The Student Who Ate 5-Day Old Pasta And His Liver Shut Down
Summary
TLDR视频脚本讲述了一个大学生因食用存放五天的意大利面而导致严重肝衰竭的案例。该案例探讨了食物中的细菌如何产生毒素,影响线粒体功能,导致脂肪代谢紊乱和急性肝衰竭。视频详细解释了线粒体在能量代谢中的作用,以及毒素如何干扰这一过程,最终导致患者需要肝脏移植。
Takeaways
- 🍝 视频中讨论了一个案例,一名学生因食用存放了五天的意大利面而导致肝脏完全衰竭。
- 💸 许多美国大学生通过接受大额贷款来支付高等教育费用,这在1990年代后可能成为终身债务的潜在机制。
- 🏫 大学生为了节省食物开支,可能会一次性准备一周的餐食,这可能导致食物安全问题。
- 🩺 该学生因低血糖、急性肝衰竭、黄疸、弥漫性出血等症状被送往急诊室。
- 🧬 肝脏是高度代谢的器官,负责分解化学物质、分泌胆汁、制造凝血因子等多种功能。
- 🔍 通过患者肝脏样本的分析,发现微泡性脂肪变性,这与常见的由酒精滥用、糖尿病和肥胖引起的大泡性脂肪变性不同。
- 🦠 导致肝衰竭的细菌是土壤中常见的蜡样芽孢杆菌,其产生的毒素专门针对线粒体,阻止其使用脂肪产生能量。
- 🔋 线粒体是细胞的能量工厂,蜡样芽孢杆菌产生的毒素(cereulide)导致线粒体内钾离子异常流入,破坏了能量生产过程。
- 🚨 由于线粒体功能障碍,肝脏无法正常处理脂肪,导致急性肝衰竭,如果不及时治疗,可能会导致死亡。
- 📚 视频还提到了医学教育中关于食物中毒的教训,强调了正确理解食物处理和保存的重要性。
Q & A
为什么大学生可能会选择吃存放了五天的意大利面?
-大学生可能会因为经济原因选择吃存放了五天的意大利面,因为意大利面价格便宜,而且提前准备一周的餐食可以节省时间和金钱。
在视频中提到的学生因为吃了五天前的意大利面而出现了什么健康问题?
-学生因为吃了五天前的意大利面而出现了急性肝衰竭,导致他的肝脏完全停止工作。
为什么吃了五天前的意大利面会导致急性肝衰竭?
-五天前的意大利面上生长的细菌产生了一种名为cereulide的毒素,这种毒素专门针对线粒体,阻止线粒体使用脂肪产生能量,导致脂肪在肝脏中迅速积累,最终导致急性肝衰竭。
线粒体在细胞中扮演什么角色?
-线粒体是细胞的能量工厂,负责产生大部分ATP(三磷酸腺苷),这是细胞能量的主要来源。
cereulide毒素是如何影响线粒体功能的?
-cereulide毒素是一种钾离子载体,它与线粒体内膜结合,允许钾离子自由流入线粒体基质,这会干扰线粒体的氧化磷酸化过程,导致ATP合成受阻,线粒体肿胀并破裂,引起肝细胞坏死。
为什么在视频中提到了Pepto-Bismol(胃乐)?
-在视频中提到了Pepto-Bismol是为了简要说明水杨酸盐(salicylates)的作用,它是一种氧化磷酸化的解偶联剂,在过量摄入的情况下可能会导致微泡性脂肪肝,因为它消耗了辅酶A(CoA),从而影响了脂肪的活化和β-氧化。
为什么视频中提到了ATP合成的电子传递链?
-电子传递链是ATP合成的关键过程,它通过一系列复杂的蛋白质复合体将电子从高能状态传递到低能状态,同时推动质子(氢离子)通过ATP合酶,释放能量合成ATP。
在视频中提到的微泡性脂肪肝(microvesicular steatosis)与常见的大泡性脂肪肝(macrovesicular steatosis)有何不同?
-微泡性脂肪肝的特点是脂肪在肝细胞中以小泡的形式积累,而大泡性脂肪肝则是脂肪在肝细胞中以大泡的形式积累,通常与酒精滥用、糖尿病和肥胖有关。
为什么视频中提到了20岁男性的健康问题?
-视频中提到20岁男性的健康问题是为了强调在这个年龄段,慢性疾病并不常见,因此急性肝衰竭更可能是由于某种特定的原因,如摄入了某种有害物质。
在视频中,为什么提到了肝脏的功能和它在代谢中的作用?
-肝脏是高度代谢活跃的器官,负责分解化学物质、分泌胆汁、制造凝血因子、处理蛋白质等多种功能,了解这些功能有助于理解为什么肝脏受损会导致如此严重的后果。
Outlines
📚 深入探讨教育贷款与健康问题
Dr. Bernard(别名Chubby Emu)介绍了他的第二频道Heme Review,该频道深入讨论主频道未涉及的话题,并提供音频播客格式。他回顾了2019年的一个案例,涉及一名大学生因食用五天前的意大利面而导致肝脏衰竭。这名学生的案例反映了许多美国年轻人为了高等教育而背负巨额贷款的现象,这可能成为他们一生的债务。Dr. Bernard讨论了大学生为节省开支而提前准备一周食物的普遍做法,以及这种习惯如何导致食物中毒的风险。他详细描述了该学生的病状,包括低血糖、肝脏衰竭的征兆,以及紧急情况下的医疗响应。
🍝 五天意大利面与肝脏衰竭的联系
Dr. Bernard讨论了五天意大利面如何可能导致肝脏衰竭。他解释了肝脏的代谢功能,包括处理食物、分泌胆汁、制造凝血因子和处理蛋白质。他提到,肝脏需要大量能量来执行这些功能,而脂肪是细胞的能量来源。通过患者肝脏样本的分析,发现微泡性脂肪变性,这是脂肪在肝脏细胞中的异常积累。Dr. Bernard推测,由于细胞无法处理脂肪,导致能量生产受阻,最终导致肝脏衰竭。他进一步解释了细菌如何在五天的意大利面上生长,并产生针对线粒体的毒素,阻止能量的产生,导致急性肝脏衰竭。
🧬 线粒体功能障碍与ATP产生
Dr. Bernard深入探讨了线粒体在细胞能量生产中的作用,特别是电子传递链和ATP合成酶如何协同工作以产生ATP。他解释了NADH如何在线粒体中产生,以及它如何参与脂肪酸的β-氧化过程。他讨论了脂肪酸如何转化为乙酰辅酶A,这是进入三羧酸循环(TCA循环)的关键步骤。Dr. Bernard还提到了由于线粒体功能障碍导致的ATP产生减少,以及这如何导致肝脏细胞的坏死和肝脏衰竭。
🏥 肝脏衰竭的临床影响与治疗
Dr. Bernard描述了肝脏衰竭的临床影响,包括凝血因子的减少导致的广泛出血、氨在血液中的积累导致的脑水肿和颅内高压。他讨论了如果没有及时进行肝脏移植,患者将无法存活。他还回顾了之前视频中添加的关于患者服用Pepto-Bismol(含有水杨酸铋)的情况,这种药物在过量时可能导致线粒体功能障碍和微泡性脂肪变性。Dr. Bernard强调了在医学实践中,必须基于当前信息做出决策,因为情况往往是复杂的,并且存在许多未知因素。
Mindmap
Keywords
💡急性肝衰竭
💡Bacillus cereus
💡线粒体功能障碍
💡五天的意大利面
💡低血糖
💡脑病
💡肝脏代谢功能
💡cereulide毒素
💡微脂滴性脂肪变性
💡能量代谢
Highlights
Dr. Bernard(Chubby Emu)在Heme Review频道深入探讨了在主频道未涉及的话题。
2019年讨论了一个案例,一名学生吃了五天前的意大利面后肝脏完全衰竭。
许多美国大学生接受大额贷款支付高等教育费用,这可能成为他们一生的债务。
意大利面价格便宜,大学生为了节省食物开支,有时会准备一周的餐食。
患者因食用五天前意大利面导致严重肝衰竭,朋友曾开玩笑说他可能会死于食物中毒。
肝衰竭的初步症状包括低血糖,但不足以确定为急性肝衰竭。
患者是一名20岁的大学生,因腹痛、恶心、呕吐和全身出血被送往急诊室。
20岁的男性不太可能患有常见于65岁以上人群的慢性疾病。
急性肝衰竭通常需要长时间发展,但在年轻人中可能因不同原因迅速发生。
患者血液中的AST和ALT水平高,出现神经症状和黄疸,但之前没有肝脏疾病。
患者可能摄入了导致急性肝衰竭的物质,考虑到年龄和社会人口统计学特征,可能是在大学环境中。
患者没有饮酒或使用刺激剂的迹象,呼吸正常,因此排除了某些药物的影响。
患者可能食用了导致急性肝衰竭的食物,特别是五天前的意大利面。
肝脏是高度代谢的器官,负责分解化学物质、分泌胆汁、制造凝血因子等。
患者的肝脏样本显示微泡性脂肪变性,与常见的大泡性脂肪变性不同。
微泡性脂肪变性与线粒体功能障碍有关,可能是由于细胞内脂肪处理和能量产生的障碍。
患者食用的五天前意大利面上的细菌是导致肝衰竭的原因,特别是产毒的芽孢杆菌。
芽孢杆菌产生的毒素专门针对线粒体,阻止其使用脂肪产生能量,导致脂肪积累和急性肝衰竭。
线粒体是细胞的能量工厂,其功能障碍会导致ATP合成减少,进而影响细胞功能。
患者因线粒体功能障碍导致肝细胞坏死,最终导致功能性肝衰竭。
患者因肝衰竭导致全身出血,因为肝脏无法产生足够的凝血因子。
患者因肝衰竭导致氨在血液中积累,流向大脑,引起脑水肿和颅内高压。
患者最终因急性肝衰竭死亡,尸检发现其肠道内容物、肝脏和加热意大利面的锅中有芽孢杆菌。
Dr. Bernard在视频中提到,患者还服用了大量Pepto-Bismol,这可能与肝衰竭有关。
Pepto-Bismol中的水杨酸盐可能干扰线粒体功能,导致ATP合成减少和脂肪积累。
Dr. Bernard强调,医学中存在许多未知和时间敏感的因素,需要基于当前知识做出决策。
Transcripts
hi everyone dr bernard here you might
know me as chubby emu this is my second
channel heme review where i go more in
depth on topics that aren't otherwise on
the main channel these episodes are also
available in audio only podcast format
link in the description below i post
here when i can sometimes alongside
chubby emu videos so if you subscribe
you'll get notifications when i do in
2019 i discussed a case about a student
who ate five-day-old pasta and his liver
completely shut down link to that video
is in the description below
aj the student was like a lot of
american people his age who went to
college in his time accepted a large
loan to pay for higher education that
depending on career choice where they
land who they met along the way or knew
beforehand and elements of luck and hard
work could serve the main purpose of
upwards socioeconomic mobility based on
scholastic merit but after the 1990s
served as a potential mechanism to
indebt someone for their entire life the
association with this machinery might be
something completely unknown to people
hundreds of years down the line but what
we do know is that pasta is cheap one
can save money on food that's a heavy
driving factor for college students and
some people like to prepare all of their
meals for the week in advance so they
don't have to think about it the
patient's practices led his friends to
joke that one day he would die of food
poisoning except this time it wasn't
going to be a joke when i started to
describe the liver failure i started
with hypoglycemia
that tells you a little probably not a
lot it's a non-specific description and
by itself it's not enough to know that
someone has acute hepatic failure i
spent maybe a whole week writing that
part and the entire video couldn't
proceed until i rectified it it really
could have gone several different ways
but starting with low sugar presence in
blood i found was the quickest way to
get to the point that i needed to for
general audience blood sugar as an idea
is in common language and it's easier to
grasp by a majority of people than
encephalopathy the word itself being
intimidating and the idea of
international normalized ratio there's
an overhead that's associated with going
that route that'll make the video longer
what's inr or prothrombin time what's
hepatic encephalopathy why does it
happen how does it happen how about
liver enzymes what's an enzyme that's
the overhead it's all technical okay so
in context of liver failure in the very
beginning of the case i tell you some
really big details aj is a 20 year old
man presenting to the emergency room
with abdominal pain nausea and diffuse
bleeding
paramedics were scrambling because he
kept vomiting in the ambulance until he
fell unconscious abdominal pain with
extreme nausea vomiting something
abdominal falling unconscious something
neurological diffuse bleeding he didn't
just get a cut somewhere it's diffuse so
he's bleeding in many different places
why would he be bleeding like that this
is someone who also has jaundice first
two sentences of the video tells you a
lot this is not a borderline case it's
an extreme one neuro exam unconscious
unarousable unresponsive to pain diffuse
bleeding so something systemic something
is wrong airway is fine breathing is
okay circulation all right heart rate
and rhythm normal in that first sentence
i also tell you that he's a 20 year old
man who is described as a student in the
title 20 is a little too old to be in
high school so this is someone at the
university undergraduate level what can
you tell me about health problems in 20
year old men
20s pretty young to have chronic
diseases that are common in people over
65 years old if we're looking at heart
attacks a 20 year old having a heart
attack is more often than not going to
have one for a different reason than a
70 year old liver damage usually takes a
long time to happen so liver failure
happening between the two age groups is
likely going to be for very different
reasons and this is acute liver failure
high ast alt in the blood neurologic
signs and symptoms jaundice hypoglycemia
no known prior liver disease so what
would be a cause of liver failure in a
previously healthy 20 year old man i
could go into all the things like
autoimmune hepatitis or ischemic
hepatopathy or scorpion sting right in
the middle of winter outside of
baltimore everything put together this
is very likely something happening due
to this person ingesting and putting
something in their body what are some
things that a 20 year old might ingest
okay heart rate and rhythm are normal so
it doesn't look like there's stimulant
use he's breathing normally so probably
not opioids because that would be
respiratory depression so what else
would you think of did he drink
something maybe that could be likely
given age and social demographic being
in college setting if it was to the
point of causing acute liver failure you
might be able to smell it off of his
breath if it happened recently enough
but in this case we know he didn't drink
any liquor did he eat something now
we're talking
one thing that i find interesting in
looking at tweets that come up randomly
about this case and the associated ones
is that this case is often met with a
lot of fear it's something that's taught
in medical pharmacy and nursing schools
because of its nature students tend to
remember that reheating pasta and rice
is dangerous
unfortunate that that ends up being the
takeaway because that's not what this
case is about
very generally reheating pasta and rice
after a day or two or three and it's
been refrigerated the whole time within
a couple of hours after it was made is
not going to cause problems so with that
how would sketchy five-day-old pasta
that was left out for at least a whole
day cause liver failure so severe that
the person eating it will die from it i
set this line in the chubby emu video
you see the liver is a highly metabolic
organ you can't live for very long
without one everything that enters your
mouth ends up in the liver as it breaks
down chemicals and red blood cells
secretes bile for digestion makes blood
clotting factors that stop you from
bleeding and processes proteins among
other functions and it maintains blood
sugar levels bringing us back to
metabolism when you think of something
being metabolically active you think of
metabolism of heat of movement the
breaking and creation of chemical bonds
involving a lot of energy being produced
and consumed an energy factory could be
called a powerhouse and because we know
that the mitochondria is the powerhouse
of the cell
now we're talking a sample of the
patient's liver revealed microvesicular
steatosis microbe meaning small vesicle
referring to a sac or a vacuole a space
and steat referring to fats or lipids
and osis meaning a disorder of a
disorder of fat contained in small sacs
this is different from
macrovesicular steatosis where the sacs
are big and they're so big that the
nucleus of the cell gets pushed off to
the side you can see that underneath a
microscope macro vesicular steatosis is
common and associated with alcohol
misuse diabetes and obesity
microvesicular
is not as common so we're talking about
the liver the liver needs a lot of
energy to function this patient had
liver failure cells use fats as an
energy source but in these samples we
see an inappropriate presence of fat in
the liver from this information we can
take one guess that fats entered the
liver cells like how they normally do
but something happened so that those
cells couldn't process and handle the
fats causing them to quickly build up
without being able to produce energy
from fats some machinery in the cell was
disturbed and couldn't make up for this
loss resulting in the big picture result
of the liver shutting down in the
extreme case that a hundred percent of
the liver no longer functions wastes in
the blood that are normally processed by
the liver accumulate quickly among them
is ammonia from gut bacteria processing
proteins and this causes disturbances in
cerebral osmolytes this results in more
water entering the brain than is normal
causing cerebral edema intracranial
hypertension herniation and then it's
over so what was that something that
happened so that cells couldn't process
and handle the fats well it was bacteria
that grew on the five-day old pasta but
it was bacillus cereus which is commonly
found in soil if it causes an illness
from food it's usually self-limiting so
it's more than just the bacteria some
strains can produce a toxin that
specifically targets the mitochondria
preventing the mitochondria from using
fats to create energy causing the
buildup and causing the acute liver
failure
in the mitochondria we have atp
production a majority of it being the
product of the electron transport chain
where protons re-enter the matrix by
traveling through a pore in atp synthase
and the energy released in that process
is used to make atp for reference the
matrix is the innermost part of the
mitochondria the inter-membrane space is
inside the mitochondria but outside the
matrix going upstream the process if atp
production ends with protons re-entering
the matrix because a gradient was
created then something must have caused
them to be pushed out of the matrix and
into the inter-membrane space if protons
were moved and those are positive
charges then we could make a guess that
electrons which are negative charges
were involved and we know in the process
of atp production there's the electron
transport chain four complexes big
proteins starting with nicotinamide
adenine dinucleotide nadh the reduced
form and it gets oxidized so two
electrons are removed and transferred to
a compound called ubiquinone the quinone
moiety is a conjugated cyclic dione so
there's two carbon double bond o's in a
structure with delocalized electrons
gaining two electrons means that the
charge becomes negative so to neutralize
it two protons are accepted and
ubiquinone becomes ubiquinol and then it
diffuses across the membrane in the
united states you see commercials
everywhere on tv for coq10 supplement
and that is ubiquinol as this conversion
happens the electron current passing
through complex one powers the active
transport so remember it's creating a
gradient of four protons in the inter
membrane space but where does nadh come
from
going upstream the process we have the
tricarboxylic acid tca cycle which
reduces nad to nadh this is all the
stuff that you learned in school
multiple times and depending on where
you end up may or may not have applied
to you you have had to memorize it
multiple times for a test without any
context of why but really all of those
times that you learned it were for
situations like this where it absolutely
applies here and it's good that you know
about it even if you don't remember it
all from school to enter the tca cycle
you need acetyl coa where does acetyl
coa come from there's one pathway where
it comes from glucose but there's
another pathway where it comes from fats
and remember we know that there's a
dysfunction of creating atp and the
pathological findings show an
inappropriate accumulation of fats in
the form of microvesicular steatosis so
this brings us to how the toxin from the
bacteria in five day old pasta caused
feminine hepatic failure to get acetyl
coa from fatty acids the pathway is
going to appear boring but there's
important steps in between that entire
diseases are based off of triglycerides
and fatty acids get converted to acyl
coa by acyl coa synthetase acyl is a
general term describing a double bond
oxygen and carbon and an alkyl group so
the number of carbons is not specific it
could be a couple it could be a lot in
any given sample you're going to have a
wide variety of different quantities
really long fatty acids which have a lot
of carbons can't cross the mitochondrial
membrane on their own but there's a
shuttle for it mediated by carnitine
diseases can happen here if there's
something wrong with the carnitine
transporter a problem with the carnitine
palmitoyl transferase enzyme that places
the carnitine on the fatty acid in or
outside the mitochondria these are all
diseases of metabolism so you can expect
highly metabolic tissue like the liver
the heart the brain to be affected in
patients who have it carnitine is bound
to the fatty acid and shuttled into the
mitochondria where the carnitine is then
taken off and acyl co-a is reformed
again and this is where it's converted
to acetyl coa through beta oxidation
completing our cycle but if we're
looking at a problem where fat is
building up into vesicles and we're
assuming that the person didn't have any
deficiencies upstream of the cycle at
this point then it's here where the
problems can form and this is called
fatty acid beta oxidation beta referring
to the second carbon from the carbonyl
group or carbon number three if you're
counting carbons starting from the
carbonyl in that first step there's
three isozymes very long chain acyl coa
dehydrogenase medium chain acyl coa
dehydrogenase and short chain acyl coa
dehydrogenase you can be born with
deficiencies of these enzymes and it's
not that uncommon medium chain acyl-coa
dehydrogenase deficiency has a
prevalence of 1 in 20 000 live births so
what happens if someone has a deficiency
for medium chain they would have primary
inhibition of fatty acid beta oxidation
what does that look like let's say it's
a kid and he's a really picky eater
mom's not having any of it she says you
know what if you don't want to eat this
dinner i'm not cooking anything extra
and i'm not going to buy you mcdonald's
chicken nuggets guess you're just going
to have to wait until morning to eat so
the kid's liver will start tapping
glycogen stores to provide glucose to
make acetyl coa to feed into the cell
machinery to produce atp but as the
hours pass those sugar stores are
getting more and more depleted and it's
harder to get a quick source acetyl-coa
provides the acetyl group for ketones
and those can be used for energy but
acetyl-coa is the precursor the
medium-chain acyl-coa dehydrogenase
deficiency which is putting a hard limit
on acetyl-coa production
that limits atp production causing a
metabolic acidosis hypoglycemia is
happening because the kid hasn't eaten
but also can't use his fat stores
because of this inhibition of fatty acid
oxidation cytoplasmic fatty acids are
converted to triglycerides which
accumulate and produces microvesicular
steatosis in the liver bringing us back
to the student who ate five-day-old
pasta the toxin made by that strain of
bacteria is called cereulide again
uncommon strain that develops from the
right conditions on rice and pasta
cereulide from what we understand is a
potassium ionophore it's a cyclic
peptide that binds to the mitochondrial
inner membrane and allows potassium to
flow freely into the matrix on the
mitochondrial inner membrane there is a
hydrogen potassium exchanger that is to
pump potassium out of the matrix and
bring hydrogen into the matrix but
there's two problems with that as an
ionophore the amount of potassium let in
would overwhelm this exchanger and not
only that remember the electron
transport chain happens here the
electron transport chain pumps hydrogen
out so that it can flow through a pore
and atp synthase to make atp so
importing hydrogen into the matrix
because you need to get rid of excess
potassium would mean that you're
disturbing the gradient that's being
created by the electron transport chain
the introduction of a lot more potassium
than normal into the matrix starts to
raise the ph of the matrix because
protons are getting pumped out while
potassium flows in
remember the electron transport chain
happens because of proteins which are
adapted to certain ph
if this changes then you could guess
that the complex's ability to function
would change because proteins can change
in different ph and there's also some
evidence that ubiquinone would also
stabilize which would then not move
electrons impairing atp synthesis as
more and more potassium floods into the
hepatocyte mitochondria oxidative
phosphorylation becomes uncoupled
reactive oxidative species form because
oxygen is supposed to be the final
electron acceptor but it can't do that
anymore the mitochondria swell up and
rupture causing hepatocellular necrosis
extensive necrosis results in functional
liver failure before the cell lysis
blebs form in the cell membrane and
enzymes start leaking out as the blebs
coalesce the cell dies and leaks out all
its contents as the liver fails it
doesn't produce the right amount of
blood clotting factors which can result
in diffuse bleeding the liver doesn't
process the ammonia that's produced by
the gut breaking down the proteins as
the ammonia flows into the liver from
the portal circulation it's supposed to
be detoxified to glutamine and urea by
the urea cycle which happens to be
another branch of the acetyl-coa
breakdown pathway but the liver is
failing and the processes are all
overloaded and normal function is not
attained ammonia spills into the blood
and flows to the brain where glutamine
synthetase in the astrocytes convert
ammonia with glutamate into glutamine
which is a cerebral osmolite causing
cerebral edema and without a liver
transplant in time nothing can be done
enough and in time to prevent what will
happen because at autopsy the bacteria
from the patient's intestinal contents
his liver and also residue from the pan
used to reheat his pasta were cultured
and it was found to be bacillus serious
the final note that i want to add here
is that in the chubby emu video at the
time i added in that the patient drank a
whole bottle of pepto-bismol to the case
because i wanted to teach briefly about
salicylates pepto-bismol is bismuth
subsalicylate being an uncoupler of
oxidative phosphorylation in the setting
of overdose it appears that it could
lead to microvesicular steatosis because
it consumes co-a which would then mean
that acetyl-coa would have trouble being
produced so there would be a decreased
fatty acid activation from low coe
levels leading to decreased beta
oxidation adding in that dual blockade
in my mind was that there would be no
question that the liver failure was
complete from a dual blockade of the
same pathway
unfortunately i could see many comments
couldn't deal with that they would go so
far as to say that it was only the
bottle of pepto-bismol that caused that
liver failure that the pasta meant
absolutely nothing but that reveals to
me that those people commenting entirely
missed everything about cerealide about
a massive intra mitochondrial shift of
potassium from a cyclic peptide acting
as an ionophore causing mitochondrial
dysfunction it didn't help that the news
articles covering the story at the time
just said that it was food poisoning
without explaining that a special strain
of bacteria that's common produced a
toxin that made this food poisoning so
much worse than normal it taught me a
lesson that two ideas at the same time
that are interwoven and related
sometimes won't be processed my videos
since 2019 have reflected that lesson
learned but the reality is in medicine
there's a lot of ifs and there's a lot
of unknowns that are time sensitive at
that particular point in time the big
bucks are made because things more often
than not are borderline and you have to
make a decision on which way to go based
on what you know at that point in time
not very many things are so obviously
unipolar and in just one dimension but
that's a quick review of microvesicular
steatosis and feminine hepatic failure
that occurred because of someone who ate
five-day-old pasta by accident
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