Misconceptions vs Myths For the purpose of this Discussion Misconception Common mistake but generally not perpetuated by schools and licensure exams This presentation will cover 5 common medical misconceptions ID: 353154
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Slide1
Common Medical Myths & MisconceptionsSlide2
Misconceptions vs. Myths
For the purpose of this Discussion:
Misconception = Common mistake, but generally not perpetuated by schools and licensure exams. This presentation will cover 5 common medical misconceptions.
Myth = More than just a common mistake; currently standard practice and propagated by schools and licensure exams. This presentation will cover 3 medical myths.Slide3
Misconception #1:
Cyclothymia
Cyclothymia
is:
An endocrine disorder that results in an underproduction of
thyroxine
An immunological disorder related to a mutation in the MHC gene
A mood disorder related to dysfunction of the thymus in the brain
None of the above
Don’t KnowSlide4
Cyclothymia
Cyclothymia
is:
An endocrine disorder that results in an underproduction of
thyroxine
An immunological disorder related to a mutation in the MHC gene
A mood disorder related to dysfunction of the thymus in the brain
None of the aboveDon’t KnowSlide5
Cyclothymia
An endocrine disorder that results in an underproduction of
thyroxine
An immunological disorder related to a mutation in the MHC gene
A mood disorder related to dysfunction of the
thymus
in the brain
None of the above (11.1%)
Don’t Know
Cyclothymia
has nothing to do with the thymusSlide6
What is the Thymus?
Cyclothymia
and
dysthymia
are named after the
greek
word “
thumos” or “thymos,” meaning spiritedness or emotion (Thumos, 2014). The thymus is also named after “thymos” though it has nothing to do with emotions, but the Greeks didn’t know that when they named it, resulting in etymological confusion that has lasted to this day.To add further confusion, the
thy
mus is right next to the
thy
roid on the trachea, and nobody ever talks about the thymus because it’s not a vital organ in children and adults, so most people don’t know what it does and the two are frequently confused.Slide7
What Does The Thymus Do?
During embryonic development lymphocytes go to the thymus to mature. Lymphocytes that fail to interact with MHCs are killed, because they wouldn’t be able to do their job if they can’t interact with MHCs
on other cells.
Lymphocytes that have strong affinity for self proteins are also killed here because they would cause autoimmunity. Failure of the thymus to kill cells that have affinity for self proteins is thought to be a possible cause of many autoimmune disorders including Diabetes Mellitus Type I (
Geenen
et al., 2005). The thymus prunes your lymphocyte population so only potentially useful lymphocytes ever make it into circulation. By your early teens your thymus starts to atrophy and turn into fat tissue and can be removed without any immune system compromise because its work has already been done (Thymus, 2015).Slide8
Misconception #2: Blood
Is blood always red?
Yes
No
Don’t KnowSlide9
Blood
Is blood always red?
Yes
No
Don’t KnowSlide10
Blood
Is blood always red?
Yes (
66.7%
)
No
Don’t KnowSlide11
Blood is Always Red.
This is a metaphor
Blood is bright red when oxygenated, and dark red when deoxygenated.Slide12
Blood is Always Red
So why are veins blue then?
This is a metaphor
And why does cyanosis happen?Slide13
Blood is Always Red
This isn’t a popular fact to share at the water cooler, because it’s a little bit complicated.
The fats and proteins in skin don’t absorb much light; they reflect it back out. Red light travels deeper than blue light before getting reflected back out (it’s better at getting through those proteins and fats).
Blood, unlike skin, absorbs light of all wavelengths, but it absorbs blue light more than red, so it appears red.
Deoxygenated blood in veins, like oxygenated blood in capillaries, reflects red light more than blue light, but compared with oxygenated blood it reflects more blue light (but still less blue than red, so it still looks red).
Kienle
et al., 1996Slide14
Even though veins absorb more blue light than red light if exposed to equal amounts of both, they don’t get exposed to equal amounts of both; they absorb a disproportionately large amount of red light under your skin because much of the blue light gets reflected back out by the proteins and fats in your skin before it can reach the vein.
Blood is Always RedSlide15
Even so, the light that comes out over top of a vein still winds up being more red than blue, but the effects discussed in the previous slide make it proportionately more blue than the surrounding skin, in a ratio of about 3 parts red to 2 parts blue (40% blue [if we ignore all the colors except red and blue for the purpose of comparison]), while the surrounding skin is 5 parts red to 3 parts blue (37.5% blue) (
Kienle
et al., 1996).
So the light from skin is mostly red, and the light from veins is mostly red, but there’s more blue in the light being reflected above veins because the veins removed more of the red light than gets removed in the surrounding skin because the red light is better at getting all the way down to the veins, and deoxygenated blood reflects more blue than oxygenated blood in surrounding capillaries.Slide16
Blood is Always Red
Color perception is skewed by our brains. The light coming out above veins is more of a reddish maroon than a blue, but it looks blue because it’s surrounded by a redder area. If you put something purple next to something red, it sometimes looks blue. This phenomenon is called relative perception.
Other examples of relative perception illusions: Different people perceive different colors in this dress.
The red squares in the top diamonds are actually the same color. The green squares in the bottom two diamonds are also the same color. Slide17
But back to the blood color responses for a second….
Is blood always red?
Yes (
66.7%
)
No
Don’t Know
But this is probably not reflective of the actual proportion of people that think that deoxygenated blood is blue, due to a type of testing bias caused by the quiz itself: the “Hawthorne effect”
Most people got it rightSlide18
The Hawthorne Effect
It is likely that people that see the question: “Is blood always red?” on a suspicious quiz will draw the conclusion that the question is only being asked because the answer is counter-intuitive, which makes the process of elimination very easy for a yes or no question, artificially inflating the proportion of correct responses.
So the blue blood misconception is likely more prevalent than these results suggest.Slide19
Misconception #3: Bipolar Disorder
Which of the following scenarios fit the diagnostic criteria for either type I or type II bipolar disorder?
No history of manic or depressive episodes. Currently experiencing a major depressive episode
No history of manic or depressive episodes. Currently experiencing a manic episode
Has experienced more than 2 years of alternating
hypomanic
and minor depressive episodes
None of the aboveDon’t knowSlide20
Bipolar Disorder
Which of the following scenarios fit the diagnostic criteria for either type I or type II bipolar disorder?
No history of manic or depressive episodes. Currently experiencing a major depressive episode
No history of manic or depressive episodes. Currently experiencing a manic episode
Has experienced more than 2 years of alternating
hypomanic
and minor depressive episodes
None of the aboveDon’t knowSlide21
Bipolar Disorder
Which of the following scenarios fit the diagnostic criteria for either type I or type II bipolar disorder?
No history of manic or depressive episodes. Currently experiencing a major depressive episode
No history of manic or depressive episodes. Currently experiencing a manic episode
(
0%
)
Has experienced more than 2 years of alternating hypomanic and minor depressive episodesNone of the above
Don’t know
All you need for a type I bipolar disorder diagnosis is mania. You almost always see depression as well, but it is not necessary for diagnosis, and it is not part of the DSM5 diagnostic criteria. Slide22
Bipolar Disorder
While Bipolar II does require at least one episode of MDD, Bipolar I does not. It doesn’t even require mild depression. It is possible for an individual to be diagnosed with Bipolar I disorder based solely on having had one or more full manic episodes (Bipolar I Disorder, 2015). These asymmetrical criteria are a product of the fact that there is a name for having depression with no elevated mood distinct from "bipolar disorder" (namely depression or MDD), but there is no special name for having elevated mood or mania with no depression distinct from bipolar disorder. This leads to a little bit of confusing
asymmetry
in the diagnostic criteria of bipolar I and bipolar II disorders.
The wording in the textbook is misleading as well. On page 429 our text says "
A bipolar disorder is characterized by mood swings from profound depression to extreme euphoria
," which makes it sound like depression is a necessary symptom for any bipolar disorder diagnosis, though it is not (Lewis et al., 2011).Slide23
Mood Disorder Chart
Depressed sometimes but never manic?
DepressionSlide24
Mood Disorder Chart
Hypo-manic sometimes & majorly depressed other times?
Type II Bipolar
Depressed sometimes but never manic?
DepressionSlide25
Mood Disorder Chart
Hypo-manic sometimes & majorly depressed other times?
Type II Bipolar
Hypomanic
sometimes &
minorly
depressed other times?
Cyclothymia
Depressed sometimes but never manic?
DepressionSlide26
Mood Disorder Chart
Manic sometimes & depressed other times?
Hypo-manic sometimes & majorly depressed other times?
Type II Bipolar
Type I Bipolar
Hypomanic
sometimes &
minorly
depressed other times?
Cyclothymia
Depressed sometimes but never manic?
DepressionSlide27
Mood Disorder Chart
Manic sometimes but never depressed?
Manic sometimes & depressed other times?
?
Hypo-manic sometimes & majorly depressed other times?
Type II Bipolar
Type I Bipolar
Hypomanic
sometimes &
minorly
depressed other times?
Cyclothymia
Depressed sometimes but never manic?
DepressionSlide28
Mood Disorder Chart
Manic sometimes but never depressed?
Manic sometimes & depressed other times?
?
We don’t really have a name for that
Hypo-manic sometimes & majorly depressed other times?
Type II Bipolar
Type I Bipolar
Hypomanic
sometimes &
minorly
depressed other times?
Cyclothymia
Depressed sometimes but never manic?
DepressionSlide29
Mood Disorder Chart
Manic sometimes but never depressed?
Manic sometimes & depressed other times?
Depressed sometimes but never manic?
?
We don’t really have a name for that
Depression
Hypo-manic sometimes & majorly depressed other times?
Type II Bipolar
Type I Bipolar
Hypomanic
sometimes &
minorly
depressed other times?
Cyclothymia
Also Type I BipolarSlide30
Our
Powerpoint
Slide on Bipolar Disorder from Psychiatric Nursing:
Not trueSlide31
Misconception #4: Osmotic Diuretics
Osmotic diuretics work because:
They are made of small molecules that pass more easily through the fenestrated membranes in the kidney
They are made of small molecules that exert a stronger colloidal osmotic pressure than large molecules
They are made of large molecules that exert a stronger colloidal osmotic pressure than small molecules
None of the above
Don’t Know Slide32
Osmotic Diuretics
Osmotic diuretics work because:
They are made of small molecules that pass more easily through the fenestrated membranes in the kidney
They are made of small molecules that exert a stronger colloidal osmotic pressure than large molecules
They are made of large molecules that exert a stronger colloidal osmotic pressure than small molecules
None of the above
Don’t Know Slide33
Osmotic Diuretics
Osmotic diuretics work because:
They are made of small molecules that pass more easily through the fenestrated membranes in the kidney
They are made of small molecules that exert a stronger colloidal osmotic pressure than large molecules
They are made of large molecules that exert a stronger colloidal osmotic pressure than small molecules
None of the above (
22.2%
)
Don’t Know Slide34
Misconception: Large molecules exert more osmotic pressure than small molecules
Blood Vessels
Same Osmotic Pressure.
Size of molecules does not affect osmotic (colloidal osmotic) pressure.
Only the number of molecules.
So the question is… Why do we specifically use large molecules for osmotic diuretics?Slide35
So the question is… Why do we specifically use large molecules for osmotic diuretics?
Because they can’t cross capillary membranes, so they never enter the interstitial fluid and they keep the relative osmotic pressure in the capillaries higher than the surrounding fluids.
As an added bonus, when they cross the fenestrated membranes in the kidney (which they can cross because the fenestrated membranes are super-permeable) they can’t get back into the blood at the semi-permeable membranes in the loop of
Henle
. Trapped in the filtrate, they draw fluid out of the vasculature with them, straight into the bladder (Pharmacological interventions for cardiopulmonary emergencies,
n.d
.).Slide36
Misconception #5: Heparin & Coumadin
What is the normal therapeutic reduction in platelet count for Coumadin and Heparin? (UVA’s normal platelet range = 150,000 – 450,000 platelets per
microliter
)
45,000 – 135,000 (about 30%)
75,000 – 225,000 (about 50%)
The goal for platelet count reduction depends on the patient’s clinical scenario and health history
None of the above
Don’t knowSlide37
Heparin & Coumadin
What is the normal therapeutic reduction in platelet count for Coumadin and Heparin? (UVA’s normal platelet range = 150,000 – 450,000 platelets per
microliter
)
45,000 – 135,000 (about 30%)
75,000 – 225,000 (about 50%)
The goal for platelet count reduction depends on the patient’s clinical scenario and health history
None of the aboveDon’t knowSlide38
Heparin & Coumadin
What is the normal therapeutic reduction in platelet count for Coumadin and Heparin? (UVA’s normal platelet range = 150,000 – 450,000 platelets per
microliter
)
45,000 – 135,000 (about 30%)
75,000 – 225,000 (about 50%)
The goal for platelet count reduction depends on the patient’s clinical scenario and health history
None of the above (22.2%
)
Don’t knowSlide39
Anticoagulants DO NOT REDUCE PLATELET COUNT
Anticoagulants reduce
coagulability
of platelets, not the number of platelets
When heparin and
coumadin
do reduce platelet count, this is a dangerous adverse reaction called heparin-induced thrombocytopenia (HIT), which means that the anticoagulants need to be discontinued immediately.
Expecting a reduction in platelet count is a dangerous misconception that can lead to a failure to recognize HIT and thrombocytopenia caused by other problemsSlide40
Bonus Slides: Physiologic Jaundice in Newborns
Physiologic Jaundice in Newborns is caused by:
Anti-
Rh
factor antibodies cross the placenta and destroy blood cells in the fetus
Breakdown of fetal hemoglobin and an immature liver & gut flora
An increase in circulating red blood cells from the mother
A, B, & CB & C
Don’t KnowSlide41
Physiologic Jaundice in Newborns
Physiologic Jaundice in Newborns is caused by:
Anti-
Rh
factor antibodies cross the placenta and destroy blood cells in the fetus
Breakdown of fetal hemoglobin and an immature liver & gut flora
An increase in circulating red blood cells from the mother
A, B, & CB & C
Don’t Know
This is a new misconception that I added after distributing the quizzes, so I have no data for prevalence of this misconception.Slide42
Blood Cells Do Not Cross the Placenta
In the Thursday OB nursing lecture in “Care of the Newborn part II” at 109:35, the lecturer states: “Increased
bilirubin
production is from an
increase in circulating red blood cells from mom
, and the fetal red blood cells also have a shorter lifespan, so between that and what’s left over from mom they have increased
hemolysis
that they have to deal with.”In “Care of the Newborn part III”, at 5:40, a guest speaker, Katie Kinsey, a pediatric nurse practitioner states: “For normal newborns this is frequently from an increase of circulating red blood cells from the mom and the fetal red blood cells have a shorter lifespan so there’s an increase in
hemolysis
.”Slide43
Blood Cells Do Not Cross the Placenta
Blood cells generally do not cross the placenta. If they could, you wouldn’t need a placenta in the first place; the umbilical cord could just plug directly into the mother’s vasculature. On occasion a few blood cells can get through, but not in any amount that would have a measurable effect on
bilirubin
levels in a fetus.Slide44
Blood Cells Do Not Cross the Placenta
Note: sometimes the fetus can swallow some of the mother’s blood during birth. In this way it is theoretically possible for maternal blood cells to contribute to physiologic jaundice in newborns by being broken down in the GI tract at which point that
bilirubin
can be absorbed into the bloodstream.Slide45
Busting Myths:
Evidence > Expert OpinionSlide46
Myth #1: Diverticulosis
Diverticulosis
is associated with:
A) Low Fiber Diets
B) High Fiber Diets
C) Neither
D) Don’t KnowSlide47
Diverticulosis
Diverticulosis
is associated with:
A) Low Fiber Diets
B) High Fiber Diets
C) Neither
D) Don’t KnowSlide48
Diverticulosis
Diverticulosis
is associated with:
A) Low Fiber Diets
B) High Fiber Diets (
16.6%
)
C) NeitherD) Don’t Know (0%)
Best current evidence suggests high fiber diets are more likely to cause
diverticulosis
, but with the general scarcity of good evidence right now, “don’t know” is a perfectly reasonable answer as well. Slide49
Diverticulosis
& Low Fiber Diet: Correlation
vs
Causation
In Fundamentals of Nursing we were told during our GI lecture that
diverticulosis
(a
blebbing-out of weak points in the colon) is associated with low fiber diets. On page 1046 our medical-surgical nursing text says: “diverticula in the sigmoid colon are thought to be associated with high luminal pressures from a deficiency in dietary fiber intake.” It also points out that, “
The disease is more prevalent in Western, industrialized populations that consume diets low in fiber […] and is uncommon in vegetarians. The disease is virtually unknown in areas of world such as rural Africa where high-fiber diets are consumed
” (Lewis et al., 2011, p. 1046)
O
ur text also cites a 2009 study in the journal of family practice that admitted: “
no direct evidence establishes a role for fiber in preventing diverticulitis” (Weisberger & Jamieson, 2009, abstract).Slide50
Diverticulosis
& Low Fiber Diet: Correlation
vs
Causation
In 2012 a study in the journal of gastroenterology with 2104 participants (as opposed to a few dozen as in most previous studies), using outpatient colonoscopy to determine incidence of
diverticulosis
(as opposed to asking patients if they felt fewer symptoms after eating more fiber as in most previous studies) found that
high fiber diets, not low fiber diets are associated with diverticulosis. (Peery et al., 2012).
This is just one study however, and history has demonstrated that no single study should be used as the basis for policy changes. The thing is though, no previous or subsequent study on the relationship between fiber and
diverticulosis
comes close to the level of evidence provided in this study. More research is badly needed.Slide51
Diverticulosis
Remember that the NCLEX still expects you to regurgitate the idea that low fiber diets cause
diverticulosis
.Slide52
Myth # 2: Contrast Media Allergies
Adverse reactions to contrast media are associated most strongly with:
Grapefruit allergies
Iodine and shellfish allergies
Nut allergies
None of the above
Don’t knowSlide53
Contrast Media Allergies
Adverse reactions to contrast media are associated most strongly with:
Grapefruit allergies
Iodine and shellfish allergies
Nut allergies
None of the above
Don’t knowSlide54
Contrast Media Allergies
Adverse reactions to contrast media are associated most strongly with:
Grapefruit allergies
Iodine and shellfish allergies
Nut allergies
None of the above (
5.6%
)Don’t knowSlide55
The Iodine & Shellfish Allergy Myth
Iodine is used in contrast media because it absorbs X-rays. Iodine is a component of proteins all over your body. It is not an allergen (
Schabelman
& Witting, 2010). If you had an allergy to iodine, you’d be dead (
Baig
et al., 2014). Even just iodine deficiency from lack of dietary intake causes hypothyroidism (Iodine Deficiency, 2015). T4 and T3 are made largely of iodine, and “70% of the body’s iodine is distributed in other tissues, including mammary glands, eyes, gastric mucosa, arterial walls, the cervix, and salivary glands. In the cells of these tissues, iodide enters directly by the sodium-iodide
symporter
(Iodine Deficiency, 2015). When an element has its own transportation mechanism in your cells, that’s a good sign that it’s important.Slide56
The Iodine & Shellfish Allergy Myth
There are no documented cases of any real allergies to iodine. As an important component of proteins used by organs all over your body it's highly
anergized
by your immune system (because it’s present in your body during embryonic development). The way our immune systems work, developing an allergy to iodine is no more possible than developing an allergy to iron. People that have an allergy to
povidone
iodine prep do not have an allergy to iodine; they have an allergy to the additives in the preparation. Slide57
The Iodine & Shellfish Allergy Myth
Moving on to the shellfish part, shellfish allergy is no more strongly associated with an adverse reaction to contrast media than any other allergy. This erroneous assumption stems from the idea that these allergies are due to iodine content in the shellfish, which is also false (shellfish allergies are due to proteins in shellfish that do not contain iodine). It is
atopy
(having a lot of allergies) in general that indicates an increased risk of an adverse reaction to contrast media, with no one allergy standing above the rest as a risk indicator (
Baig
et al., 2014).Slide58
Contrast media allergies aren’t even allergies
“Allergies” to contrast media are not even an allergy at all. Rather, people who have lots of allergies tend to have hyperactive inflammatory systems, and the
hyperosmolality
of contrast media can irritate the vasculature (
Sicherer
, 2004), causing a “direct stimulation of mast cells and
basophils
to release mediators leading to “anaphylactoid” reactions (pseudo-allergy). This may lead to urticaria, bronchospasm, hypotension, and even cardiac arrest (
Baig
et al., 2014). There are two basic types of contrast media: non-ionic low
osmolality
and ionic high osmolality
, both of which have iodine in them. The non-ionic kind generates less dissociation, which means fewer particles floating around in the blood. Recall medical misconception #4, where we discussed how osmolality is determined by the number of molecules suspended in a solvent. “These [low osmolality] compounds are usually about one-half to one-third as osmotically active as the ionic forms, and associated with fourfold or greater reduction in all adverse reaction and fivefold decrease in severe adverse reactions” (Baig et al., 2014). The iodine and shellfish assessment question we all memorized for the NCLEX is BS (bad science)Slide59
So What Should Radiologists Be Assessing For?
We discussed how people with allergies tend to have more active inflammatory systems. This means that people with any type of allergy at all are at a higher risk for an adverse reaction to contrast media. Obviously, people with a previous history of a reaction to contrast media are at the highest risk.
Radiologists should be assessing first for previous reaction to contrast media, followed by any history of any allergies, and the type and severity of reactions to those allergens.Slide60
Iodine & Shellfish Allergy Myth
Remember that the NCLEX still expects you to regurgitate the idea that iodine allergies exist and they, along with shellfish allergies indicate an increased risk of adverse reactions to contrast media.
On Tests the truth isn’t important. It’s what the test-makers think is true that’s important.Slide61
Myth # 3?: Salt Intake
Speaking of which, you had better watch out for
all of you iodine allergy people.Slide62
Salt
Reducing sodium intake to below 2300mg in the general population:
Reduces all-cause mortality
Increases all-cause mortality
Has no significant effect on all-cause mortality
Don’t know
“Salt: It’s the thing that makes food taste bad when it’s not in it.”
- unknownSlide63
Salt
Reducing sodium intake to below 2300mg in the general population:
Reduces all-cause mortality
Increases all-cause mortality
Has no significant effect on all-cause mortality
Don’t knowSlide64
Salt
Reducing sodium intake to below 2300mg in the general population:
Reduces all-cause mortality
Increases all-cause mortality
Has no significant effect on all-cause mortality
Don’t know
A new meta-analysis suggests that the safe intake range for sodium is 2645-4945mg, well above the AHA-recommended 2300mg maximum limit, which may be unhealthily low. Given the scarcity of strong evidence, “don’t know” is currently the only reasonable answer here.Slide65
How much does sodium intake reduction reduce blood pressure?
I tried asking nurses how much they thought a reduction from the national average sodium intake of 3400mg to the AHA-recommended 2300mg limit would reduce average blood pressure.
Guesses ranged from 5 to 15 points systolic and diastolic, with the average guess being 10 points systolic and 9 points diastolic.Slide66
How much does sodium intake reduction reduce blood pressure?
A Large Cochrane meta-analysis found that reducing sodium intake by 1729mg reduced BP by 4.18/2.06. A 2358mg reduction in daily sodium intake yielded 5.39/2.82 in hypertensive people and 2.42/1.00 in
normotensive
people. Note that if a person with average sodium intake (3400 mg) reduces their intake by 2358mg they would be at 1042mg/day. (He, Li, & Macgregor, 2013). Assuming a linear relationship between sodium intake reduction and BP reduction for the purpose of roughly guessing what the reduction in BP would be when reducing sodium intake from 3400mg to 2300 mg, one would expect a drop of
3.43/1.79
mmHg for hypertensive people and
1.54/0.636
mmHg for normotensive people.
So sodium intake reduction does reduce blood pressure. Just not as much as you’d think.Slide67
Salt
Until the past few years, nobody ever checked for an association between sodium intake reduction from the average amount to 2300mg with incidence of heart attacks or strokes. The logic for the 2300mg sodium restriction has always been a three-step model as illustrated below:
Sodium intake is positively correlated with blood pressure
High blood pressure is correlated with adverse cardiovascular events
Reducing sodium intake in the general population will save livesSlide68
Salt
Let’s generate a model for this logic:
A is associated with B
B is correlated with increased mortality
Reducing A will save livesSlide69
Salt
Now let’s apply that logic to automobile accidents:
Most motor vehicle crashes occur at traffic lights
Motor vehicle crashes are positively correlated with death
Removing traffic lights from cities will save lives
This logic doesn’t work. Blood pressure cannot be used as a stand-alone surrogate for the risk of adverse cardiovascular events.Slide70
Salt
The AHA recommends (ideally) reducing sodium intake to
1500 mg/day
The FDA, CDC, WHO, USDA (US department of agriculture), AND (academy of nutrition and dietetics), ADA (
american
diabetes association), and many other reputable organizations currently recommend a maximum sodium intake of
2300mg/day
for the general population.
A recent meta-analysis published in March of 2014 observed sodium intake via 24-hour urine collection and all-cause-mortality rates and found that mortality followed a J-shaped curve with an actual safe range of sodium intake to be between 2645mg and 4945mg, for both
normotensive
and hypertensive people, suggesting that the 2300mg limit is unhealthily low. Intake below 2645mg was associated with no change in the incidence of adverse cardiovascular events, but it
was
associated with an increase in all-cause-mortality, especially with hypertensive patients that suffered from
comorbidities
(Alderman et al., 2014).
In other words, according to this study, whether you’re hypertensive or not, reducing your sodium intake to 1500mg or 2300mg/day
makes you more likely to die
.Slide71
The Problem(s) With Scholarly Articles
They are hard to read.
Scholarly articles are full of esoteric, field-specific jargon and statistical expressions that researchers may be familiar with, but most health care professionals are not. Unless you’re well-educated in the specific systems being discussed in a given article, and you’re a seasoned professional at reading scholarly articles or you’ve recently taken a course in statistics, you’re lucky to get through two sentences in the methods or results section without having to spend five minutes looking something up.
Sometimes scholarly articles are wrong.
And whether an article is based on strong evidence or not, odds are you didn’t read and understand the entire article.
People like to cite them without understanding them.
Because they’re hard to read, people don’t take the time to judge an article’s research methods before they cite it.Slide72
For Example:
A recent study published in 2014 demonstrates that salt causes hypertension and kidney damage in rats!
“Salt-induced epithelial-to-
mesenchymal
transition in Dahl salt-sensitive rats is dependent on elevated blood pressure” (Wang et al., 2014)
=
Rats on a high sodium diet suffered from hypertension and kidney damage. Rats on the normal sodium diet were perfectly healthy by comparison.
Looks bad for salt. But a study is only as good as its methods.Slide73
The rats in this study received a
0.3%
NaCl
diet as a “normal” sodium diet. The rats on the “high sodium” diet received an
8%
NaCl diet. How Much salt is that? https://www.youtube.com/watch?v=gENVB6tjq_M Let’s do a few back of the envelope calculations to see how much salt that is.Americans eat an average of 3400 mg of sodium per day. Americans eat on average 4 pounds of total food (1814.37G) per day. This translates to a 0.18739287% Na diet, or 0.4572386028% NaCl diet (multiply %Na by 2.44 to get %
NaCl
).
Now that we know that Americans eat a
0.46%
NaCl diet we have a basis for comparison.The 0.3% “normal” NaCl would equate to 5.44311G NaCl = 2230mg Na/day for humans (right around the AHA maximum limit, and only a couple hundred below my meta-analysis’ minimum healthy limit, so a reasonably safe-looking number). How much salt did the “high salt” diet rats get?Deliberate Obscurantism vs. Curiosity & Free TimeSlide74
Deliberate Obscurantism vs. Curiosity & Free Time
The rats on the “high sodium” diet received an 8%
NaCl
diet, the human equivalent of 145.2G
NaCl
, or 59.49G =
59,488mg
of sodium/day. That’s 25.86 times the AHA’s recommended maximum, and 11.9 times the maximum recommended by the meta analysis that I provided, and 17.5 times the current average American intake (One of my frozen TV dinners has 1500mg of sodium. That’s like eating 40 TV dinners every day).Something worth noting: Even at this ridiculously high salt intake, only the modified salt-sensitive rats experienced a markedly higher blood pressure. The Brown Norway rats they used “do not develop elevated blood pressure on a high-salt diet as do SS rats” (Note: the term “salt resistant” they use to describe the brown Norway rats is misleading; they are not bred for special tolerance to salt. They are just normal rats, just as the terms “salt sensitive” and “salt resistant” when referring to people refer to individuals that are especially sensitive to increased salt intake and normal people, respectively). In the United States, about 25% of the population is salt-sensitive.
X 40Slide75
Deliberate Obscurantism vs. Curiosity & Free Time
Not only does this study not trump the meta-analysis, it doesn’t even disagree with it. The meta-analysis asserts that the safe sodium intake range is 2645 to 4945mg, with higher intakes resulting in hypertension and increased mortality. This study asserts that if you feed a rat the human equivalent of 60,000mg of salt it will have really bad hypertension (provided it’s a salt-sensitive rat and not a normal rat). Slide76
If you cite scholarly articles without taking the time to read and understand them
You’re going to have a bad time.Slide77
Many Studies on Sodium Intake are Deceptive
Many studies by researchers that support a reduction in sodium intake suffer from the same problems:
When using an animal model they drown the subjects in ridiculous amounts of salt that no human would be capable of eating the equivalent of
They use increased blood pressure as a proxy for an increased incidence of adverse cardiovascular events, which fails to take into account the other side effects of reducing sodium intake.
They do not examine the effects of low salt intake. They only compare a healthy salt intake with a ridiculously high salt intake, leading agencies like the AHA, FDA, and CDC to suggest restricting sodium below a maximum amount and say nothing about a lower healthy limit.Slide78
Salt
A lot of recent research and position statements by prominent national and international organizations suggest lowering sodium intake
“A reduction in salt intake lowers blood pressure and, thereby, reduces cardiovascular risk”
- “Effect of longer-term modest salt reduction on blood pressure”
(He, Li, & Macgregor, 2013)
“Reduced sodium intake results in reduced blood pressure levels. High blood pressure increases your risk for heart disease and stroke”
- Heart & Stroke Foundation
(Dietary sodium, heart disease & stroke, 2014).
“Sodium increases blood pressure,” “eating less sodium now will help curb that rise and reduce your risk of developing other conditions associated with too much sodium, such as stroke, heart failure, osteoporosis, stomach cancer, and kidney disease”
- American Heart Association
(About Sodium, 2014).
To name just a fewSlide79
Salt
There is also a lot of recent research that criticizes the 1500 and 2300mg sodium intake limits
“Fatal and nonfatal outcomes, incidence of hypertension, and blood pressure changes in relation to urinary sodium excretion”
http://www.ncbi.nlm.nih.gov/pubmed/21540421
“Low-salt intake during mating or gestation in rats is associated with low birth and survival rates of babies”
http://www.ncbi.nlm.nih.gov/pubmed/25197564
“The science upon which to base dietary sodium policy”
http://advances.nutrition.org/content/5/6/764.full
“Reducing dietary sodium the case for caution”
http://jama.jamanetwork.com/article.aspx?articleid=185293
“Data rather than opinion dictates that a definitive clinical trial must determine if the US government’s sodium guideline is safe and effective
http://ajh.oxfordjournals.org/content/24/8/859.extractSlide80
This Wouldn’t Be the First Time
Peanuts
(Huang, F., & Nowak-
Wegrzyn
, 2008)
Cholesterol
Saturated Fats
MSG (FDA & WHO say it’s fine)
Gluten
(
Biesiekierski
, 2013)Thankfully Health & Nutrition Authorities didn’t jump on the MSG or anti-gluten bandwagonshttps://www.youtube.com/watch?v=exi7O1li_wA&list=PL723E862403291665 Tom
Naughton’s
“Big Fat Fiasco”Slide81
Subjective Validation
Subjective validation is where a person believes two unrelated events are related because their hypothesis demands that they be related.
A significant amount of research is done not for the purpose of discovering causal relationships, but for the purpose of proving the researchers’ hypotheses correct.Slide82
Clarification:
Sodium restrictions are very often necessary and useful for individuals with liver and kidney dysfunction (because dysfunctional kidneys can’t dispose of excess sodium). The question is whether sodium intake reduction would be beneficial for the general population and for individuals with hypertension and otherwise healthy kidneys and livers.Slide83
The Controversy
The American Heart Association (AHA) stands by its advisory that everyone should restrict sodium intake to under 2,300 mg, or 1,500 in certain groups, warning consumers to be WARY of this new study. President elect of AHA and cardiologist at Brigham and Women’s Hospital, Dr. Elliot Altman comments,
“Given the abundance we have about excess sodium in diet and its relationship to hypertension and the ability of us as health professionals to recommend to patients that if they lower their blood pressure they will reduce their risk of heart disease and stroke, we are not distracted by these analyses [by the IOM] that have significant methodological flaws.”
Further, AHA CEO Nancy Brown cautions,
“In short, this new analysis of these studies should not be used as rationale to reverse public health policy recommendations.”
The authors of the study insist, “The findings here lend support to those who have questioned the scientific basis for sodium reduction [recommendations], which are based primarily on the assumed blood pressure effect obtained in selected intervention studies and a selected meta-analysis of intervention studies.” Gradual’s team references previous results, published by Cochrane review, supporting modest reductions in salt intake to improve blood pressure.
The American Council on Science and Health (ACSH)’s Dr. Gil Ross had this comment:
“The AHA persists in its ivory-tower warning, which is both scientifically unsound and impractical to say the least, among humans who actually eat. Again and again we’ve seen studies showing that population-wide sodium restriction is fraught with potential consequences: while it may help some groups with severe high blood pressure or fluid retention, it may harm others. Further, the AHA’s response is mere blather, as Dr. Altman immediately shifted the discussion from sodium restriction to the benefits of reducing elevated blood pressure. While the latter is indisputable, the former is at least a matter of academic discussion”
(Our sodium intake is just right, a new study finds, 2014).Slide84
The Controversy
In 2013 the Institute of Medicine (IOM) convened a committee to review the effects of sodium intake on health outcomes other than blood pressure, focusing on intake from 1500 to 2300 mg/day. The final report supported population-wide efforts to lower sodium, but concluded that there were insufficient data to support a lowering of sodium to less than 1500 mg/day as recommended by the AHA, or less than 2000 mg/day as recommended by the WHO (Cook,
Appel
, &
Whelton
, 2014).
Which leads me to a question that I find myself asking frequently: Slide85
Wikipedia, what should I believe?
“The effect of a low salt diet on mortality or cardiovascular disease is unclear with any benefit in either hypertensive or normal
tensive
people being small if present” (Low sodium diet, 2014).
WIKIPEDIA HAS SPOKENSlide86
The only thing that’s clear right now is that more research is needed as to the health effects of sodium intake reduction.
For the NCLEX, remember that the 2300mg limit is still recommended in the US. Just know that the evidence is shaky.
SaltSlide87
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