#hypertension is from #sugar not #salt #health

2011.{11..12}.1: health/hypertension
2012: summary:
. hypertension is not caused by excessive salt;
but rather by a high-glycemic diet
that provokes too much insulin
which is then disabling the kidneys
by preventing them from removing salt .
. another factor is arterial tension
that is controlled by magnesium .
. here again, insulin abuse is the culprit,
causing magnesium resistance,
requiring higher doses to the same job .
. high amounts of dietary fructose
can be another source of high blood pressure .
. some salty seaweed seems to have
little effect on pressure;
that's because the pressure problem comes only from
the kidney's inability to clear sodium chloride;
whereas some seaweed has no chloride:
its sodium comes in the form bound to proteins .
. Wrack seaweed is a great source of minerals
and is safe for those with high blood pressure .
. conversely,
higher levels of dietary fructose from added sugars
are responsible for not only high blood pressure,
but an epidemic of kidney disease .
11.10: web.health/hypertension/
sodium restriction vs seaweed:

. what is the controversy about salt causing hypertension;
isn't that just stale hypothesis like dietary cholesterol?
. there are hypertensive animal models
that do get strokes with excessive salt
-- the reference was found in Caduceus:
Strazzullo P et al, Salt intake, stroke, and cardiovascular disease:
meta-analysis of prospective studies,
BMJ 2009;339:b4567.
The most recent meta-analysis,
examining the results of 13 published studies on
‘habitual salt intake’, stroke and cardiovascular disease rates
in 170,000 people in 5 countries including the US and Japan,
concluded that a 5g reduction in salt intake in the population
could achieve a 23% drop in the number of strokes
and a 17% drop in total cardiovascular disease.

[2012.1.17: but that is mere medical trickery;
it only manipulates symptoms, not the cause;
instead, listen to Gary Taubes as he explains in
Good Calories, Bad Calories:
 . the evidence for the salt-
hypertension theory
is epidemiological, not from
controlled experiments
and the same evidence
could support a non-salt theory
since any time you have salt
in a modern diet
you also have refined grains,
added glucose, and fructose .
. water retention is not happening from excess salt;
rather, it is carbs' raising of insulin
that is causing the kidneys to resorb even excessive salt;
so then to compensate for the excessive saltiness,
the kidneys also retain more water
-- all for the high insulin provoked by our
modern, high-glycemic diet .
. not only does fructose cause hypertension directly,
but also a high-glycemic diet and excessive fructose
create an insulin resistance
that in turn creates magnesium resistance
which makes arteries tense .
. see magnesium as cure for hypertension;
the real problem is being insensitive to normal amounts .]

. Dr.Lustig alerted us to a trick of the foods industry
which uses disarmingly small quantities of salt
to make their sugary drinks more addictive .
. here is where salt, in ironically innocuous doses,
does indeed get involved in hypertension,
but not in the way we would assume .
. there could be a money problem here:
the modern diet's affect on our health
doesn't show up during the reproductive years,
hence it works fine for survivalists;
and, while civilization would like to feed both
hungry tummies and ravenous sex drives
they have no way of doing so without dirt-cheap grains .
. since you can't give up grains,
then it may help a little to give up salt .
. this was seen in the fat vs carbs debates too;
fats must be bad because giving up refined grains
would simply devastate the current budget of our
industrial government complex
-- and it is this complex which is funding
the academic papers that support our theories
about salt, fat, and grains .
the case for seaweeds:
. potassium and magnesium work with sodium
to regulate water balance, nerve impulses, and muscle tone .
The more sodium you get,
the more potassium and magnesium you need.
Few of us get enough greens,
yet we add high amounts of sodium to foods .
This leads to potassium and magnesium deficiency,
where nerves are over-stimulated [by a
relative excess of calcium? ]

. sodium needs a buffer, such as chloride,
and chloride is essential for gastric acid .
. sodium chloride is about 60% chloride;
there is  27mg of sodium per gram of seaweed
but, no chloride;
therefore, seaweed alone is a safe salt substitute;
[because only the chloride form of seaweed
is worsening the high blood pressure .]
[ 2012.1.18: news.health/hypertension/
blame the chloride not seaweed's sodium:
. only the chloride form of sodium causes hypertension:
Morris et al., showed that sodium bicarbonate (baking soda)
does not raise blood pressure in salt-sensitive folks,
they recommend that the
bicarbonate or citrate form of potassium,
and not the chloride form,
be the replacement for sodium chloride .
science mag 1983, dec` UCSF` Theodore Kurtz, Curtis Morris,
. sodium chloride but not other forms of sodium
is what causes hypertension in rats,
eg, sodium ascorbate is a vitamin-c-based preservative
that did not cause high blood pressure;
neither did sodium bicarbonate .
Dietary chloride as a determinant of
"sodium-dependent" hypertension:
Science 9 December 1983: Vol. 222 no. 4628 pp. 1139-1141
The uninephrectomized rat given desoxycorticosterone (DOC)
provides a classic model of "sodium-dependent" hypertension.
In such rats, the extent to which
a given dietary intake of sodium
induced an increase in blood pressure
depended on whether or not the
anionic component of the sodium salt
was chloride.
With normal and high dietary intakes of sodium,
sodium chloride induced increases in blood pressure
much greater than that induced by
approximately equimolar amounts of
sodium bicarbonate, sodium ascorbate,
or their combination .
A normal amount of dietary sodium chloride
induced hypertension,
whereas an equimolar amount of sodium bicarbonate
did not increase blood pressure.
This difference could not be attributed to
differences in sodium or potassium balances,
weight gain, or caloric intake.
The DOC model of "sodium-dependent" hypertension
might better be considered to be
sodium chloride -dependent hypertension. ]-2012
 the case for seaweeds:
. most dietary salt in Westernized nations
comes from processed foods – particularly bread,
responsible for some 75% of the excess !

biggest risk factors for hypertension:
# obesity, and physical inactivity;
[ getting more glucose than you can use,
and then getting too much insulin; ]
# [high fructose:
causes insulin resistance,
which then causes magnesium resistance,
which may contribute to hypertension;
and by another route: elevated uric acid  .]
# regular analgesic use
[is this how kidneys are messed by aspirins?]

. there are 4.5 grams of seaweed in
the traditional Japanese diet,
among the healthiest in the world.
-- Japanese 1964 population statistics, Caduceus 2009, 75, p18.

Seaweed removes toxic metals,
reduces cholesterol,  dissolve fats in the blood,
and its special polysaccharides are anticoagulants .
Japanese research has shown wrack seaweed
to act as an antidote to excessive salt.
It was discovered that
when stroke-prone rats were overfed salt,
only those also fed seaweed powder
did not have strokes’.
[ Yamori Y et al]
A chronic lack of dietary iodine ‘is largely responsible for
 an epidemic of hypo-thyroid linked illnesses
and breast cancer’.
[ Miller D, 2008;75. ]
Wrack seaweed ingredients:
-- 10 gram with 12% moisture (tsp/4)  --
protein 0.75 g
fiber carbs 0.5 g
polysaccharide carb's (including fucoidan) 80 mg
other carbs 4.5g
fat 0.320 g
iodine 3.9 mg
-- electrolytes:
sodium 350 mg (bonded to proteins not chlorine)
chloride 0
magnesium 70 mg
potassium 310 mg
-- essential enzyme precursors:
manganese 300 mic
selenium 1.5mic -- is this right? lower than I expected .
zinc 1300 mic
cu 2 mg
sulphur 300 mg
-- bone essentials:
calc 200 mg
boron 600 mic
silicon 10 mg
phosphorus 15 mg
-- misc:
iron 5.75 mg
cobalt 54 mic
gold 3.9 mg

. the Seaweed Health Foundation,
at the Centre for Food Innovation in Sheffield,
pursues a holistic approach in seaweed research.
-- see also Worldwide Action on Salt & Health (WASH),
and UK's Consensus Action on Salt & Health (CASH).
seaweed has no chloride; what does?
the use of chloride in the body:
(ncbi.nlm.nih.gov and wiki)
. sodium, needed for balance of blood volume,
can be bound to bicarbonate instead of chloride;
however, chloride is still essential:

. the stomach's Gastric acid is composed of
0.5% hydrochloric acid (HCl),
and large quantities of potassium chloride (KCl)
and sodium chloride (NaCl)
. hydrochloric acid is neutralized by sodium bicarbonate
to form NaCl and carbonic acid (carbon dioxide and water).
. sodium bicarbonate is also useful for
neutralizing dieter's ketones or other blood acidifiers .

. there might be 2g of sodium in food per day,
and 0.5 g lost by sedentary (imperceptable) sweating .
. 10g of salt contains 6g chloride . [2012.1.18:
. chloride's rda is 1.7 .. 5g /day .]
Chloride: The Forgotten Essential Mineral!
Chloride toxicity has been observed in humans
in cases of impaired sodium chloride metabolism,
e.g. in congestive heart failure.
[Seelig M.]
. vegetables are a healthier sources of chloride;
but there's not enough there
to meet the needs of an active adult,
[Altschul AM, Grommet JK.]
. the potassium in fruits and veg' is not chloride?
apparently most of the chloride we need
must be coming from our sodium chloride intake .
. while a high level of potassium in food
correlates with a high level of buffers,
those buffers need not include chloride .]-2012
. fluid retention and high blood pressure
 are attributed to the high sodium and potassium levels.
[Beard TC.]
 --[ 2012.1.18: that is refuted:
the key to fluid retention and high pressure is
the combination of sodium and chloride;
while sodium and potassium often come bound to chloride,
sodium and potassium alone are not the problem
-- blame the chloride not wrack seaweed's sodium .]
theory of salt reduction isn't working:
diuretic hypertension treatment isn't working:
. diuretic therapy over the past 50 years
has resulted in a dramatic reduction in deaths from
stroke and coronary heart disease (CHD);
[cardiac failure from clogged arteries]
yet, cardiac and renal failure steadily increase .
Uric Acid, the Metabolic Syndrome, and Renal Disease
J Am Soc Nephrol 17: S165–S168, 2006.
Metabolic syndrome, characterized by truncal obesity,
hypertriglyceridemia, elevated BP, and insulin resistance,
is recognized increasingly as a
major risk factor for kidney disease
and also is a common feature of patients who are on dialysis.
The rise in metabolic syndrome indirectly may be
a major contributor to the general rise in renal disease
that has been observed throughout the world
in the past few decades.

One feature that is common to patients with
metabolic syndrome
is an elevated uric acid.
Although often considered to be
secondary to hyperinsulinemia,
recent evidence supports a primary role for uric acid
in mediating this syndrome. Specifically, fructose,
which rapidly can cause metabolic syndrome in rats,
also raises uric acid;
and, lowering uric acid in fructose-fed rats
prevents features of the metabolic syndrome.
Uric acid also can accelerate renal disease
in experimental animals
and epidemiologically is associated with
progressive renal disease in humans.
It is proposed that fructose- and purine-rich foods
that have in common the raising of uric acid
may have a role in the epidemic of metabolic syndrome
and renal disease that is occurring throughout the world.

. recent studies have emphasized that metabolic syndrome
also is both associated with and a risk for
the development of chronic kidney disease (CKD)
--[related to glomerulosclerosis .]
. how might metabolic syndrome accelerate renal disease ?
Obesity has been associated with a type of
focal segmental glomerulosclerosis (FSGS) called
“obesity-related glomerulopathy”
Obesity also increases the risk factor for
diabetes and hypertension
and has been shown to lead to glomerular hypertension
and hyperfiltration .
The metabolic syndrome also is associated with
the release of inflammatory cytokines
and the presence of endothelial dysfunction
and oxidative stress,
all which could contribute to the
development of glomerulosclerosis.
Insulin resistance also may have a direct role
as a consequence of stimulating the
sympathetic nervous system
and the renin-angiotensin-aldosterone system .
Dyslipidemia, which is a feature of the metabolic syndrome,
[and directly correlates with high insulin levels]
may induce toxic and inflammatory tubulointerstitial injury .

Finally, the metabolic syndrome is also associated with
an elevated serum urine acid, and fructose intake .
Fructose rapidly raises uric acid as a consequence of
activation of fructokinase with ATP consumption,
intracellular phosphate depletion,
and stimulation of AMP deaminase .
Fructose constitutes 50% of table sugar
and also is a major component in high-fructose corn syrup,
which is used in the United States as a sweetener.
. fructose intake correlates well with
the recent rise in the epidemic of metabolic syndrome,
diabetes, hypertension, and kidney disease .

The main pathophysiologic mechanism by
which uric acid causes these conditions
involves an inhibition of
endothelial nitric oxide bioavailability
(which may  induce insulin resistance),
activation of the renin angiotensin system,
and direct actions on endothelial cells
and vascular smooth muscle cells .

Hyperuricemia predicts the development of both
hypertension and diabetes .
Mild hyperuricemia in normal rats
induces systemic hypertension,
renal vasoconstriction, glomerular hypertension
and hypertrophy,
and tubulointerstitial injury independent of
intrarenal crystal formation (30 –32).
Lowering uric acid in fructose-fed rats
ameliorates much of the metabolic syndrome,
including a reduction in BP, serum triglycerides,
hyperinsulinemia, and weight gain .

Epidemiologic studies also have found that
hyperuricemia is an independent risk factor for
renal dysfunction in the normal population
and in patients with hypertension, diabetes, and CKD .
This leads to the hypothesis that fructose intake
may be a novel mediator of
the epidemic of renal disease.
--. this reminds that one problem with Atkins diet
could be that most will have metabolic syndrome,
and have kidneys that are already in bad shape
from fructose abuse;
so, this would be a bad time to stress them with high fats .
. it might be safer to try a 2-phase approach:
first quit the sugars and quick carbs
without trying to lose weight;
use a lot beans with olive oil, whey protein folded in,
and a few eggs on separate occasions .
. with sugar out of the way,
it's safe moving to the induction phase .

magnesium supplements may help
Dr. Cohen's Magnesium Solution
is addressing only blood pressure;
Dr. Carolyn Dean `The Miracle of Magnesium,
relates magnesium deficiency to
emotions (anxiety, panic attacks, depression),
metabolic disorder (fatigue, diabetes,
heart disease, osteoporosis, insomnia),
muscular problems( asthma, migraines ).

a nutritional anthropologist:
(author of Deadly Harvest)
. up to 75% of Americans
are deficient in magnesium;
--[. this is actually measuring
magnesium resistance;
magnesium sensitivity depends upon
insulin sensitivity,
and this loss of sensitivity
can be due to dietary abuse
or chronic high stress
as seen in the mentally ill,
and in those minorities who are
trapped in cycles of poverty .
. without adequate magnesium sensitivity,
artery walls can't relax and flex;
hence, it is one reason for hypertension .]
Dr. Cohen's main message is that
magnesium is often overlooked;
the usual non-medicinal interventions
are confined to addresssing
obesity, lack of exercise, low fiber,
salt, alcoholism, and smoking .
--[. notice that obesity implies either
high insulin or insulin resistance .
. alcoholism, smoking, and lack of exercise
all worsen insulin resistance .
. fast carb's are safe for youth only because
youth still have good insulin response,
and so their insulin doesn't get high enough
to block the salt from exiting the kidneys,
so, they don't collect the water .
. additional magnesium has the effect of
decreasing the insulin resistance,
along with relaxing the arteries .]
Dr. Cohen with magnesium.
cured his own vascular disease
he offers a mountain of scientific references
to  support that conclusion .
beware blood tests:
. your blood level of magnesium remains normal
while your bones are still becoming weakened.
. a normal test of blood magnesium means little.
your body removes magnesium from the bones
in order to maintain
the level required in the blood.
beware the wrong version of
"(High Blood Pressure Solution):
. Dr.Moore has the establishment's
recommendations (near vegetarian
and an extreme phobia of fats).
. proof?
he mentions primitive people diets
in terms of hunter/gatherer,
but uses farming communities as proof.
He also chooses to ignore the fact that
the majority of hunter/gather societies
relied far more on fats than carb's
(mentions Eskimos as proof,
but fails to acknowledge
they didn't get any carbs in their diet;
also seems unaware of
Pemmican - 50/50 fat/meat -
which was a staple diet of the
healthy, long-lived Plains Indians).
-- . see Dr. Ellis's
Ultimate Diet Secrets
or Faigin's
Natural Hormonal Enhancement

for proof that Zone diets
are perfectly healthy .

. one reviewer suggests a particular
form of Magnesium 
Taurate (from Cardiovascular Research)
for heart health and also sleep.
. another user clarifies:
(Chelated magnesium is absorbed
without diarrhea)
Krebs cycle chelated minerals.
eg, Enzymatic Therapy
[Chelated with citrate, fumarate, malate,
succinate, and alpha ketoglutarate]
and Source Naturals
[Magnesium Malate is their
Krebs cycle chelate
-- the one they label as "(Chelate)
is bound to amino acids from
hydrolyzed vegetable protein .]
wiki's chelate FAQ for how to bind Mg:
. Virtually all biochemicals exhibit the ability to dissolve
certain metal cations. (like magnesium)
Thus, proteins, polysaccharides, and polynucleic acids
are excellent polydentate ligands for many metal ions.
-- contrasted with monodentate ligands,
which form only one bond with the central atom
and are thus not as effective at keeping a mineral
soluble and not producing precipitates or scale.
Organic compounds such as
the amino acids glycine and histidine,
organic di-acids such as malate,
and polypeptides such as phytochelatin
are also typical chelators .