August 7, 2025 • 22 mins
Beriberi: What is it? What causes it? What are the types? In this episode, we will go over the interesting history of beriberi, the symptoms that can occur, and how we treat it. Tune in to learn more!
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References:
https://www.pbs.org/wgbh/americanexperience/features/bataan-prisoners-diseases/
https://www.who.int/news-room/fact-sheets/detail/dengue-and-severe-dengue
https://www.riken.jp/en/news_pubs/news/2015/20150806_1/
https://hormonesmatter.com/beriberi-the-great-imitator/
https://medlineplus.gov/ency/article/000339.htm
https://www.healthline.com/health/beriberi
https://my.clevelandclinic.org/health/diseases/thiamine-deficiency
https://pmc.ncbi.nlm.nih.gov/articles/PMC2889456/
https://www.imdb.com/title/tt5555342/
https://www.mayoclinic.org/diseases-conditions/scarlet-fever/symptoms-causes/syc-20377406
https://coleswildbird.com/fact-or-fiction-never-feed-rice-to-birds/
*This podcast is for entertainment purposes only. If you suspect you have a medical condition, please seek out an opinion of a medical professional.*
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:00):
Lately, you have been feeling strange. Your hands and feet are tingly. It is pretty much the only
(00:05):
thing you can feel in them. When you try to walk, it is a struggle. It feels almost as if you are
trying to drag your feet through cement. Everything hurts, especially your legs. You call your mother
to try to ask her about what may be going on. However, you struggle to get the words out,
feeling more confused than ever. When you eventually manage to tell her, she tells you that
(00:25):
that horrendous diet you have at college is not doing you any favours. You need to go and see a
doctor. Hello and welcome to Anatomy of Illness. Today's episode is about beriberi. Before we get
(00:51):
into the condition, we are going to start with the history. So why do we know beriberi exists?
In this episode, I may also refer to the condition as thiamine deficiency or B1 deficiency. Now onto
the history. For this, we are going to begin all the way back in 808 in Japan as this is where
documents have been found suggesting beriberi occurred. This is not what it was called in
(01:14):
ancient Japan though. It was known as kakké or leg disease. It was also known as this around that
time in ancient China. Between 1603 and 1867, this would have been due to the polished white rice in
the diet in Japanese cities. So rice that had the outer husk removed, which contains most of
the thiamine. This was due to the popularity of rice milling as having white rice on the table
(01:37):
symbolised affluence because it looked more presentable on the table than brown rice. Now
we are going to jump back quickly to 1629 and over to Java in Indonesia. With the first western
description of the condition, this being by Jacobus Bontius, who was a Dutch physician.
There is no real record as to who was the first to start using the Sinhalese term beriberi to
(01:59):
describe the condition, this term meaning I cannot, I cannot, but both the Dutch and the
English would use the term. The English getting the term from communications with the Dutch.
We see this with the first descriptive English account given by Thomas Christie. This was
between the late 1790s and early 1800s in what at the time was known as Ceylon but is now modern day
(02:20):
Sri Lanka. He observed the condition to primarily affect the soldiers of the English East India
Company that were recruited from the south eastern coast of India. This also being where the
condition was widely spread at the time in the local population, not just soldiers recruited
from there. He saw that this condition would affect both Europeans and Indians. Seeing many
(02:41):
cases actually affecting the white soldiers. In his descriptions, he would note that those with
the condition would suffer from paralysis of the lower limbs, edema or dropsy, dropsy being the
old term for edema type swelling. He would forward his observations to William Hunter in London who
would inquire about the Indian sailors on board their mortality rate specifically. During this
(03:02):
time, Christie was working on differentiating it from scurvy, which is another disease caused by
vitamin deficiency with a very interesting history we covered it back in episode 11.
He would comment on the absence of the swollen gums, fetid breath and spotted limbs. He would
also mention that the condition did not respond to the anti-scorbiotic lime juice, meaning it's
not scurvy. Christie would claim moisture impure air, despondency and dirtiness as contributing
(03:28):
factors for the development of beriberi. However, he primarily attributed it to a want of a
stimulating and nourishing diet. This being due to the fact that the majority of the soldiers diet
consisted of rice, hulled rice. Christie's account would mention much about the diet being a cause
and a cure of this disease. However, in Hunter's account of Lascar diseases, it became an
(03:53):
afterthought. Lascar being the soldiers that manned these ships. Moving on to the 1830s and into South
India, here we see an offer for a prize for papers written about beriberi by the Madras Medical Board.
This was done in an attempt to encourage research into beriberi due to this condition being known
to be insidious in its attack, rapid in its progress and fatal in its termination. After this,
(04:17):
four papers were written and the prize would be awarded to John Grant Malcolmson, who was, like
the others who submitted the papers, an army medical officer. He of course had his own
observations on the condition, believing that the term beriberi was actually derived from
the Hindustani word for sheep. He suggested this due to an awkward sheep-like gait that
he claimed was a characteristic of the condition. He would also note in his paper that the local
(04:42):
population did not distinguish beriberi from other conditions. The Tegulu people use the name
Timmeree waivo as a term to encompass conditions like beriberi, palsy, tingling sensations and
even rheumatism. He would describe beriberi as mostly occurring in one particular area of India
and in the soldiers stationed there. Around the same time, in 1835, a British naval surgeon
(05:06):
by the name of James Bankier would make his own comments about beriberi. However, these could be
seen as less than helpful. He referred to it as the salon palsy, suggesting both an ill-defined link
with poor vegetarian diets and hinting that the condition was contagious, like the cholera
outbreaks that were happening in the same area, describing it as a very troublesome complaint.
(05:30):
And note on this, beriberi is a vitamin deficiency. If I sneeze in your direction,
you are not going to catch a vitamin deficiency. It is not contagious. Because of other conditions
that were spreading at the time, like smallpox, malaria, and of course cholera, beriberi was a
bit like the ignored middle child. Yes, it was there, but it was not seen as an important disease.
(05:53):
It was not contagious. It was not killing as many people. We see this with the medical accounts of
the Madras famines of both 1866 and the 1876 to 1878 famine. These records focus primarily on
cholera, dysentery, malaria, and smallpox, with no mention of beriberi. When literature did mention
beriberi in the mid to late 19th century, it was often spoken of as exclusively occurring in the
(06:16):
northern Circars, this being a part of India at the time. It was considered non-contagious and
mostly blamed on climate, with the occasional suggestion of it being diet related. In the 1880s,
we would see the lectures of a former Surgeon General with the Indian Army by the name of
W.C. Maclean, discussing diseases of tropical climates over at the Netley Army Medical School.
(06:37):
His discussions on beriberi mainly talked about the condition being something that he had
predominantly seen in South India, or South Indian troops that were taken to Burma. At this time,
the cause was still obscure. However, Maclean did have some suggestions for the cause. He believed
that the condition developing could be blamed on the water, the soil, and the climate in the area,
along with poverty, insufficient food, and clothing. Interestingly enough, even at this
(07:01):
time other conditions were still being described as beriberi, when they were not the same condition,
like anemia in Assam and Ceylon. Assam being an Indian state, and Ceylon of course being again
Sri Lanka. This would change with the 1877 paper by W.R. Kynsey. “The anemia, or beriberi, of Ceylon.”
The anemia was identified as a condition caused by hookworm, which symptoms were different from
(07:27):
beriberi. In 1886, we would have another deviation from understanding of beriberi with the work of
Norman Chevers. He would claim that the condition was actually a form of the epidemic dropsy,
and that it should be called beriberi fever, as the condition must be the result of an earlier
fever. Claiming that the symptoms were similar to scarlatina, this is another term for scarlet
(07:48):
fever, this condition is caused by a bacterial infection after having strep throat. It can be
life-threatening, but anyway, back to beriberi. Chevers claimed that beriberi was closer to an
infection like scarlet fever, and it would cause widespread confusion and misreporting of beriberi
or epidemic dropsy up until the 1930s. In the early 1900s, two pioneers would begin to hone in
(08:11):
on the potential problem at hand for so many. These would be Kanehiro Takaki in Japan, and
Christiaan Eijkman in Java. Eichmann finding that when chickens were fed a diet of white rice,
they developed polyneuritis, or leg paralysis. When they were fed brown rice, they would not
develop this. They would both suggest that rice diets may be to blame for beriberi. But something
(08:33):
would be missing from this conclusion. So in 1907, W.L. Braddon identified a potential unknown
culprit, suggesting that it may in fact be a rice ergot or Toxi-infection causing the issue,
an ergot being a type of fungus that you don't want to be eating. Braddon suggested that there
was a poison present on the surface of the grain of rice. The rice was simply the agent of delivery,
(08:57):
not the actual cause of disease. However, in just three short years, a more likely answer was
suggested in 1910. This was by Henry Fraser and A.T. Stanton, suggesting that it is more likely to
be a nutritional issue affecting the rice. Our researchers have conclusively shown that beriberi
can be prevented by the use of unpolished rice, and as surely produced by the use of highly
(09:22):
polished rice. This meaning those who had a diet that was mostly white rice, this was causing them
to develop beriberi. However, in the year of 1910, we still did not know the real cause of this
condition. So with this, white rice was seen as the main villain of the story, which would lead
to some interesting things occurring, like the call by Victor Heiser, who was head of the Asian
(09:43):
operations of the Rockefeller board, to call for an international tax on white rice. This was not
a suggestion that anyone actually wanted, as rice was a large part of the diet there, and by taking
it and making it too expensive to buy and eat, it would cause even worse outcomes, considering
people would not be able to afford their typical food. However, there would be some lesser known
(10:05):
advancements in 1910. This being the isolation of vitamin B1 from rice bran. This was done by
Umetaro Suzuki. He originally called it a baric acid, but this would largely be ignored. Between
1911 and 1912, we would have the work of Polish biochemist Casimir Funk. He would also isolate
the vitamin from rice bran. He would suggest the term "vitamin" as it had an amino acid and was
(10:30):
essential for life. So vitamins were an amine of life. In 1926, vitamin B1 would be discovered.
Again, this was when Barend Jansen and Willem Donarth isolated and crystallized a substance,
that when they fed it to pigeons with polyneuritis, they were cured. Polyneuritis in pigeons and
chickens was the animal model of choice for many. Complete side note, this is potentially why you
(10:54):
should not throw white rice for your wedding. Yeah, as it turns out, pigeons don't actually
explode when they eat white rice. Thanks, Dad. I will not admit how old I was when I learned that.
From the early 1900s up into the 1930s, Burma would have an increase in the rice mills,
but there was no increase in the deaths from beriberi. Which led to interesting comments,
(11:15):
like that of the superintendent of Dacca Central Jail, who asked the question, "The organism of
beriberi only attacks rice from the further east? Good question." Interestingly enough,
due to changes in the literature during the early 1900s, beriberi began to be seen as something that
only affected Chinese populations. This was in part due to the literature coming from Singapore.
(11:37):
The institutions that had those affected by beriberi happened to be primarily occupied by
Chinese people. So the people being discussed in the Singaporean literature as having beriberi all
happened to be Chinese labourers, prisoners, and asylum inmates. They were significantly
discussed and photographed, leading to the idea that true beriberi only affect Chinese bodies.
(11:58):
This was also amplified by Braddon's observations in Malaya. He would point out that the Chinese
immigrants ate white rice that was uncured. So it was cooked after hulling, whereas the
Tamil locals cured their rice. This is done by parboiling, it then removing the husk.
The Chinese suffered from beriberi, however the Tamil did not. This being due to an interesting,
(12:21):
yet undiscovered factor at the time. Parboiling before removing the husk of the rice actually
retains enough thiamine to prevent beriberi. Moving on to 1936. This is when we would have
the first successful creating of synthesised thiamine by Robert Williams. Now we are going
to move to between 1942 and 1945 with the Second World War. Here we would have the accounts of
(12:44):
several prisoners of war, including from the Cabanatuan Prisoner of War camp in the Philippines.
One of the more prominent diseases in the camp was beriberi. This was due to the diet
fed to prisoners kept in the camp. They were fed something that was called lugao. This was
described by an ex-POW by the name of Harold Amos. He would state, "They gave us a little lugao.
(13:06):
That was rice mixed with water. The worms and bugs and weevils would float to the top. And at first
you'd pick them out. And then after a couple of meals, why, you just, as a little protein,
you just ate raw." Those who were kept here as prisoners would eat less than 300 calories a day
of this rice porridge. Almost all who were kept at this camp as POWs ended up with beriberi due to
(13:29):
the diet being low in thiamine, among many other things, as the rice had the husks removed. The husks
containing the thiamine. Cabanatuan, like other camps, was host to many diseases, due to the
amount of nutrition and poor sanitation. One of the camp doctors, Dr Hibbs, would claim that,
"The whole place was a pathological museum. Most doctors would never see such cases in their entire
(13:51):
lives." We also see this with the account of one of the captives in the camp, Bob Body.
"It was malaria I had to begin with. Then I had dengue fever. Which, well, you are worse with
dengue fever than malaria, but it is not fatal like malaria can be. Then I had amoebic dysentery and
there was nothing you could do. Then beriberi came along and there were two types. There was wet and
(14:12):
there was dry. I had the wet. My head swole up and everything swole up. And then there was dry and
there was no swelling. It just hurt. Your feet hurt all the time. You couldn't put them on the ground.
And then I went blind for a couple of days from some lack of vitamin." A little note, both dengue
and malaria can be deadly. Dengue is less often deadly. Either way, don't go frolicking with
(14:34):
mosquitoes. They aren't your friends. Hate to break that to you. If you're enjoying this episode
so far and think someone else might enjoy it, you should share it with them. It helps us grow.
So what actually causes beriberi? Simply put, this condition is caused by a prolonged deficiency in
the vitamin B1, which is also known as thiamine. This can be due to several reasons, like having
a low intake of thiamine-rich foods. So if you predominantly eat highly processed carbohydrates
(14:59):
like white rice, white sugar, and white flour, this can increase your risk of developing beriberi,
as these do not have adequate levels of thiamine unless they are enriched. A little note to this,
all foods have a place in diets unless you are allergic to it or do not like it. However,
emphasis on this as a balanced diet is necessary to avoid nutritional deficiencies. Don't be
(15:21):
sitting in the corner of a cupboard just chowing down on a bag of white flour. Otherwise, beriberi
isn't going to be the only problem you have. Along with diet, having an eating disorder like anorexia
nervosa also increases your risk of developing a thiamine deficiency due to the restrictive
food intake. There are also several other causes that can lead to the development of this condition,
(15:42):
like conditions that increase thiamine needs, an example of this being hyperthyroidism,
so an overly functional thyroid, medications like some diuretics, anti-seizure medications,
and cardiovascular medications. Conditions that prevent the absorption of thiamine,
an example of this is having chronic diarrhoea, or conditions that affect how your body metabolises
(16:03):
thiamine, like liver disease. What are some of the risk factors for developing beriberi?
Well, there are many risk factors that can increase your chances of developing beriberi.
These include drinking heavily, or having an alcohol use disorder,
having Wernicke-Korsakoff syndrome. This condition is linked to having a thiamine deficiency
along with alcohol use disorder. It is a type of memory disorder, poor diet or starvation,
(16:26):
having a lack of access to nutritional foods, having prior gastric bypass surgery, kidney
disease and dialysis. During pregnancy, beriberi can develop if you have hyperemesis gravidarum.
This is extreme nausea and vomiting during pregnancy. Children who are breastfed by
mothers who are thiamine deficient also have a higher risk of developing beriberi.
(16:48):
Congenital beriberi. This is when a child is born without the ability to absorb thiamine.
Infants who are fed formulas that do not have enough thiamine are also at an increased risk
of developing beriberi. What are the types of beriberi?
Well, there are two types of beriberi. These types classify what is being affected.
The two types are wet beriberi. This form affects your cardiovascular system
(17:09):
and dry beriberi. This form can be seen alongside Wernicke-Korsakoff syndrome,
and this form affects the central nervous system. However, Wernicke-Korsakoff syndrome does not
always occur with dry beriberi. Sometimes you can just have dry beriberi without it.
How do we diagnose beriberi? Well, doctors will first do an exam. With this,
they will check for obvious signs and symptoms that may hint into a diagnosis of a thiamine
(17:32):
deficiency. After this, they will order blood tests. The blood test for thiamine deficiency
does not actually check the levels of the vitamin in your blood as we are unable to do this directly.
However, we do have a test that indirectly tests for this. This test checks for the levels of an
enzyme known as transketolase. Now thiamine is important in transketolase actually working.
(17:54):
So if the activity of this enzyme is low, then it suggests that your thiamine is likely low,
causing you to have symptoms of beriberi. We will get right
into symptoms and presentation right after this little break.
(18:15):
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What symptoms might you have if you had beriberi? The symptoms you may experience
if you had beriberi will depend on the form of beriberi you develop.
For those with wet beriberi, this being the kind that affects your cardiovascular system,
the symptoms that you may experience include waking up in the middle of the night feeling
(18:36):
short of breath, experiencing shortness of breath with activity or exercise,
swelling in the lower legs and having an increase in your heart rate.
For those who have dry beriberi, this being the kind that affects the central nervous system,
the symptoms you may have include experiencing decreased function of the muscle. This can be
found especially in the lower legs, tingling or loss of feeling in both the hands and feet.
(18:58):
This is on both sides of the body, not just one. Experiencing pain, having mental confusion,
having difficulties with speaking, experiencing strange eye movements. So nystagmus. This is a
backward and forward left to right movement of the eye. This is rapid, repeated and uncontrollable.
Vomiting. Paralysis. This occurs if the condition is left untreated.
What should a doctor be aware of when it comes to beriberi? Well, there are several complications
(19:22):
a doctor should be aware of when it comes to beriberi. These include
Wernicke-Korsakoff syndrome. This can occur with beriberi in extreme cases.
This condition is actually two different forms of brain damage caused by thiamine deficiency.
Wernicke encephalopathy. This affects your hypothalamus and thalamus.
Symptoms of this include confusion, memory loss, visual problems like rapid eye movement
(19:44):
and double vision, and also a loss of muscle coordination.
Korsakoff syndrome. This is a permanent damage to the part of the brain that allows us to form
memories. The symptoms of this include loss of memory and inability to form new memories,
and even hallucinations, sometimes delirium as well. This may be called Korsakoff's psychosis.
So the hallucinations and delirium, Korsakoff's psychosis. This is not the only complication
(20:09):
that a doctor should be aware of when it comes to beriberi. This condition can also cause coma,
congestive heart failure, and death. How do we treat beriberi?
When it comes to beriberi, the treatment for this condition is replacing the missing thiamine
that your body has been lacking. So for this, doctors may recommend an injection or supplements
to be taken by mouth. Doctors will also follow up on your condition to ensure that you are actually
(20:30):
recovering. This can be done through blood tests and making sure these symptoms are actually going
away. Doctors may also recommend changes in the diet or taking other supplements alongside
vitamin B supplements to prevent beriberi from occurring again if the thiamine deficiency was
due to diet. They may recommend other supplements just in case you were deficient in other things.
In most cases, beriberi is easily treated with no lasting effects. However, if caught later,
(20:54):
some people may experience remaining symptoms or other medical conditions. So for those who have
experienced acute heart failure due to beriberi, their heart is damaged and they may have a poor
outlook depending on how severe that condition is. For those who had nervous system damage,
if the condition was not caught early, some of those symptoms may remain after treatment like
those of Korsakoff's syndrome. Are there any famous people who have or have had beriberi?
(21:17):
In recent history, no. And that is a good thing. Why is this? Well, it means that we have a better
understanding of health and nutrition, which means people are not getting beriberi as often as the
distant past, meaning that people are not getting these preventable conditions due to poor nutrition
as often. Some people still do get them. But if you would like to check out a depiction of
(21:37):
beriberi in the media, there is actually at least one. If you are interested in watching an episode
of a South Korean drama that features beriberi, there is the historical drama known as Jewel in
the Palace or Dae Jong Geum. It has an episode titled Beriberi, which obviously has the condition
as the main plot of the episode, considering it's called that. As beriberi is considered to
be mostly eradicated, considering we know the cause of the condition, there are not really any
(22:01):
foundations that focus solely on beriberi. If you want to check out the sources, social media links,
or any other links, you can head to anatomyofillness.com. If you enjoyed this episode and
would like to hear more, subscribe to be notified about our latest episodes. If you'd like to join
our community, you can join us on Discord or Instagram. Otherwise, stick around for the next
episode.
Did you know that the name thiamine actually comes from its structure? Thi comes from thio
(22:35):
because it has sulfur and amine because it has an amino group. Thiamine being the deficiency
in beriberi.
Lately, you have been feeling strange. Your hands and feet are tingly. It is pretty much the only
(00:05):
thing you can feel in them. When you try to walk, it is a struggle. It feels almost as if you are
trying to drag your feet through cement. Everything hurts, especially your legs. You call your mother
to try to ask her about what may be going on. However, you struggle to get the words out,
feeling more confused than ever. When you eventually manage to tell her, she tells you that
(00:25):
that horrendous diet you have at college is not doing you any favours. You need to go and see a
doctor. Hello and welcome to Anatomy of Illness. Today's episode is about beriberi. Before we get
(00:51):
into the condition, we are going to start with the history. So why do we know beriberi exists?
In this episode, I may also refer to the condition as thiamine deficiency or B1 deficiency. Now onto
the history. For this, we are going to begin all the way back in 808 in Japan as this is where
documents have been found suggesting beriberi occurred. This is not what it was called in
(01:14):
ancient Japan though. It was known as kakké or leg disease. It was also known as this around that
time in ancient China. Between 1603 and 1867, this would have been due to the polished white rice in
the diet in Japanese cities. So rice that had the outer husk removed, which contains most of
the thiamine. This was due to the popularity of rice milling as having white rice on the table
(01:37):
symbolised affluence because it looked more presentable on the table than brown rice. Now
we are going to jump back quickly to 1629 and over to Java in Indonesia. With the first western
description of the condition, this being by Jacobus Bontius, who was a Dutch physician.
There is no real record as to who was the first to start using the Sinhalese term beriberi to
(01:59):
describe the condition, this term meaning I cannot, I cannot, but both the Dutch and the
English would use the term. The English getting the term from communications with the Dutch.
We see this with the first descriptive English account given by Thomas Christie. This was
between the late 1790s and early 1800s in what at the time was known as Ceylon but is now modern day
(02:20):
Sri Lanka. He observed the condition to primarily affect the soldiers of the English East India
Company that were recruited from the south eastern coast of India. This also being where the
condition was widely spread at the time in the local population, not just soldiers recruited
from there. He saw that this condition would affect both Europeans and Indians. Seeing many
(02:41):
cases actually affecting the white soldiers. In his descriptions, he would note that those with
the condition would suffer from paralysis of the lower limbs, edema or dropsy, dropsy being the
old term for edema type swelling. He would forward his observations to William Hunter in London who
would inquire about the Indian sailors on board their mortality rate specifically. During this
(03:02):
time, Christie was working on differentiating it from scurvy, which is another disease caused by
vitamin deficiency with a very interesting history we covered it back in episode 11.
He would comment on the absence of the swollen gums, fetid breath and spotted limbs. He would
also mention that the condition did not respond to the anti-scorbiotic lime juice, meaning it's
not scurvy. Christie would claim moisture impure air, despondency and dirtiness as contributing
(03:28):
factors for the development of beriberi. However, he primarily attributed it to a want of a
stimulating and nourishing diet. This being due to the fact that the majority of the soldiers diet
consisted of rice, hulled rice. Christie's account would mention much about the diet being a cause
and a cure of this disease. However, in Hunter's account of Lascar diseases, it became an
(03:53):
afterthought. Lascar being the soldiers that manned these ships. Moving on to the 1830s and into South
India, here we see an offer for a prize for papers written about beriberi by the Madras Medical Board.
This was done in an attempt to encourage research into beriberi due to this condition being known
to be insidious in its attack, rapid in its progress and fatal in its termination. After this,
(04:17):
four papers were written and the prize would be awarded to John Grant Malcolmson, who was, like
the others who submitted the papers, an army medical officer. He of course had his own
observations on the condition, believing that the term beriberi was actually derived from
the Hindustani word for sheep. He suggested this due to an awkward sheep-like gait that
he claimed was a characteristic of the condition. He would also note in his paper that the local
(04:42):
population did not distinguish beriberi from other conditions. The Tegulu people use the name
Timmeree waivo as a term to encompass conditions like beriberi, palsy, tingling sensations and
even rheumatism. He would describe beriberi as mostly occurring in one particular area of India
and in the soldiers stationed there. Around the same time, in 1835, a British naval surgeon
(05:06):
by the name of James Bankier would make his own comments about beriberi. However, these could be
seen as less than helpful. He referred to it as the salon palsy, suggesting both an ill-defined link
with poor vegetarian diets and hinting that the condition was contagious, like the cholera
outbreaks that were happening in the same area, describing it as a very troublesome complaint.
(05:30):
And note on this, beriberi is a vitamin deficiency. If I sneeze in your direction,
you are not going to catch a vitamin deficiency. It is not contagious. Because of other conditions
that were spreading at the time, like smallpox, malaria, and of course cholera, beriberi was a
bit like the ignored middle child. Yes, it was there, but it was not seen as an important disease.
(05:53):
It was not contagious. It was not killing as many people. We see this with the medical accounts of
the Madras famines of both 1866 and the 1876 to 1878 famine. These records focus primarily on
cholera, dysentery, malaria, and smallpox, with no mention of beriberi. When literature did mention
beriberi in the mid to late 19th century, it was often spoken of as exclusively occurring in the
(06:16):
northern Circars, this being a part of India at the time. It was considered non-contagious and
mostly blamed on climate, with the occasional suggestion of it being diet related. In the 1880s,
we would see the lectures of a former Surgeon General with the Indian Army by the name of
W.C. Maclean, discussing diseases of tropical climates over at the Netley Army Medical School.
(06:37):
His discussions on beriberi mainly talked about the condition being something that he had
predominantly seen in South India, or South Indian troops that were taken to Burma. At this time,
the cause was still obscure. However, Maclean did have some suggestions for the cause. He believed
that the condition developing could be blamed on the water, the soil, and the climate in the area,
along with poverty, insufficient food, and clothing. Interestingly enough, even at this
(07:01):
time other conditions were still being described as beriberi, when they were not the same condition,
like anemia in Assam and Ceylon. Assam being an Indian state, and Ceylon of course being again
Sri Lanka. This would change with the 1877 paper by W.R. Kynsey. “The anemia, or beriberi, of Ceylon.”
The anemia was identified as a condition caused by hookworm, which symptoms were different from
(07:27):
beriberi. In 1886, we would have another deviation from understanding of beriberi with the work of
Norman Chevers. He would claim that the condition was actually a form of the epidemic dropsy,
and that it should be called beriberi fever, as the condition must be the result of an earlier
fever. Claiming that the symptoms were similar to scarlatina, this is another term for scarlet
(07:48):
fever, this condition is caused by a bacterial infection after having strep throat. It can be
life-threatening, but anyway, back to beriberi. Chevers claimed that beriberi was closer to an
infection like scarlet fever, and it would cause widespread confusion and misreporting of beriberi
or epidemic dropsy up until the 1930s. In the early 1900s, two pioneers would begin to hone in
(08:11):
on the potential problem at hand for so many. These would be Kanehiro Takaki in Japan, and
Christiaan Eijkman in Java. Eichmann finding that when chickens were fed a diet of white rice,
they developed polyneuritis, or leg paralysis. When they were fed brown rice, they would not
develop this. They would both suggest that rice diets may be to blame for beriberi. But something
(08:33):
would be missing from this conclusion. So in 1907, W.L. Braddon identified a potential unknown
culprit, suggesting that it may in fact be a rice ergot or Toxi-infection causing the issue,
an ergot being a type of fungus that you don't want to be eating. Braddon suggested that there
was a poison present on the surface of the grain of rice. The rice was simply the agent of delivery,
(08:57):
not the actual cause of disease. However, in just three short years, a more likely answer was
suggested in 1910. This was by Henry Fraser and A.T. Stanton, suggesting that it is more likely to
be a nutritional issue affecting the rice. Our researchers have conclusively shown that beriberi
can be prevented by the use of unpolished rice, and as surely produced by the use of highly
(09:22):
polished rice. This meaning those who had a diet that was mostly white rice, this was causing them
to develop beriberi. However, in the year of 1910, we still did not know the real cause of this
condition. So with this, white rice was seen as the main villain of the story, which would lead
to some interesting things occurring, like the call by Victor Heiser, who was head of the Asian
(09:43):
operations of the Rockefeller board, to call for an international tax on white rice. This was not
a suggestion that anyone actually wanted, as rice was a large part of the diet there, and by taking
it and making it too expensive to buy and eat, it would cause even worse outcomes, considering
people would not be able to afford their typical food. However, there would be some lesser known
(10:05):
advancements in 1910. This being the isolation of vitamin B1 from rice bran. This was done by
Umetaro Suzuki. He originally called it a baric acid, but this would largely be ignored. Between
1911 and 1912, we would have the work of Polish biochemist Casimir Funk. He would also isolate
the vitamin from rice bran. He would suggest the term "vitamin" as it had an amino acid and was
(10:30):
essential for life. So vitamins were an amine of life. In 1926, vitamin B1 would be discovered.
Again, this was when Barend Jansen and Willem Donarth isolated and crystallized a substance,
that when they fed it to pigeons with polyneuritis, they were cured. Polyneuritis in pigeons and
chickens was the animal model of choice for many. Complete side note, this is potentially why you
(10:54):
should not throw white rice for your wedding. Yeah, as it turns out, pigeons don't actually
explode when they eat white rice. Thanks, Dad. I will not admit how old I was when I learned that.
From the early 1900s up into the 1930s, Burma would have an increase in the rice mills,
but there was no increase in the deaths from beriberi. Which led to interesting comments,
(11:15):
like that of the superintendent of Dacca Central Jail, who asked the question, "The organism of
beriberi only attacks rice from the further east? Good question." Interestingly enough,
due to changes in the literature during the early 1900s, beriberi began to be seen as something that
only affected Chinese populations. This was in part due to the literature coming from Singapore.
(11:37):
The institutions that had those affected by beriberi happened to be primarily occupied by
Chinese people. So the people being discussed in the Singaporean literature as having beriberi all
happened to be Chinese labourers, prisoners, and asylum inmates. They were significantly
discussed and photographed, leading to the idea that true beriberi only affect Chinese bodies.
(11:58):
This was also amplified by Braddon's observations in Malaya. He would point out that the Chinese
immigrants ate white rice that was uncured. So it was cooked after hulling, whereas the
Tamil locals cured their rice. This is done by parboiling, it then removing the husk.
The Chinese suffered from beriberi, however the Tamil did not. This being due to an interesting,
(12:21):
yet undiscovered factor at the time. Parboiling before removing the husk of the rice actually
retains enough thiamine to prevent beriberi. Moving on to 1936. This is when we would have
the first successful creating of synthesised thiamine by Robert Williams. Now we are going
to move to between 1942 and 1945 with the Second World War. Here we would have the accounts of
(12:44):
several prisoners of war, including from the Cabanatuan Prisoner of War camp in the Philippines.
One of the more prominent diseases in the camp was beriberi. This was due to the diet
fed to prisoners kept in the camp. They were fed something that was called lugao. This was
described by an ex-POW by the name of Harold Amos. He would state, "They gave us a little lugao.
(13:06):
That was rice mixed with water. The worms and bugs and weevils would float to the top. And at first
you'd pick them out. And then after a couple of meals, why, you just, as a little protein,
you just ate raw." Those who were kept here as prisoners would eat less than 300 calories a day
of this rice porridge. Almost all who were kept at this camp as POWs ended up with beriberi due to
(13:29):
the diet being low in thiamine, among many other things, as the rice had the husks removed. The husks
containing the thiamine. Cabanatuan, like other camps, was host to many diseases, due to the
amount of nutrition and poor sanitation. One of the camp doctors, Dr Hibbs, would claim that,
"The whole place was a pathological museum. Most doctors would never see such cases in their entire
(13:51):
lives." We also see this with the account of one of the captives in the camp, Bob Body.
"It was malaria I had to begin with. Then I had dengue fever. Which, well, you are worse with
dengue fever than malaria, but it is not fatal like malaria can be. Then I had amoebic dysentery and
there was nothing you could do. Then beriberi came along and there were two types. There was wet and
(14:12):
there was dry. I had the wet. My head swole up and everything swole up. And then there was dry and
there was no swelling. It just hurt. Your feet hurt all the time. You couldn't put them on the ground.
And then I went blind for a couple of days from some lack of vitamin." A little note, both dengue
and malaria can be deadly. Dengue is less often deadly. Either way, don't go frolicking with
(14:34):
mosquitoes. They aren't your friends. Hate to break that to you. If you're enjoying this episode
so far and think someone else might enjoy it, you should share it with them. It helps us grow.
So what actually causes beriberi? Simply put, this condition is caused by a prolonged deficiency in
the vitamin B1, which is also known as thiamine. This can be due to several reasons, like having
a low intake of thiamine-rich foods. So if you predominantly eat highly processed carbohydrates
(14:59):
like white rice, white sugar, and white flour, this can increase your risk of developing beriberi,
as these do not have adequate levels of thiamine unless they are enriched. A little note to this,
all foods have a place in diets unless you are allergic to it or do not like it. However,
emphasis on this as a balanced diet is necessary to avoid nutritional deficiencies. Don't be
(15:21):
sitting in the corner of a cupboard just chowing down on a bag of white flour. Otherwise, beriberi
isn't going to be the only problem you have. Along with diet, having an eating disorder like anorexia
nervosa also increases your risk of developing a thiamine deficiency due to the restrictive
food intake. There are also several other causes that can lead to the development of this condition,
(15:42):
like conditions that increase thiamine needs, an example of this being hyperthyroidism,
so an overly functional thyroid, medications like some diuretics, anti-seizure medications,
and cardiovascular medications. Conditions that prevent the absorption of thiamine,
an example of this is having chronic diarrhoea, or conditions that affect how your body metabolises
(16:03):
thiamine, like liver disease. What are some of the risk factors for developing beriberi?
Well, there are many risk factors that can increase your chances of developing beriberi.
These include drinking heavily, or having an alcohol use disorder,
having Wernicke-Korsakoff syndrome. This condition is linked to having a thiamine deficiency
along with alcohol use disorder. It is a type of memory disorder, poor diet or starvation,
(16:26):
having a lack of access to nutritional foods, having prior gastric bypass surgery, kidney
disease and dialysis. During pregnancy, beriberi can develop if you have hyperemesis gravidarum.
This is extreme nausea and vomiting during pregnancy. Children who are breastfed by
mothers who are thiamine deficient also have a higher risk of developing beriberi.
(16:48):
Congenital beriberi. This is when a child is born without the ability to absorb thiamine.
Infants who are fed formulas that do not have enough thiamine are also at an increased risk
of developing beriberi. What are the types of beriberi?
Well, there are two types of beriberi. These types classify what is being affected.
The two types are wet beriberi. This form affects your cardiovascular system
(17:09):
and dry beriberi. This form can be seen alongside Wernicke-Korsakoff syndrome,
and this form affects the central nervous system. However, Wernicke-Korsakoff syndrome does not
always occur with dry beriberi. Sometimes you can just have dry beriberi without it.
How do we diagnose beriberi? Well, doctors will first do an exam. With this,
they will check for obvious signs and symptoms that may hint into a diagnosis of a thiamine
(17:32):
deficiency. After this, they will order blood tests. The blood test for thiamine deficiency
does not actually check the levels of the vitamin in your blood as we are unable to do this directly.
However, we do have a test that indirectly tests for this. This test checks for the levels of an
enzyme known as transketolase. Now thiamine is important in transketolase actually working.
(17:54):
So if the activity of this enzyme is low, then it suggests that your thiamine is likely low,
causing you to have symptoms of beriberi. We will get right
into symptoms and presentation right after this little break.
(18:15):
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What symptoms might you have if you had beriberi? The symptoms you may experience
if you had beriberi will depend on the form of beriberi you develop.
For those with wet beriberi, this being the kind that affects your cardiovascular system,
the symptoms that you may experience include waking up in the middle of the night feeling
(18:36):
short of breath, experiencing shortness of breath with activity or exercise,
swelling in the lower legs and having an increase in your heart rate.
For those who have dry beriberi, this being the kind that affects the central nervous system,
the symptoms you may have include experiencing decreased function of the muscle. This can be
found especially in the lower legs, tingling or loss of feeling in both the hands and feet.
(18:58):
This is on both sides of the body, not just one. Experiencing pain, having mental confusion,
having difficulties with speaking, experiencing strange eye movements. So nystagmus. This is a
backward and forward left to right movement of the eye. This is rapid, repeated and uncontrollable.
Vomiting. Paralysis. This occurs if the condition is left untreated.
What should a doctor be aware of when it comes to beriberi? Well, there are several complications
(19:22):
a doctor should be aware of when it comes to beriberi. These include
Wernicke-Korsakoff syndrome. This can occur with beriberi in extreme cases.
This condition is actually two different forms of brain damage caused by thiamine deficiency.
Wernicke encephalopathy. This affects your hypothalamus and thalamus.
Symptoms of this include confusion, memory loss, visual problems like rapid eye movement
(19:44):
and double vision, and also a loss of muscle coordination.
Korsakoff syndrome. This is a permanent damage to the part of the brain that allows us to form
memories. The symptoms of this include loss of memory and inability to form new memories,
and even hallucinations, sometimes delirium as well. This may be called Korsakoff's psychosis.
So the hallucinations and delirium, Korsakoff's psychosis. This is not the only complication
(20:09):
that a doctor should be aware of when it comes to beriberi. This condition can also cause coma,
congestive heart failure, and death. How do we treat beriberi?
When it comes to beriberi, the treatment for this condition is replacing the missing thiamine
that your body has been lacking. So for this, doctors may recommend an injection or supplements
to be taken by mouth. Doctors will also follow up on your condition to ensure that you are actually
(20:30):
recovering. This can be done through blood tests and making sure these symptoms are actually going
away. Doctors may also recommend changes in the diet or taking other supplements alongside
vitamin B supplements to prevent beriberi from occurring again if the thiamine deficiency was
due to diet. They may recommend other supplements just in case you were deficient in other things.
In most cases, beriberi is easily treated with no lasting effects. However, if caught later,
(20:54):
some people may experience remaining symptoms or other medical conditions. So for those who have
experienced acute heart failure due to beriberi, their heart is damaged and they may have a poor
outlook depending on how severe that condition is. For those who had nervous system damage,
if the condition was not caught early, some of those symptoms may remain after treatment like
those of Korsakoff's syndrome. Are there any famous people who have or have had beriberi?
(21:17):
In recent history, no. And that is a good thing. Why is this? Well, it means that we have a better
understanding of health and nutrition, which means people are not getting beriberi as often as the
distant past, meaning that people are not getting these preventable conditions due to poor nutrition
as often. Some people still do get them. But if you would like to check out a depiction of
(21:37):
beriberi in the media, there is actually at least one. If you are interested in watching an episode
of a South Korean drama that features beriberi, there is the historical drama known as Jewel in
the Palace or Dae Jong Geum. It has an episode titled Beriberi, which obviously has the condition
as the main plot of the episode, considering it's called that. As beriberi is considered to
be mostly eradicated, considering we know the cause of the condition, there are not really any
(22:01):
foundations that focus solely on beriberi. If you want to check out the sources, social media links,
or any other links, you can head to anatomyofillness.com. If you enjoyed this episode and
would like to hear more, subscribe to be notified about our latest episodes. If you'd like to join
our community, you can join us on Discord or Instagram. Otherwise, stick around for the next
episode.
Did you know that the name thiamine actually comes from its structure? Thi comes from thio
(22:35):
because it has sulfur and amine because it has an amino group. Thiamine being the deficiency
in beriberi.
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