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.​”[1]

Now,​ ​as​ ​Mark​ ​Antony​ ​said,​ ​“​I​ ​have​ ​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​ ​worsens​ ​its​ ​reputation.
However,​ ​just​ ​because​ ​someone​ ​is​ ​associated​ ​with​ ​something​ ​nefarious​ ​doesn’t​ ​always
mean​ ​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.[​2​]​ ​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.”[​3​]

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.[​4​]

This​ ​is​ ​because​ ​one​ ​of​ ​insulin’s​ ​functions​ ​is​ ​to​ ​have​ ​your​ ​kidneys​ ​hold​ ​onto​ ​more
sodium.[​5​]​ ​ ​So,​ ​if​ ​you​ ​lower​ ​your​ ​insulin​ ​levels​ ​by​ ​decreasing​ ​carbohydrate,​ ​you​ ​will​ ​lose
a​ ​lot​ ​of​ ​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​.”[​6​]​ ​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.[n]​ ​As​ ​the​ ​study​ ​says:​ ​“​Low-salt​ ​(LS)​ ​diet
activates​ ​the​ ​renin-angiotensin-aldosterone​ ​and​ ​sympathetic​ ​nervous​ ​systems,​ ​both​ ​of
which​ ​can​ ​increase​ ​insulin​ ​resistance​ ​(IR).”​[​7​]

And,​ ​As​ ​mentioned​ ​last​ ​in​ ​my​ ​last​ ​video,​ ​a​ ​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.[​8​]​ ​The​ ​WHO,​ ​by​ ​the​ ​way,​ ​recommends​ ​getting​ ​no​ ​more​ ​than​ ​one
teaspoon​​ ​of​ ​salt​ ​per​ ​day.[​9​]

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.​ ​[​10​]​ ​In​ ​fact,​ ​aldosterone​ ​blocking​ ​drugs​ ​-
A​ngiotensin​ ​C​onverting​ ​E​nzyme​ ​inhibitors​ ​or​ ​ACE​ ​inhibitors​ ​are​ ​being​ ​explored​ ​as​ ​a
treatment​ ​for​ ​insulin​ ​resistance.​ ​As​ ​this​ ​study​ ​says:​ ​“​The​ ​positive​ ​effects​ ​of​ ​ACE​ ​inhibitor
drugs,​ ​particularly​ ​on​ ​hypertriglyceridemia​ ​and​ ​insulin​ ​resistance​,​ ​might​ ​bring​ ​them
forth​ ​as​ ​first-line​ ​drugs​ ​in​ ​the​ ​treatment​ ​of​ ​obese​ ​and​ ​hypertensive​ ​children​.​”[​11​]

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.[​12​]

So​ ​that’s​ ​sugar,​ ​but​ ​what​ ​happens​ ​with​ ​low​ ​salt?​ ​As​ ​this​ ​study​ ​says:​ ​“​In​ ​summary,​ ​the
insulin​ ​resistance,​ ​induced​ ​by​ ​LS,​ ​is​ ​tissue-specific​ ​and​ ​is​ ​accompanied​ ​by​ ​activation
of​ ​JNK​ ​and​ ​IRS-1(ser307)​ ​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​ ​LS​ ​rats.​”[​13​]​ ​Increased
adiposity​ ​simply​ ​means​ ​increased​ ​fatness.

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​ ​already​ ​probably​ ​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.​ ​[​14​]​ ​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.​”[15]

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.[​16​]​ ​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​ ​production​ ​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.​“[15]

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.​ ​“[​17​]

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.​ ​In​ ​one​ ​study,​ ​the​ ​average​ ​fat​ ​content​ ​of​ ​the​ ​Pacu​ ​went​ ​from​ ​10​ ​to​ ​28
percent.​ ​After​ ​the​ ​flood​ ​waters​ ​recede,​ ​the​ ​Pacu​ ​returns​ ​to​ ​the​ ​low​ ​water​ ​where​ ​food​ ​is
scarce.​ ​Luckily,​ ​the​ ​Pacu​ ​has​ ​stored​ ​so​ ​much​ ​fat​ ​that​ ​it​ ​can​ ​go​ ​without​ ​eating​ ​for​ ​as​ ​long
as​ ​six​ ​months.[15,​ ​18​]

Humans​ ​have​ ​always​ ​liked​ ​fructose,​ ​and​ ​especially​ ​since​ ​1820,​ ​consumption​ ​of​ ​it​ ​began
to​ ​rise​ ​dramatically.[​19​]​ ​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.[20,​ ​21​]”​ ​If​ ​we​ ​go​ ​back​ ​to​ ​Robert​ ​Lustig’s​ ​paper,​ ​we​ ​can
see​ ​a​ ​pathway​ ​through​ ​which​ ​fructose​ ​causes​ ​this​ ​production​ ​of​ ​uric​ ​acid.​ ​[12]

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​.”[6]​ ​Another​ ​2017​ ​study​ ​shows​ ​that​ ​“​Serum​ ​uric​ ​acid​ ​fell
significantly​ ​in​ ​both​ ​the​ ​moderate​ ​and​ ​high​ ​[sodium]​ ​interventions​ ​compared​ ​to​ ​the​ ​low
sodium​ ​intervention.​”[​22​]​ ​Keep​ ​in​ ​mind​ ​that​ ​high​ ​uric​ ​acid​ ​means​ ​higher​ ​insulin​ ​and
worsened​ ​insulin​ ​resistance.

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.​”[​23​]​ ​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.​"[24]
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​ ​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.​ ​There’s​ ​all​ ​kinds​ ​of​ ​healthy​ ​sources​ ​of​ ​sodium​ ​than​ ​what​ ​is​ ​sitting​ ​in​ ​most​ ​salt
shakers.​ ​Just​ ​leave​ ​tortoises​ ​alone,​ ​they​ ​already​ ​have​ ​enough​ ​trouble​ ​with​ ​butterflies
harassing​ ​them​ ​and​ ​drinking​ ​their​ ​salty​ ​tears.

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