Low Sodium’s link to Fat Gain & Insulin Resistance (Salt vs. Sugar)

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This episode is brought to you by Skillshare. In 1979 at an FDA panel hearing in Washington,
Frito-Lay’s research director Alan Wohlam, along with an NYC cardiologist and a cancer
researcher from buffalo, defended salt on behalf of the Potato Chip and Snack Foods
Association. They warned that salt restricting guidelines
would be dangerous. That “The risks associated with too little
salt in the diet, were particularly high among infants and children, diabetics, pregnant
women and women using estrogen-based contraceptives.” Now, as Mark Antony said, “I come to bury
Caesar, not to praise him.” Potato Chips, Snack Foods and Processed Foods
are the last thing someone should eat, unless they are literally starving. Even if they are defending it, having someone
affiliated with such food products speak on salt’s behalf probably doesn’t help its
reputation. However, just because someone is associated
with something nefarious doesn’t always mean that they’re wrong – even if we really
don’t want to trust them. It was said that salt restriction would be
dangerous for pregnant women, infants and children, and diabetics. I mentioned in my last video that studies
have shown that pregnant women develop a marked craving for salt, and that women on a low
salt diet compared to a high salt diet, caused more miscarriages, stillbirths and premature
babies. Salt is critical for proper growth in general. As this article from the Journal of Biomedical
Science points out, salt restriction impedes fetal growth and specifically stunts development
of cardiovascular organs or decreases the number of nephron in the kidney, predisposing
the baby to hypertension in adulthood. It also says that “salt restriction is associated
with a decrease in insulin sensitivity.” As diabetes is a state of insulin resistance,
this overlaps with the notion that salt restriction could be dangerous for diabetics. But what could salt possibly have to do with
diabetes? Well, it actually relates to why people sometimes
feel sick on a very low carbohydrate or ketogenic diet. This sick feeling, better known as the keto-flu,
involves headache, fatigue, nausea and muscle weakness. These symptoms also match those of sodium
depletion. This happens because a higher level of ketones,
greater release of glucagon, and in particular lower levels of insulin – all things that
occur during carbohydrate restriction, increase the body’s excretion of sodium. This is because one of insulin’s functions
is to have your kidneys hold onto more sodium. A lot of people talk about the “keto flu”
like it’s an unavoidable phase of the ketogenic diet, but you can avoid this by simply replacing
the sodium that you lose. The flip side of this, is that when you are
on a low salt diet, the body will actually use insulin as a tool for preserving and holding
on to the salt that it has. This study, done on 147 people with normal
weight and blood pressure found that “With dietary salt restriction serum total- and
LDL-cholesterol as well as serum insulin and uric acid concentrations increased significantly.” The effect on insulin seems to be so significant
that, a study published in the Metabolism Journal, found that just one week on a low
sodium diet caused onset of insulin resistance in a group of healthy volunteers. In fact, doctors have known that diuretics,
which deplete salt, can also promote insulin resistance and diabetes. As the study says: “Low-salt diet activates
the renin-angiotensin-aldosterone and sympathetic nervous systems, both of which can increase
insulin resistance.” And, this study in the New England Journal
of medicine shows that when salt intake drops below just 1.5 teaspoons per day, a significant
increase in renin occurs, indicating the renin-angiotensin-aldosterone system is being activated. The WHO, by the way, recommends getting no
more than one teaspoon of salt per day. Another study specifically implicates increased
aldosterone as a pathway for low salt’s causing of Insulin resistance. Aldosterone is a key hormone that is secreted
as part of the renin-angiotensin-aldosterone system. In fact, aldosterone blocking drugs – Angiotensin
Converting Enzyme inhibitors or ACE inhibitors are being explored as a treatment for insulin
resistance. Other than insulin resistance, aldosterone
is better known for raising blood pressure. ACE inhibitors are frequently prescribed for
the treatment of hypertension. Let me point out again that you can also keep
aldosterone levels low by simply getting enough salt. Now there’s a different white crystal that
you do want to avoid. Cardiovascular research scientist, James DiNicolantonio
points out in his book “The Salt Fix” several of the uncanny ways in which salt
and sugar have almost directly opposite effects. Not only do both a high sugar intake and low
salt intake provoke insulin resistance and therefore diabetes, the pathways by which
this occurs are remarkably similar. Table sugar, sucrose, is one part glucose
and one part fructose. About a year ago I put out a video explaining
the biochemistry behind why fructose is particularly fattening, damaging to the liver and how it
provokes insulin resistance. It was based on the work of Robert Lustig,
Andrew Bremer and Michele Snyder. I’ll spare you the explanation of all the
reactions here, but there’s just one thing I want to point out. This diagram is showing that during fructose
metabolism, this enzyme JNK-1 is activated, leading to insulin receptor IRS-1 phosphorylation. Just remember that: JNK-1 activation leads
to IRS-1 phosphorylation. Simply put, this insulin receptor IRS-1 is
being deactivated. Now, for insulin to work properly, the insulin
secreted from the pancreas needs to bind to this receptor. Due to fructose’s deactivating of this insulin
receptor, the pancreas has to work harder and pump out more insulin to get its job done,
leading to insulin resistance. So that’s sugar, but what happens with low
salt? As this study says: “In summary, the insulin
resistance, induced by Low Salt, is tissue-specific and is accompanied by activation of JNK and
IRS-1 phosphorylation.” (Sound familiar?) The article continues, to say: “The impairment
of the insulin signaling in these tissues, but not in adipose tissue, may lead to increased
adiposity and insulin resistance in Low Salt rats.” Increased adiposity simply means increased
fatness. Now, The idea that low salt could make someone
fat and put them on a path to diabetes may sound dubious, especially to certain people
because, ironically, the people who are putting themselves on a low salt diet are doing so
probably because they are already very health conscious in general and far from being fat. That said, it is possible for people to be
very lean and still have insulin resistance. Low salt is more likely to be a contributing
factor to, rather than the sole factor in insulin resistance. Insufficient salt intake could be one factor
in the that little bit of stubborn fat you haven’t gotten rid of, or maybe the weight
loss plateau you’ve hit. Now, there’s just a little bit more to be
explained about how else low salt could make it easier to gain weight and even worsen insulin
resistance. In his book “The Fat Switch,” physician and
researcher at the University of Colorado, Richard Johnson makes the case that there
is some sort of “switch” that activates weight gain. While it’s something we humans all want
to avoid, In the animal world, weight gain is a very strategic move. Animals have essentially learned how to become
obese so they can survive. As Johnson says: “While Darwin emphasized
the principle of the survival of the fittest, there is an equally important concept of survival
of the fattest.” Johnson gives several examples of animals
employing this strategy: “The 13-lined ground squirrel routinely
doubles its fat content in the late summer in preparation for hibernation during winter. The Emperor penguin also doubles its weight
in fat prior to protecting and warming its eggs during the fierce Antarctic winter. The bar-tailed dogwit markedly increases its
fat in its liver and blood prior to migrating thousands of miles to its winter home.” Johnson explains in a 2013 paper of his that
these animals aren’t just making themselves fat, they are essentially inducing metabolic
syndrome in themselves. They get fatty liver, insulin resistance and
accumulate visceral fat. For us, this is a diseased state, but for
these animals, it’s a damn good way to store fat for the winter. So, what is causing this insulin resistance
and fat storage? What is flipping the fat switch? Johnson says that the key factor is increased
levels of uric acid. Uric acid is commonly viewed as a simple waste
product and most physicians are only concerned with it in the context of gout and kidney
stones. However, as Johnson points out: “an elevated
serum uric acid is extremely common in people who are obese, especially if they have fatty
liver or are insulin resistant.“ If you look at a person with gout, a disease
characterized by elevated levels of uric acid, you commonly see: Abdominal obesity, fatty
liver, elevated triglycerides, hypertension, and… insulin resistance and diabetes. For a while, it was thought that elevated
uric acid was not a cause, but simply a consequence of obesity, fatty liver and insulin resistance. However, this study in the Journal of Biological
Chemistry found that if you put uric acid on liver cells, they will begin to produce
fat. The conclusion was very straightforward: “Rather
than a consequence, uric acid induces fatty liver.” The way this works is quite interesting. Uric acid induces oxidative stress in the
cells’ mitochondria. This specifically inhibits an enzyme called
Aconitase in the citric acid cycle, leading a build up of citrate. Citrate is a substance that stimulates fat
production. Uric acid also inhibits another enzyme required
for the burning of fatty acids, leading to less ATP being produced. This all means: more fat synthesis, less fat
burning, and less energy production. If you’re a human with things to do and
places to be, this isn’t so great, but it’s perfect for an animal trying to prepare for
the winter. When animals have used up their fat stores
and need to start foraging for more food, there is a marked rise in uric acid to help
store that food as fat. But there’s another way to increase uric
acid and that’s by consuming fructose. Every spring tropical rains fall heavily on
the Amazon basin, causing the forest to flood. When this happens, as many as 200 different
types of fruit eating fish come in to eat the ripe sweet fruit that the trees are dropping. One of these fish is the Pacu, which looks
like a piranha but is larger and doesn’t have sharp teeth. The Pacu eats as much sweet, fructose containing
fruit as it can and converts it to fat, which it stores as oils in its liver and tissues. One study found that the average fat content
of the Pacu went from 10 to 28 percent after gorging on fruit. After the flood waters recede, the Pacu returns
to the low water where food is scarce. Luckily, the Pacu has stored up so much fat
that it can go without eating for as long as six months. Humans too have always liked fructose, and
especially since 1820, consumption of it began to rise dramatically. Of course this wasn’t fructose from fruit,
but from table sugar. John Yudkin, British physiologist and author
of the 1972 book “Pure, White and Deadly,” was able to show multiple times that just
a few weeks on a high-sugar diet, would result in elevated insulin and uric acid.” If we go back to Robert Lustig’s paper,
we can see a pathway through which fructose causes this production of uric acid. And, of course all this ties back to low salt
diets. As shown in the earlier mentioned 1991 study,
“With dietary salt restriction … serum insulin and uric acid concentrations increased
significantly.” Another 2017 study shows that “Serum uric
acid fell significantly in both the moderate and high [sodium] interventions compared to
the low sodium intervention.” One study even found that when diabetic patients
were placed on a higher-sodium diet, their insulin response improved. The authors even suggested that some people
should even supplement with sodium, stating that “an abundant sodium intake may improve
glucose tolerance and insulin resistance, especially in diabetic, salt-sensitive, or
medicated essential hypertensive subjects.” As Dr. DiNicolantonio writes in the Salt Fix:
“We’re finding that increasing your salt intake, even above what’s generally considered
a normal intake, may help improve your insulin sensitivity.” However, hypertension is a very common complication
of diabetes. Unfortunately, as per common practice, diabetic
patients are very likely to be prescribed a low-salt diet in order to attempt to deal
with their blood pressure. As mentioned last time Around 12 grams of
salt per day (which contains about 4.5 grams of sodium) seems to be the optimal intake
for most people. However, if you drink more than 3 cups of
coffee a day, or you’re on a low carbohydrate diet or you are sweating alot from exercise
or heat exposure, you may want to try and see how you feel on a few more grams of salt. Also, everyone’s situation is of course
different, so if you do have insulin resistance, you may want to look further into this topic
or check with an expert before ramping up your salt intake. I started this video off talking about Frito
Lay, but snack foods and processed foods should not be your source of sodium. Where you get your sodium does matter. Most salts have anti-caking agents in them,
which you definitely want to avoid. There’s all kinds of higher quality salts
from celtic sea salt to the recently popular pink himalayan salt. So, I think that while the editing in my videos
is acceptable, it’s not like I have the most impressive animations or infographics. I have to rely on my writing to make a narrative
that presents somewhat complicated or dry concepts in an interesting way. And, like Kurt Vonnegut said: “When I write,
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