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Author Topic: mp siin - kui sul ei ole midagi asjalikku öelda, tee seda mujal.  (Read 99070 times)

mp

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Re: mp siin - kui sul ei ole midagi asjalikku öelda, tee seda mujal.
« Reply #600 on: January 15, 2018, 19:43:10 »


https://www.ncbi.nlm.nih.gov/pubmed/29301002

Nephrol Dial Transplant (2018) 1–10
doi: 10.1093/ndt/gfx340

Should we eat more potassium to better control blood pressure
in hypertension?

Michel Burnier

* What kind of potassium supplement should be given?
One of the practical questions is in what form should potassium
supplement be prescribed in order to be effective? Most
clinical studies have used potassium chloride. However, in fruits
and vegetables, the anion accompanying potassium is not chloride.
To answer this question, He et al. [49] performed the first
randomized crossover study in a small group of hypertensive
patients comparing the effects on BP of potassium chloride and
potassium citrate given for 1 week. The BP-lowering effect
was comparable with the two forms of potassium supplementation.
In contrast, a recent double-blind, placebo-controlled
study compared the effects of potassium magnesium citrate
(KMgCit), potassium chloride (KCl) and potassium
citrate (KCit) on 24-h ambulatory BP in hypertensive and prehypertensive
subjects, using a randomized crossover design.
The goal of this study was to clarify which of the three components
of K, Mg and citrate is important in lowering BP [50].
Interestingly, a significant reduction of BP was found with KCl
but not with the two other preparations of potassium, indicating
that potassium is the key element and that KCl and KMgCit
or KCit supplementation have differential effects on BP. Thus
these data differ from the initial observation reporting no difference
between potassium chloride and potassium citrate.

* CONCLUSIONS
Primitive humans consumed a diet very rich in potassium and
poor in sodium. Today this pattern is completely reversed. Food
manufacturing is probably responsible for both the increased
sodium and reduced potassium content of food products. There
is now sufficient scientific evidence to support an increase in
potassium intake to reach a urinary potassium excretion between
90 and 120 mmol/day in patients with essential hypertension and
preserved renal function (eGFR> 60 mL/min/1.73 m2
) in order to help lower their BP. There is also rather good evidence that a
high-potassium diet decreases the incidence of stroke and CVDs,
although for these latter there is no level A evidence from trials at
the moment. Regarding patients with impaired renal function,
there is a definite need for new randomized prospective trials in
all CKD stages in order to determine the potential benefits and
risks of increasing potassium in the diet.
In clinical practice, these conclusions could be translated as a
change in the conventional lifestyle recommendations given to
patients with hypertension or cardiovascular or renal disease.
Indeed, physicians could give a more positive recommendation
for better nutrition, encouraging the consumption of more
healthy products with a high potassium content rather than the
sempiternal message ‘Don’t eat salt!’ As illustrated in Figure 5,
the recommendations on salt could thus be tailored to the urinary
potassium excretion or to the Na:K ratio in urine, recommending
primarily an increase in potassium intake with fruits,
vegetables and nuts in patients with a moderate excess of salt
intake or a combined reduction of sodium and increase in
potassium intake in those with excessive salt consumption. In
any case, the definite answer to the title of this article is yes, one
should eat more potassium to lower BP and prevent cardiovascular
events.
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mp

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Re: mp siin - kui sul ei ole midagi asjalikku öelda, tee seda mujal.
« Reply #601 on: January 20, 2018, 09:16:22 »


https://www.ncbi.nlm.nih.gov/pubmed/29238244

Influence of A Thermogenic Dietary Supplement on Safety Markers, Body Composition, Energy Expenditure, Muscular Performance and Hormone Concentrations: A Randomized, Placebo-Controlled, Double-Blind Trial.

"No unfavorable effects of supplementation were reported, and the supplement did not adversely affect safety markers. However, the supplement did not reduce fat mass or increase lean mass relative to placebo. In the supplement group, lower body maximal strength was increased relative to placebo (+18%, d=1.1 vs. +10%, d=0.5), and cortisol concentrations were decreased relative to placebo (-16%; d=-0.4 vs. +15%, d=.75). However, no differences were observed for upper body maximal strength or muscular endurance. REE increased in response to both supplement and placebo ingestion (placebo: +5%; supplement: +11.5%), but the difference between conditions was not statistically significant. Overall, some select parameters may have been beneficially modified by supplementation, but this did not result in superior weight or fat loss over 6 weeks of supplementation and resistance training."
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