Jag får många frågor om salt och har därför valt att skriva lite mera om salt och natrium.
Det är inte själva saltet som är en hälsofara utan natriumbalansen, då höga halter av natrium i kosten (genom förbrukning av vanligt salt, natriumklorid) är förknippat med högt blodtryck och ohälsa inom hjärt-och kärl. Trots detta så är fokusering på natriumminskningen begränsat till ett fåtal länders folkhälsoarbete.
Undersökningar påvisar att de flesta vuxna i världens befolkningen har ett genomsnittligt natriumintag som ligger över det som påvisats hälsosamt. I europeiska och nordamerikanska länder, dominerar natriumintag från bearbetade livsmedel (vilket ligger på cirka 75% av intaget). Spannmål och bakverk var den största enskilda källan till natriumintaget hos vuxna medborgare i Storbritannien och USA. I Japan och Kina kom merparten av natriumtillförseln från salt i hemmamatlagning och från sojasås.
Slutsatserna är att det finns ett ofördelaktigt högt natriumintag i världen. Natriumbegränsning rekommenderas ofta som en åtgärd för att sänka blodtrycket och därmed också för att minska kardiovaskulär sjukdom (CVD) m.m.
Tänk på att salt är nödvändigt för syra/basbalansen och därmed också bindningen av vatten till kroppen. Att minska på salt är således inte det som bidrar till hälsosammare mat, utan det faktum att saltet bör ha mindre innehåll av natrium. Välj gärna naturliga salter som havs- och bergssalt. För hela studien, följ länken ”läs mer”.
In the appended article, once again, we see research validating one of your
primary theses… that is – protein dietary restriction.
Coming from a performance athletic background, your low protein diet
admonition was a hard sell for me. I used to take protein supplements by
the hand full, and I consumed protein bars constantly in addition to taking
Creatine and other protein building supplements. You have conclusively
shown that muscle mass can be just as easily be built and maintained on a
low protein vegetarian diet as on a high animal protein diet. It’s all in
the quality of the blood.
The attached article points out how high-energy protein synthesis at the
cellular mitochondrial level works. Our bodies produce more of a ”high
energy” protein (d4EBP) in the mitochondria when the ingestion of protein is
restricted. The article is silent on whether the beneficial effects of a
low protein diet, still hold up IF all ingested protein is vegetarian in
origin.
You certainly seem to be correct again, when you say that we should avoid
ALL animal protein. BUT….I wonder if it is also necessary to avoid
vegetarian protein as well?
The population of Loma Linda, CA is statistically one of the longest-lived
in the world. It is thought that the reason for this statistical variance
is that most inhabitants of Loma Linda are Seventh Day Adventists, who are
largely vegetarian. Yet Adventists don’t intentionally restrict vegetarian
protein… and still the added longevity shows up in the statistical
evidence. This Loma Linda statistical variance may indicate that it is not
necessary to restrict vegetarian protein to get the the enhanced d4EBP
mitochondrial activity to which the appended article refers.
Regards,
John Baird
Sr. VP, Chief Legal Officer (CLO)
Director of Corporate Affairs
pH Miracle Center
Young pHorever, Inc.
————————–Referenced Article——————–
’Anti-Atkins’ Diet Extends Life in Flies
October 5, 2009
(Ivanhoe Newswire) — Flies fed an ”anti-Atkins” low protein diet live
longer because their mitochondria function better, according to a new study
from the Buck Institute for Age Research in California. The research shows
that the molecular mechanisms responsible for the lifespan extension in the
flies have important implications for human aging and diseases such as
obesity, diabetes and cancer.
Mitochondria act as the ”powerhouse” of the cells. It is well known that
mitochondrial function worsens with age in many species, and especially in
humans with Type II diabetes and obesity. ”Our study shows that dietary
restriction can enhance mitochondrial function, hence offsetting the
age-related decline in its performance,” Buck faculty member Pankaj Kapahi,
PhD, lead author of the study, is quoted as saying.
The research calls into question the health benefits of the high-protein
diets often used to lose weight. Kapahi said that while the long-term
impacts of such diets have not been examined in humans, he believes they are
likely to be harmful. ”In flies, we see that the long-lived diet is a low
protein diet and what we have found here is a mechanism for how that may be
working,” he said.
The researchers reported that while there is a reduction in protein
synthesis with the low protein diet, the activity of specific genes involved
in generating energy in the mitochondria are increased. That activity —
conversion of RNA to protein — is important for the protective effects of
dietary restriction, said Kapahi. ”There have been correlative studies that
show mitochondria change with dietary restriction, [and] this research
provides a causal relationship between diet and mitochondrial function.”
The study describes the mechanism by which mitochondrial genes are converted
from RNA to protein by a particular protein (d4EBP). Flies fed a low protein
diet showed an uptick in activity of d4EBP, which mediates cell growth in
response to nutrient availability. The research showed that d4EBP is
necessary for lifespan extension.
When the activity of the protein was genetically ”knocked out” the flies did
not live longer, even when fed the low protein diet. When the activity of
d4EBP was enhanced, lifespan was extended, even when the flies ate a rich
diet.
The Buck Institute study provides a significant advance in understanding the
role of 4EBP, said Kapahi, and implies an important role for 4EBP and
mitochondrial function as excellent targets to explore their role in
lifespan extension in mammals.
SOURCE: Cell, October 2, 2009
Reference: http://ivanhoe.com/channels/p_channelstory.cfm?storyid=22560
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