, and walking are the safe and effective alternatives for losing weight.
Just don’t eat as much and bingo with no drugs
WIKI
Wernicke encephalopathy (WE), also Wernicke’s encephalopathy, or wet brain is the presence of neurological symptoms caused by biochemical lesions of the central nervous system after exhaustion of B-vitamin reserves, in particular thiamine (vitamin B1). The condition is part of a larger group of thiamine deficiency disorders that includes beriberi, in all its forms, and alcoholic Korsakoff syndrome. When it occurs simultaneously with alcoholic Korsakoff syndrome it is known as Wernicke–Korsakoff syndrome.
Classically, Wernicke encephalopathy is characterised by a triad of symptoms: ophthalmoplegia, ataxia, and confusion. Around 10% of patients exhibit all three features, and other symptoms may also be present. While it is commonly regarded as a condition particular to malnourished people with alcohol misuse, it can be caused by a variety of diseases. It is treated with thiamine supplementation, which can lead to improvement of the symptoms and often complete resolution, particularly in those where alcohol misuse is not the underlying cause. Often other nutrients also need to be replaced, depending on the cause. Medical literature notes how managing the condition in a timely fashion can avoid worsening symptoms.
Wernicke encephalopathy may be present in the general population with a prevalence of around 2%, and is considered underdiagnosed; probably, many cases are in patients who do not have commonly-associated symptoms.
The classic triad of symptoms found in Wernicke encephalopathy is
Ophthalmoplegia: later expanded to include other eye movement disorders; typically affecting the lateral rectus muscle. Lateral nystagmus is the most commonly seen disorder, but lateral rectus palsy—usually bilateral—is common, as well.
Ataxia: later expanded to include imbalance or any cerebellar dysfunction.
Confusion: later expanded to include any neuropsychological disturbances. Prevalent in roughly eight in 10 diagnosed cases.
Korsakoff syndrome, characterised by memory impairment, confabulation, confusion, and personality changes, has a strong and recognised link with WE. A very high percentage of patients with Wernicke–Korsakoff syndrome also have peripheral neuropathy, and many people who consume excess alcohol have this neuropathy without other neurologic signs or symptoms. Korsakoff’s occurs much more frequently in WE due to chronic alcoholism. It is uncommon among those who do not consume excessive amounts of alcohol. Up to 80% of WE patients who misuse alcohol develop Korsakoff’s syndrome. In Korsakoff’s, atrophy of the thalamus and the mammillary bodies and frontal lobe involvement is usually observed. In a study, half of Wernicke–Korsakoff cases had good recovery from the amnesic state, which may take from 2 months to 10 years.
Thiamine deficiency and errors of thiamine metabolism are believed to be the primary cause of Wernicke encephalopathy. Thiamine, also called B1, helps to break down glucose. Specifically, it acts as an essential coenzyme to the TCA cycle and the pentose phosphate shunt. Thiamine is first metabolised to its more active form, thiamine diphosphate (TDP), before it is used. The body only has 2–3 weeks of thiamine reserves, which are readily exhausted without intake, or if depletion occurs rapidly, such as in chronic inflammatory states or in diabetes.
Thiamine is involved in:
Metabolism of carbohydrates, releasing energy.
Production of neurotransmitters including glutamic acid and GABA.
Lipid metabolism, necessary for myelin production.
Amino acid modification. Probably linked to the production of taurine, of great cardiac importance.
Brain lesions in WE are usually credited to focal lactic acidosis. An absence of thiamine can lead to too much pyruvate within the cells since it is not available to help convert pyruvate through the TCA cycle. An increase in pyruvate causes an increase in lactate concentration leading to focal lactic acidosis.
Lesions can be reversed in most cases with immediate supplementation of thiamine.
In 1949, the idea that WE lesions are a result of a disruption to the blood-brain barrier was introduced. Large proteins passing into the brain can put neurological tissue at risk of toxic effects. The blood-brain barrier junctions are typically found to have WE lesions located at that region of the brain.
An altered blood–brain barrier may cause a perturbed response to certain drugs and foods.
There are hospital protocols for prevention, supplementing with thiamine in the presence of: history of alcohol misuse or related seizures, requirement for IV glucose, signs of malnutrition, poor diet...
In patients suspected of WE, thiamine treatment should be started immediately. Blood should be immediately taken to test for thiamine, other vitamins and minerals levels. Following this an immediate intravenous or intramuscular dose of thiamine should be administered two or three times daily. Thiamine administration is usually continued until clinical improvement ceases.
Considering the diversity of possible causes and several surprising symptomatologic presentations, and because there is low assumed risk of toxicity of thiamine, because the therapeutic response is often dramatic from the first day, some qualified authors indicate parenteral thiamine if WE is suspected, both as a resource for diagnosis and treatment. The diagnosis is highly supported by the response to parenteral thiamine, but is not sufficient to be excluded by the lack of it. Parenteral thiamine administration is associated with a very small risk of anaphylaxis.
People who consume excessive amounts of alcohol may have poor dietary intakes of several vitamins, and impaired thiamine absorption, metabolism, and storage; they may thus require higher doses.
WE was first identified in 1881 by the German neurologist Carl Wernicke, although the link with thiamine was not identified until the 1930s.
https://en.wikipedia.org/wiki/Wernicke_encephalopathy
Wow…how come none of these people ever figured that out? You are a genius.
Pitching prescription meds direct to the consumer on TV is America’s OTHER drug problem.
Shocking! Unexpected! Who could have guessed?
Wow…how come none of these people ever figured that out? You are a genius.
My pension was reduced by $292.00 a month and that’s half my food money , lost 11 pounds in a little over a month and a half , I have no choice ,LOL
GLP 1 Signals the brain to reduce appetite . Some people never get a signal to quit eating. Since Covid I am having a weight problem because I never feel satisfied and I have urges to eat even when full . That all started when my sense of smell was diminished and never came back all the way. I am thinking about trying GLP 1
Mother’s little helper....
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