Post by Enrico CPost by Enrico CAppro'... Ho appena trovato un articolo sulla Zona dal Journal of the
American College of Nutrition che, dalle prime righe, mi pare
piuttosto
Post by Enrico Cprudente, se non addirittura scettico, rispetto ad alcuni dei
"benefici"
Post by Enrico Cdella Zona... però su altri (vedi omega3) mi pare più possibilista
:)
Post by Enrico CDevo ancora leggerlo fino in fondo però.
Quel poco d'inglese che mastico non mi permette di leggere un
articolo così complesso. Se dopo averlo letto mi fai un sunto, ti
ringrazio.
Ci provo, sperando di evitare troppi errori e imprecisioni! ^^
http://www.jacn.org/cgi/content/full/22/1/9
Journal of the American College of Nutrition, Vol. 22, No. 1, 9-17 (2003)
Published by the American College of Nutrition
Review Article
"The Zone Diet Phenomenon: A Closer Look at the Science behind the Claims"
Samuel N. Cheuvront, PhD, RD
U.S. Army Research Institute of Environmental Medicine, Natick, Maine
L'argomento sono i "The purported health benefits" della Zona, cioè i
benefici asseriti dalla Zona. L'articolo passa in rassegna la
documentazione scientifica esistente per verificare quali effetti siano
dimostrati e quali no... Tra i benefici documentati, secondo l'articolo,
i vantaggi degli Omega-3. Sugli altri aspetti della teoria della Zona però
l'articolo dice che mancano studi scientifici verificabili, quindi non
resta che passare in rassegna gli studi esistenti su argomenti vicini.
Questi studi, secondo l'articolo, portano a conclusioni diverse da quelle
della Zona, per esempio riguardo al rapporto proteine/carboidrati
raccomndato, e quindi alla distribuzione dei macronutrienti...
[Nell'articolo però non si prendono in considerazione i possibili effetti
psicologico, lo stimolo positivo a cambiar vita, di cui parlavamo nel
thread.]
L'articolo esordisce con un parorama generale sulla diffusione delle diete
"low-carb", intendendo "low" come basso rispetto alle raccomandazioni
ufficiali... in questo senso include tra le "low carb" anche la Zona, anche
se come sappiamo non è a bassissimi carb, anzi...
ABSTRACT [Sintesi]
The purported health benefits of low-carbohydrate diets have been advocated
intermittently over the last century and have enjoyed increasing popularity
over the last decade. Although most revolve around the emphatic theme that
carbohydrates are to blame for many chronic diseases, their specific
ideologies are more variable and in some cases quite sophisticated. The
Zone Diet phenomenon represents a new generation of modern low carbohydrate
food fad with sales placing it among the most popular diet books in recent
history.
Si ricordano quindi alcuni dei postulati della Zona, e alcuni dei benefici
asseriti... [per ora solo in sintesi]
The Zone is a 40% carbohydrate, 30% protein and 30% fat eating plan that
advocates only sparing use of grains and starches. The precise 0.75 protein
to carbohydrate ratio required with each meal is promoted to reduce the
insulin to glucagon ratio, which purportedly affects eicosanoid metabolism
and ultimately produces a cascade of biological events leading to a
reduction in chronic disease risk, enhanced immunity, maximal physical and
mental performance, increased longevity and permanent weight loss.
Si dice, però, che certi collegamenti non sono stati dimostrati, anzi la
letteratura scientifica suggerisce che chi ci siano alcune contraddizioni
nella teoria della Zona. Ci si propone quindi di discutere cosa della Zona
ha solidi fondamenti scientifici e cosa no...
There is presently little scientific support for the connections made
between diet, endocrinology and eicosanoid metabolism. In fact, a review of
the literature suggests that there are scientific contradictions in the
Zone Diet hypothesis that cast unquestionable doubt on its potential
efficacy. The purpose of this review is to evaluate the scientific merit of
the Zone Diet and its health claims in an effort to help delineate what is
and what is not sound nutrition science.
Le conclusioni dell'articolo sono anticipate in questi punti (traduco
velocemente e saltando qualche dettaglio che mi pare meno decisivo, scusate
le approssimazioni...):
Key teaching points:
• The Zone Diet is a carbohydrate-restricted diet that postulates a
connection between diet, hormones and eicosanoids that ultimately leads to
improved health.
La zona è una dieta a bassi carbo che postula un collegamento tra dieta,
ormoni e eicosanoidi per ottenere risultati benefici sulla salute.
• There is no evidence that a 0.75 protein to carbohydrate ratio
(40/30/30), whether eaten as a small test meal or in the form of a complete
mixed diet, reduces the insulin response when compared to traditional
dietary guideline meal/food intakes and may even potentially produce a
larger area under the insulin curve.
Non ci sono prove, secondo l'articolo, che un rapporto 0.75 tra proteine e
carbo (dieta 40/30/30) riduca la risposta insulinica, a confonto di
un'alimentazione da linee guida, e anzi potrebbe portare persino,
potenzialmente, a un'area più grande sotto la curva dell'insulina. Questo
sia per piccoli pasti di test si per pasti completi come nell'alimentazione
reale.
• The Zone classification of eicosanoids as "bad" or "good" based on
receptor binding or on gross physiological functions is oversimplified, but
the recommendation to supplement the diet with omega-3 fatty acids or
progenitors of series-1 eicosanoids has some documented health merit.
La classificazione degli eiconosanoidi tra "buoni" e "cattivi" della Zona è
troppo semplificata. Tuttavia, la raccomandazione di integrare la dieta con
grassi acidi omega-3 o "progenitori di eicosanoidi della serie-1", ha
qualche merito salutistico documentato.
• Although carbohydrate, protein, insulin and glucagon can impact delta
desaturase enzyme activity, those activities reported by the Zone clearly
and selectively ignore the known effects of macronutrients and hormones
that contradict the Zone theory.
Sebbene carbo, proteine, insulina e glucalone possono effettivamente aver
effetto sull'attività dell'enzima desaturasi, la teoria della Zona ignora
però altri effetti conosciuti di macronutrienti ed ormoni che contraddicono
la Zona...
• The scientific literature is in opposition to the purported benefits of
adopting a Zone Diet for improved health.
La letteratura scientifica si trova in contrasto con i benefici asseriti
della Zona...
Segue il testo di dettaglio... Introduco [tra parentesi quadre] qualche mia
nota che forse può aiutare la lettura... sempre se ho capito bene anch'io!
^^
INTRODUCTION
The purported [asseriti] health benefits of low-carbohydrate diets have
been advocated [sostenuti] intermittently over the last century and have
enjoyed increasing popularity over the last decade [decennio]. Although the
extremity of dietary carbohydrate restriction varies among popular low
carbohydrate diets, the belief that carbohydrates are in one way or another
to blame for most chronic diseases [da incolpare per la maggior parte delle
malattie croniche] remains a consistent [costante] and emphatic theme. On
the other hand [D'altra parte], the theories offered to explain the
association between lower carbohydrate intakes and improved health are more
variable and have become progressively more sophisticated. For the
credulous consumer identifying with the recognized link between science,
nutrition and health, the appearance of a scientific basis for popular low
carbohydrate diet claims is alluring. [in parole povere: le teorie sempre
più sofisiticate invocate alla base delle diete low carb finiscono per
attrarre il consumatore credulo, anche se a volte si tratta solo di
apparenza di scientificità]. The Zone Diet phenomenon represents a new
generation of modern low carbohydrate food fad with sales placing it among
the most popular diet books in recent history.
The Zone Diet’s theoretical basis is intricate, and some of its detailed
content enigmatic. As a result, many health and nutrition scientists choose
simply to dismiss its health claims. [molti nutrizionisti si limitano
semplicemente a non dar valore ai benefici asseriti dalla Zona]. However,
while the Zone Diet is generally regarded as fiction, the foundations for
its theories are based on real scientific facts. [Però, anche se le Dieta a
Zona è generalmente considerata come "fiction", le fondamenta delle sue
toerie sono costruite a partire da alcuni fatti scientifici reali]. Since
even a pure myth usually contains a particle of truth [particella di
verità], an unbalanced dismissal of the Zone Diet argument is ineffective
in combating its claims and may even serve to perpetuate confusion among
the popular media when nutrition and health professionals attempt
communicating to the consumer what is and what is not sound nutrition
science. [in parole povere: la semplice scrollata di spalle del
nutrizionista ufficiale non chiarisce le idee alla gente, perché anche
nelle teorie infondate c'è pur sempre un granello di verità, e quindi per
fare chiarezza occorre spiegare bene cosa ha fondamento scientifico e cosa
no].
Carbophobia is a form of nutrition misinformation infused into the
American psyche through multiple advertising avenues that include magazine
ads, television infomercials and especially best selling diet books.
[La paura dei carboidrati è una forma di disinformazione nutrizionale
infusa nella psiche americana da molti canali di propaganda, come gli
annunci pubblicitari, gli spot che mischiano informazione alla pubblicità,
e i libri best-seller sulle diete popolari]]
Due to the freedom of press guaranteed under the First Amendment, the
lucrative publication of dubious nutrition information is difficult to
combat. The success of the Zone Diet book by Barry Sears [1] in 1995 led to
publication of at least ten Zone-related books or Zone "knock-offs". The
American Dietetic Association promotes dissemination of sound,
science-based nutrition information to correct and counter pervasive
nutrition misinformation [2]. Therefore, the purpose of this review is to
evaluate the scientific merit of the Zone Diet and its health claims in an
effort to help delineate what is and what is not sound nutrition science.
WHAT IS THE ZONE DIET?
The recommendation to achieve a dietary macronutrient distribution of
approximately 55% carbohydrate, 15% protein and 30% fat is widely
acknowledged and based upon an extraordinary depth of scientific research
spanning more than 25 years [3–7]. [in sintesi: la raccomandazione
ufficiale di circa 55C-15P-30G è basata su ricerche scientifiche
approfondite nel corso di oltre 25 anni].
In contrast, the Zone Diet is defined as a 40% carbohydrate, 30% protein
and 30% fat eating plan that specifically advocates sparing use of grains
and starches [1]. [All'opposto, la Zona 40-30-30 sostiene un uso contenuto
di cereali e amidi]. More importantly, the protein to carbohydrate ratio
(P:C) of the diet is 0.75, or 3g of protein for every 4g of carbohydrate.
[E soprattutto, il rapporto p/c 0,75, cioè 3 g di proteine ogni 4 di
carbo]. This is approximately three times the ratio (0.25) resulting from
conventional diet recommendations. [Ovvero, il triplo del rapporto p/c 0,25
delle linee guida]. According to Zone Diet doctrine, every meal must
conform to this 0.75 P:C in order to realize the purported health benefits.
[Per la Zona, ogni singolo pasto deve avere un p/c 0,75 per ottenere
benefici]. The Zone Diet prescription is centered primarily on protein
intake, which is specified as 1.1–2.2 g/kg fat-free mass, depending on
activity level [1]. [La Zona suppone un fabbisogno di proteine da 1,1 a 2,2
g per Kg di massa magra, a seconda dell'attività fisica]. The carbohydrate
component is derived from the desired 0.75 P:C, while fat intake makes up
the remaining 30% of total energy. [Di conseguenza si calcolano i carbo, e
il restante 30% delle calorie in grassi]. The Zone Diet prescription for
three body mass indexes (BMI) [indice di massa corporea] and corresponding
body fat percentages [8] associated with the need for weight loss are
presented in Table 1. Assuming a sedentary lifestyle, Table 1 makes it
clear that a Zone Diet is both a low energy and low carbohydrate diet.
[Come si vede dalla tabella 1, che appare cliccando, la Zona è una dieta
ipocalorica, oltre ad essere low carb]. Once a desired amount of body fat
is lost, dieters [coloro che fanno la dieta] may add fat back to the diet
to maintain appropriate body fat levels while keeping the P:C of the diet
and every meal at 0.75. [Una volta raggunto il dimagrimento desiderato, per
la Zona si può aggiungere grassi alla dieta, mantenendo però il rapporto
p/c di 0,75]. In this way, the Zone transforms from a weight loss diet to a
lifestyle diet [1,9]. [In questo modo, la Zona si trasforma da dieta
dimagrante in regime alimentare ordinario per la vita].
View this table:
[in this window]
[in a new window]
Table 1. Sample Zone Diet Prescriptions at Three Undesirable Body Mass
Indexes
The "Zone" is defined as a metabolic state in which the human body operates
at optimal efficiency [1]. [La Zona viene definita come uno stato
metabolico in cui il corpo umano opera ad efficienza ottimale]. The
specific health benefits of the Zone Diet purportedly include, but are not
limited to, permanent weight loss, prevention of chronic diseases, enhanced
immunity, maximum physical and mental performance and even greater
longevity [1]. [Tra i benefici asseriti, dimagrimento, prevenzione di
malattie croniche, rafforzamento immunitario, massime performance fisiche e
mentali e persino maggior longività]. Zone Diet claims of maximum physical
performance have been both refuted [10–13] and rebutted 14]; however, all
benefits attributed to the Zone Diet are based on the same mechanistic
premise. [I vanti di massima performance fisica sono stati "confutati" (se
capisco bene "refuted and rebutted"), ma tutti i benefici attribuiti alla
Zona si basano sulle stessa premessa]. Fig. 1 illustrates the proposal that
a 0.75 P:C will reduce the insulin to glucagon ratio (I:G), allow excess
body fat to be "burned" (weight loss) and ultimately lead to the production
of "good" eicosanoids [1,9]. According to the Zone theory, eicosanoids are
extremely powerful biological agents and the specific production of "good"
eicosanoids is responsible for all the diet’s purported health benefits
[1]. Therefore, the Zone Diet is a carbohydrate-restricted diet that
postulates a connection between diet, hormones and eicosanoids that
ultimately leads to improved health. [Secondo la Zona, il rappporto p/c di
0,75 riduce il rapporto tra insulina e glucalone, consente di bruciare il
grasso corporeo in eccesso e porta infine alla produzione di eicosanoidi
"buoni", agenti biologici estremamente potenti che sarebbero responsabili
di tutti i benefici asseriti.] The scientific questions of interest in this
review are 1) Does changing the dietary P:C from 0.25 to 0.75 alter the
insulin to glucagon ratio (I:G) enough to reduce or suppress the anabolic
actions of insulin? 2) Can an alteration in the I:G result in the precise
control of eicosanoid metabolism? [Le questioni scientifiche da chiariree
sono: 1) se davvero il rapporto p/c 0,75 modifichi il rapporto I:G tra
insulina e glucalone e 2) se tale modifica porti a un preciso controllo del
metabolismo degli eicosanoidi.]
Fig. 1. Postulated biological sequence of events linking a lower
carbohydrate intake with a state of superior health known as the Zone [1,9]
(P:C = protein to carbohydrate ratio; I:G = insulin to glucagon ratio).
THE SCIENCE BEHIND THE ZONE: A CLOSER LOOK
Diet and Blood Glucose Homeostasis [La dieta e l'omeostasi (equilibrio) del
glucosio nel sangue].
The endocrine pancreas produces two hormones that regulate blood glucose
concentrations. [Il pancreas produce due ormoni che regolamo le
concentrazioni del glucosio nel sangue]. Insulin is a glucose-lowering
hormone produced by pancreatic beta cells while neighboring alpha cells
produce its antagonist glucose-raising hormone glucagon. [L'insulina è un
ormone che abbassa la concentrazione di glucosio mentre il glucalone è
l'ormone suo antagonista, che invece tiene alto il glucosio]. The exact
mechanisms to explain the control of blood glucose homeostasis have been
recently clarified in a series of intricate glucose, insulin and glucagon
clamping studies. [L'esatto meccanismo di azione che spiega uk controllo
del glucosio sanguigno è stato recentemente chiarito in una serie di studi
sugli intricati rapporti tra glucosio, insulina e glucalone]. Fig. 2
illustrates that, within the physiological range of fasting and
postprandial blood glucose concentrations, glucose homeostasis is achieved
almost exclusively by variations in insulin release and withdrawal
[16–18].. It is only when blood glucose concentrations fall below this
biological range that glucagon and other counterregulatory hormones prevent
or correct hypoglycemia in a hierarchical manner. [In sostanza: Nei valori
fisiologici normali, il livello del glucosio è in sostanza controllato dai
rilasci di insulina. Solo quando il glucosio sanguigno scende sotto certi
livelli, intervengono anche il glucalone e altri ormoni per correggere e
prevenire l'ipoglicemia] Both glucagon activity and release are suppressed
through one or more mechanisms involving direct or indirect alpha cell
inhibition by glucose, glucose transport, glucose metabolism, or insulin
[16,19–22]. In the most simplistic sense, the net metabolic trend toward
anabolism (insulin) or catabolism (glucagon) depends on the insulin to
glucagon ratio (I:G). However, the metabolic release of insulin and
glucagon are so highly sensitive to blood glucose concentrations that the
activity of glucagon is largely suppressed in the postprandial period so
long as blood glucose concentrations remain within the physiological range
[16–18] (Fig. 2). [Nei termini più sempplicistici, il metabolismo tende
all'anablismo (insulina) o catabolismo (glucalone) in base al rapporto I_G
tra insulina e glucalone. Però, l'attività del glucalone è largamente
sopressa durante il periodo post-pranzo, finché il glucosio e l'insulina
restano nei valori fisiologici, come nell'esempio che segue...]. For
example, ordinary postprandial insulin concentrations (25–100 µU/mL)
abolish the lipolytic actions of glucagon (200 pg/mL) [23] during
euglycemia both in vitro [24] and in vivo [25]. [Per esempio, una normale
concentrazione di insulina post-pranzo di 200..., sopprime l'azione
lipolitica del glucalone (l'azione cioè di "bruciare i grassi", se non
erro...)]
Fig. 2. Construct of normal blood glucose regulation and associated
glycemic thresholds [soglie] suggests that insulin release and withdrawal
[rilascio o ritiro di insulina] exclusively regulates [regola in maniera
esclusiva] plasma glucose in the resting, postabsorptive state. Adapted
from reference [17].
[Insomma, se ho ben capito, si dice che a dirigere il gioco normalmente è
l'insulina, ma il glucalone entra in gioco quando si tratta di evitare
l'ipoglicemia o abbassamento eccessivo del glucosio sanguigno]
The classic insulin and glucagon responses to the ingestion of single
nutrients are well documented. Carbohydrates (hyperglycemia) stimulate
insulin release while protein (hyperaminoacidemia) stimulates the release
of glucagon and insulin [16,26–28]. The hormonal response to protein intake
promotes amino acid uptake and protein synthesis (insulin) while preventing
hypoglycemia (glucagon) [16]. This is conceivably an advantageous
evolutionary adaptation for any carnivorous animal subsisting largely on a
meat diet. However, when protein and carbohydrate are consumed mixed
together, a synergy is produced resulting in a larger release of insulin
when compared to carbohydrate or protein eaten alone [29–31]. According to
the principles of the Zone Diet [1], a 0.75 P:C (acceptable range of
0.6–1.0) represents the ideal macronutrient balance to reduce plasma
insulin and shift the I:G ratio in favor of the catabolic, lipolytic
hormonal milieu most suitable for weight loss and "good" eicosanoid
production (discussed below). Because there are no peer-reviewed scientific
data on the Zone Diet that would specifically allow an explicit examination
of this claim, related literature must be examined and the implications of
these data extrapolated to the Zone condition.
[Le classiche risposte dell'insulina e del glucalone all'ingestione di
singoli nutrienti sono ben documentate. I carbo stimolano il rilascio di
insulina mentre le proteine stumolano il rilascio di glucalone e insulina,
in modo da favorire l'assorbimento degli aminoacidi e la sintesi proteica
(con l'insulina) evitando però l'ipoglicemia (grazie al glucalone). Perà,
quando proteine e carbo sono consumati nello stesso pasto, si produe una
sinergia che risulta in un rilascio maggiore di insulina rispetto a un
pasto solo di carbo o solo di proteine. Secondo i principi della Zona, un
rapporto p/c di 0,75 [con un range accettabile tra 0,6 e 1] rappresenta
l'equilibrio ideale per ridurre l'insulina nel plasma e modificare il
rapporto I:G insulina-glucalone in modo da favorire l'azione ormonale
catabolica e lipolitica che porta al dimagrimento e alla produzione di
eicosanoidi "buoni" (discussi in seguito). Occorre però sottoporre a vaglio
queta affermazione, e siccome non ci sono dati scientifici relativi alla
Zona "peer-reviewed", verificati cioè da altri scienziati, occorre
esaminare la letteratura scientifica connessa e le implicazioni che si
possono trarre rispetto alla Zona. Di sequito, quindi, si citano alcuni
esperimenti che hanno verificato le concentrazoni di insulina e glucosio
sanguigno dopo pasti di test con diversi rapporti p/c...].
Protein/Carbohydrate Ratios and the Endocrine Pancreas
Spiller et al. [29] fed different combinations of liquid P:C food boluses
to normal subjects and measured their acute (2 hour) glucose and insulin
responses to those meals. The results of these experiments [29] showed that
the area under the curve (AUC) for glucose was significantly greater for a
P:C of 0.27 (conventional diet recommendations) than either 0.58 or 0.86
(ratios within Zone Diet recommendations). However, this difference was due
solely to what occurred in the first 30-minute postprandial period, and
blood glucose levels returned to normal in each condition within ~60
(0.27), ~45 (0.58) and ~35 (0.86) minutes, respectively [29]. More
importantly, the AUC for insulin was not different among the three P:C’s.
Therefore, the release and withdrawal of insulin required to regulate these
small differences in blood glucose was similar for all three dietary
ratios.
[L'esperimento di Spiller ha mostrato che un p/c più alto, 0,58 o 0,86,
anziché lo 0,27 convenzionale, riduce l'"Area sotto la curva" AUC del
glucosio sanguigno (limitatamente ai primi 30 minuti dopo il pasto) ma non
l'AUC dell'insulina].
Westpahl et al. [30] also examined the effects of food bolus P:C’s (mixed
solid and liquid food) similar to conventional (0.20) and Zone Diet (0.60,
1.0) levels on 4 hour glucose, insulin and glucagon measurements. This
study showed no differences in glucose, insulin or glucagon AUC
attributable to P:C ratios [30]. There was, however, a clear trend for both
insulin and glucagon concentrations to be higher in proportion to higher
P:C ratios. This is not surprising given the known metabolic effects of
this macronutrient combination. No statistical comparison was made among
the I:G of the diets, but the data do support a reduction in I:G when the
P:C is increased. However, this is of little metabolic consequence when
blood glucose concentrations are within the physiological range (fasting
and postprandial), since insulin suppresses the activity of glucagon. In
fact, because absolute insulin areas rose in step-wise fashion as the P:C
increased [30], a higher P:C could be argued to stimulate a more anabolic
condition, perhaps favorable for weight gain and "bad" eicosanoid
production (discussed below).
[L'esperimento di Westpahl non ha trovato differenze nelle AUC di insulina,
glucalone e glucosio attribuibili a variazioni del rapporto p/c. Si è
notato, comunque, una tendenza all'aumento sia dell'insulina che del
glucalone all'aumentare del p/c, con presumibile riduzione del rapporto
I:G, ma ciò ha scarse conseguenze metabiliche quando le concentrazioni di
glucosio sono all'interno dei limiti fisiologici normali ("fasting and
postprandial", che credo si traduca: a digiuno e dopo un pranzo), perché
l'insulina sopprime l'attività del glucalone. Addirittura, nota l'articolo,
l'aumento assoluto dell'insulina al crescere del p/c potrebbe favorire
l'aumento di peso e la produzione di eicosanoidi "cattivi"...!]
In one of the only peer-reviewed studies to examine and compare long-term
(six months) effects of Zone-like (0.78) and conventional (0.24) P:C’s on
human metabolism, Linn et al. [32] showed that 1) there was no significant
difference in fasting lipid oxidation when people consumed either diet, 2)
glucagon suppression (release) by insulin was equally sensitive on both
diets, 3) the glucose threshold for insulin release was reduced by 15%
after a 0.78 P:C diet, and 4) glucose sensitivity was reduced by 26% on the
0.78 P:C diet. All of these data indicate that consuming a diet with a
Zone-recommended P:C (0.6–1.0) has no greater potential to promote fat
burning, weight loss or any other phenomenon related to I:G alterations
(see below) when compared to a diet consistent with conventional
nutritional recommendations because associated insulin levels are likely to
be as high or higher in response to increasing the P:C.
[In uno dei soli studi peer-reviewed che abbiano confrontato gli effetti
sul metabolismo di diete tipo Zona (p/c 0,78) e convenzionali (p/c 0,24)
sul lungo termine (sei mesi), non si sono notate differenze sul metabolismo
che porta a bruciare grasso corporeo, perdere peso o altri fenomeni
collegati a modefiche del rapporto I:G insulina - glucalone, poiché i
livelli di insulina sono altrettanto o più alti aumentando il rapporto p/c
rispetto a quello delle raccomandazioni nutrizionali...]
More complicated, but applicable, metabolic interactions of dietary protein
and carbohydrate in whole-foods diets must be carefully considered. Added
fat, fiber and the type of dietary carbohydrate fed can all significantly
affect the I:G ratio. Coulston et al. [33] compared the effects of
consuming two whole foods diets (60% carbohydrate, 21% fat vs. 40%
carbohydrate, 41% fat) for ten days each on the postprandial insulin
response measured at the noon-time meal (mean of days 9 and 10). The
insulin response was significantly blunted for two hours following the 40%
carbohydrate meal when compared to the higher carbohydrate meal. These data
might wrongfully be interpreted to support the validity of the Zone Diet
concept when in fact neither diet was Zone-like in its P:C (60% = 0.32 vs.
40% = 0.48). Since fiber intake was similar (26–35 g) for both trials, the
delayed gastric emptying afforded by the higher fat intake probably
explains the lower insulin levels best. There were no differences in
chronic fasting glucose or insulin levels when comparing the two trials
after ten days. Clearly, the metabolic response to whole food diets is not
as predictable as those measured when consuming single or dual nutrients.
Similarly, other complicating factors may explain many of the putative
deleterious effects attributed to "high carbohydrate" diets. For example,
studies of diets that provide a large portion of carbohydrates as simple
sugars often observe transiently higher insulin concentrations and
unfavorable blood lipid changes [33–35] (see Frayn and Kingman [36] for
review). However, these have employed "high carbohydrate" diets not
representative of those outlined by conventional food intake
recommendations (~55% carbohydrates from fruits, vegetables, legumes and
whole grains) [3–7]. To conclude, there is no evidence that a 0.75 P:C
(40/30/30), whether eaten as a small test meal or in the form of a complete
mixed diet, reduces the insulin response when compared to traditional
dietary guideline food intakes and may even potentially produce a larger
area under the insulin curve.
[Molto sinteticamente: in pasti che si avvicinano di più alle condizioni
reali rispetto ai pasti di test fatti solo di proteine e carbo, cioè che
includono anche fibre, grassi, e diversi tipi di carbo, anche questi
fattori hanno effetto sul rapporto I:G insulina-glucalone e la situazione è
più complessa. Coulston, per esempio, ha confrontato gli effetti di diete
con "whole foods" (60% carbohydrate, 21% fat vs. 40% carbohydrate, 41% fat)
per dieci giorni sulla risposta insulinica postprandiale misurata a pasto
di mezzzogiorno (media dei giorni 9 e 10). La risposta insulinica era
significativamente meno alta per due ore dopo il pasto con 40% di carbo
rispetto a quello con più carbo. Questi dati potrebbero erroneamente
(secondo l'articolo) essere interpretati per supportare la validità della
Zona mentre in realtà nessuna delle due diete era nel p/c della Zona (60% =
0.32 vs. 40% = 0.48). /mia nota: però, lasciatemi osservare, la seconda
dieta era più vicina alla Zona, mmmh... ma continiamo con la traduzione/
Poiche la quantità di fibre era simile (26–35 g), il ritardo nello
svuotamento gastrico dovuto alla maggiore percentuale di grassi spiega
probabilmente meglio i livelli più bassi di insulina. Non si sono notate
differenze, comunque, nei livelli cronici di insulina e di glucosio a
digiuno confrontando le due diete dopo dieci giorni. Chiaramente, il
responso metabolico a diete con "whole foods" non è così prevedibile come
quello misurato quando si consumano un solo nutriente o soli due nutrienti.
Analogamente, altri fattori complicanti, come alti apporti di zuccheri
semplici, possono spiegare l'osservazione di sbalzi insulinici maggiori ed
effetti sfavorevoli sui lipidi sanguigni, cioè degli "effetti deleteri"
attribuiti alle diete cosiddette "high carb". (mentre, se ho capito quanto
vuol dire l'articolo, il problema non è la quantità di carbo ma il *tipo*
di carbo).].
With regard to body weight control, any weight loss experienced by
adherents to the Zone Diet prescription (40/30/30) is easily explained by
the severe energy restriction of the diet (Table 1) rather than enhanced
fat metabolism resulting from manipulations in the dietary P:C. Weight loss
produced by a negative energy balance is hardly a new concept. However, the
Zone Diet also purports that this same P:C and presumed I:G alteration
provides health benefits beyond weight loss via changes in eicosanoid
metabolism. Despite a lack of scientific support for the enhancement of fat
metabolism claimed by Zone Diet proponents, the Zone Diet eicosanoid theory
deserves evaluation since it is a relatively new and obscure wrinkle in the
low carbohydrate diet phenomenon that is generally not well understood, but
is widely touted as the "key" to optimal health [1].
[Per quanto riguarda il controllo del peso corporeo, le perdite di peso
sperimentate da chi aderisce alle prescrizioni della Zona (40/30/30) sono
facilmnte spiegabili con le restrizioni di calorie nella dieta, cioè dal
regime fortemente ipocalorico, piuttosto che dalle modifiche nel rapporto
p/c proteine/carbo. Perdere peso con un bilancio calorico negativo non è
una novità. Però, la Zona asserisce che altri benefici per la salute si
ottengono grazie al rapporto p/c raccomandato e quindi alle modifiche nel
rapporto I:G insulina/glucalone, attraverso il metabolismo degli
eicosanoidi, considerato dalla zona come "chiave" alla salute ottimale...]
DIET, HORMONES, AND EICOSANOID METABOLISM
[Questa parte sugli eiconsanoidi l'ho scorsa solo velocemente per ora...
Vale comunque quanto si diceva all'inizio, cioè pur criticando una
suddivisione troppo semplicistica tra "buoni" e "cattivi", e nonostante
alcuni meccanismi di azione restino ancora oscuri, si riconosce un certo
valore al consiglio di curare l'apporto di Omega-3, considerando tra
l'altro che nella dieta occidentale "americana" con molta carne e poco
pesce i pochi omega-3 a catena lunga che si ottengono dal pesce subiscono
la "concorrenza" degli omega-6 a catena lunga della carne... "more longer
chain omega-6’s from animal meats, fewer longer chain omega-3’s from fatty
fish [42], competitive pressure against omega-3 fatty acid incorporation
into membrane phospholipids can occur [44–46]."
Essential Fatty Acids and Eicosanoid Metabolism
Eicosanoids are the ubiquitous hormone-like products of essential dietary
fatty acid (omega-3 and omega-6) metabolism. In fact, part of the
essentiality of omega-3 and omega-6 fatty acids in human nutrition is
attributed to the role of each in the biosynthesis of eicosanoids [37–40].
The major dietary sources of omega-6 and omega-3 fatty acids are
polyunsaturated vegetable oils. The typical occidental diet provides
roughly three times the omega-6 fatty acid (linoleic acid) necessary to
prevent deficiency [41,42]. This is approximately ten times higher than
omega-3 fatty acid ({alpha}-linolenic acid) intakes [41–43]. Because
Americans also consume more longer chain omega-6’s from animal meats, but
fewer longer chain omega-3’s from fatty fish [42], competitive pressure
against omega-3 fatty acid incorporation into membrane phospholipids can
occur [44–46].
Arachidonic acid (AA) is formed primarily from the elongation and
desaturation of linoleic acid or is obtained directly from the diet and
acts as the predominant tissue precursor of eicosanoids [45,47] (Fig. 3).
The action of phospholipase releases AA from phospholipids within the
plasma membranes of cells. AA acts as a precursor for different eicosanoids
depending on the nature of both the tissue and the stimulus involved. Fig.
3 illustrates that when the metabolic pathway involves the cyclo-oxygenase
(COX) enzyme system, unstable intermediates are formed that produce
prostaglandins (PG), prostacyclins (PGI) or thromboxanes (TX), depending on
the action of additional tissue-specific enzymes. When the pathway involves
the lipoxygenase enzyme, leukotrienes (LT) are formed. Therefore, the
physiological actions of eicosanoids in vivo depend largely on the
tissue(s) in which they are synthesized.
Fig. 3. Simplified schematic of eicosanoid biosynthesis from food sources
of omega-6 and omega-3 fatty acids or their derived metabolic intermediate
progenitors GLA, DGLA, AA, and EPA (GLA = gamma linolenic acid, DGLA =
dihomo-gamma linolenic acid, AA = arachidonic acid, EPA = eicosapentaenoic
acid; COX = cyclooxygenase, LIPOX = lipoxegenase; PG = prostaglandin, PGI =
prostacyclin, TX = thromboxane, LT = leukotriene, OH-DGLA =
15-hydroxydihomo-gamma linolenic acid; {Delta}5, {Delta}6 = delta 5 and 6
desaturase enzymes). Subscripts denote the total number of double bonds in
each molecules structure and the series to which it belongs.
The major physiological actions of the series-2/4 eicosanoids (e.g., PGE2,
PGI2, TXA2, LTB4) are presented in Table 2. Similar functions are observed
for series-1 and series-3/5 eicosanoids arising from homologue AA
precursors (Fig. 3), but with notable caveats. For example, the conversion
of {alpha}-linolenic acid or omega-3 metabolic intermediates into
series-3/5 eicosanoids is less efficient than for the omega-6’s and their
actions in vivo are also noticeably weaker [48]. However, the consumption
of dietary omega-3 fatty acids or their homologue AA precursor
eicosapentaenoic acid (EPA) impacts series-2/4 eicosanoid metabolism by
competing for receptor sites, enzyme activity and also by competing for
acylation into membrane phospholipids [43,45,49–51], thus diminishing
omega-6 eicosanoid formation and function. Other series-1 and series-3
metabolites, such as 15-hydroxydihomo gamma linolenic acid (OH-DGLA) and
docosahexaenoic acid (DHA) also directly inhibit rate-limiting enzymes
involved in series-2/4 leukotriene [52] and prostaglandin [53] formation,
respectively. These metabolic interactions play important roles in human
physiology, health and disease.
Table 2. General Effects of Series-2/4 Eicosanoids in Regulating Biological
Processes
Eicosanoids in Health and Disease
The possibility that excessive omega-6 intakes and subsequent series-2/4
eicosanoid synthesis may influence untoward physiological outcomes and
increase the risk for a variety of chronic diseases is receiving more
attention [40,43,45,46,54]. Lands et al. [44,45] describe an algorithm that
accurately predicts dietary intakes of essential fatty acids and eicosanoid
precursors from their plasma levels measured in triacylglycerols and
phospholipids (reciprocal prediction also valid). The omega-6 to omega-3
fatty acid ratio from these measures may actually be useful as a biomarker
in predicting morbidity and mortality related to cellular events linking a
compromised vascular system to excessive omega-6, series-2/4 eicosanoid
synthesis [45,46]. Because essential fatty acids serve as substrates for
eicosanoid production, alterations in the balance of omega-3 and omega-6
fatty acid membrane phospholipid pools can influence eicosanoid synthesis
and, thus, the specific physiological processes in which they are involved
[39,43,45].
Most eicosanoids produce local (autocrine/paracrine) intracellular effects
by binding to plasma membrane receptors to activate or inhibit second
messenger systems (cAMP, cGMP or IP3/DAG) [55]. The membrane receptors for
the most common second messenger system (cAMP) are coupled to adenylate
cyclase through separate stimulatory or inhibitory G-proteins. Therefore,
whether an eicosanoid stimulates or inhibits cAMP formation depends on
whether the eicosanoid binds to an inhibitory or stimulatory receptor
[55,56]. In this way, eicosanoids are hormone-like in their temporal
activation of intracellular second messengers and bi-directional mediation
(stimulation or inhibition) of cellular activity.
According to the Zone theory, "bad" eicosanoids (series-2/4, Table 2) are
those operating through the IP3/DAG second messenger pathway, while "good"
eicosanoids (PGE1) operate through cAMP [14]. This classification is
probably based on the observation that ischemic and thrombotic
cardiovascular diseases are aggravated by pathologic arteriolar
vasoconstriction and platelet aggregation [45,49,51]. Increasing cellular
cAMP inhibits a myriad of Ca2+ dependent signal transduction pathways
involved in the manufacture of platelets and platelet aggregation [57,58],
while IP3/DAG second messengers promote Ca2+ release in the cell cytoplasm
[51,55], thereby stimulating those pathways for platelet formation and
aggregation. However, the designation of IP3/DAG as the pathway by which
"bad" eicosanoids act ignores the fact that activation of this same second
messenger system is critical in the mechanism to vasodilate the cerebral
microvasculature [59], an action that reduces the potential for thrombotic
cerebrovascular accident.
Some eicosanoids also bind to multiple receptors, thereby stimulating more
than one second messenger system. The Zone theory suggests that EP2
receptors for PGE2 are "good" because they stimulate cAMP formation, while
EP3 receptors are "bad" because they inhibit cAMP formation [14]. This
explanation is correct, but critically incomplete. There are also at least
three other EP3 isoforms which have no effect on cAMP because they operate
through different second messenger systems [60]. In addition, although EP3
knock-out mice demonstrate a reduced risk for thromboembolism [61], the
absence of the EP3 receptor also produces derangements in febrile responses
to pyrogens and on the regulation of bicarbonate secretion in response to
duodenal acidification [62]. Clearly, an overgeneralized classification of
eicosanoids as "good" or "bad" ignores the balanced effects produced by
diverse actions of eicosanoids in human physiological regulation [63].
The Zone Diet recommendation to supplement with omega-3 fatty acids
(specifically EPA or fish oil) and progenitor series-1 eicosanoid
homologues of AA (GLA/DGLA) is not novel but is consistent with
conventional diet and health recommendations. The modest intake of fish,
fish oil, EPA supplements or plant omega-3 fatty acids is generally
associated with a reduced risk for morbidity and mortality from various
chronic vascular and inflammatory diseases [40,42,49,51,64,65–67]. The
mechanism to explain this health benefit has generally centered on EPA
competition with AA for phospholipid membrane acylation, rate-limiting
enzyme activity and receptor sites [43,45,49–51]. Although the use of
omega-3 fatty acids to diminish omega-6 eicosanoid signaling is well
documented, the direct impact of omega-6 eicosanoid progenitors (GLA, DGLA)
on series-1 eicosanoid synthesis (Fig. 3) and reduced series-2/4 eicosanoid
signaling is more equivocal.
The importance of GLA or DGLA supplementation in human nutrition has
recently been reviewed as particularly promising in relieving inflammatory
and rheumatic conditions [52,53,66–68]. However, human GLA and DGLA
supplementation studies illustrate greater unpredictability associated with
eicosanoid production and platelet aggregation. Dietary supplementation
with GLA or DGLA in humans given 1–6 g doses for three to four weeks
results in a rise in serum DGLA and AA concentrations [69–71]. Although 21
days of GLA supplementation decreased inflammatory LTB4 formation by 58% in
one study [71], a similar dose given over 42 days increased platelet
aggregation in another [72]. These conflicting results may reflect the
potential for the DGLA metabolite OH-DGLA to either inhibit lipoxygenase
activity directly [52] or, alternatively, undergo metabolism to AA and TXA2
(Fig. 3), thus stimulating vasoconstriction and platelet aggregation. Stone
et al. [69] observed an increase in the production of both PGE1 and PGE2
after 28 days of DGLA supplementation [69]. Therefore, supplemental GLA
undergoes elongation to DGLA, which undergoes ample desaturation ({Delta}5)
to AA in vivo [70,73], despite a reportedly low {Delta}5 desaturase
activity in man [69,73].
The Zone classification of eicosanoids as "bad" or "good" based on receptor
binding or on gross physiological functions is oversimplified, but the
recommendation to supplement the diet with omega-3 fatty acids or
progenitors of series-1 eicosanoids has some documented health merit.
Although much of how to control or manipulate omega-6 fatty acid metabolism
is still unknown, according to the Zone Diet theory, dietary and hormonal
control of desaturase enzyme activity can regulate eicosanoid production
and metabolism with drug-like precision [1].
Dietary and Hormonal Control of Desaturase Activity
Dietary and hormonal effects on essential fatty acid desaturase enzyme
activity have been studied for decades [73,74–83], but heretofore, no
connection between diet, endocrinology, eicosanoids and health [1,15] is
documented. Diet-induced reductions in the I:G are promoted by Zone Diet
advocates as the key to controlling eicosanoid metabolism through
manipulation of desaturase enzyme activity [1,15]. However, as explained
above, any alteration in the I:G is likely to be very small and of no
foreseeable metabolic consequence due to the synergistic release of insulin
resulting from carbohydrate and protein eaten together and the dominant
physiological actions of insulin over glucagon. Nevertheless, to be
complete this analysis of the Zone theory must be considered for its
proposed effects on desaturase enzyme activity because Zone advocates
misleadingly offer only select scientific information in support of this
health promoting metabolic pathway.
According to the Zone [1,15], carbohydrates inhibit the {Delta}6 desaturase
enzyme ({Delta}6), while insulin accelerates its {Delta}5 desaturase
counterpart ({Delta}5). In contrast, protein intake is said to stimulate
{Delta}6, while the accompanying glucagon stimulus is purported to inhibit
{Delta}5. Therefore, a smaller insulin and larger glucagon release
accompanying a low carbohydrate, high protein diet would result in greater
omega-6 desaturation to GLA (more active {Delta}6 enzyme) and less DGLA
desaturation to AA (less active {Delta}5 enzyme), thus producing more
series-1 and less series-2/4 eicosanoids (Fig. 3). However, this
explanation ignores scientific findings to the contrary.
In vitro animal studies clearly demonstrate that carbohydrate diets ranging
from 50% to 73% of energy intake inhibit both {Delta}5 and {Delta}6
desaturase enzyme activity [74,77], an effect mediated by elevated blood
glucose concentrations [83], but desaturase enzyme inhibition by glucose is
rapidly reversed in vivo following insulin injection [73,83]. Dietary
protein intakes ranging from 20% to 73% of energy intake stimulate both
{Delta}5 and {Delta}6 enzymes [74,77,78,82], while glucagon inhibits both
enzymes [79,80]. These observations concerning the effects of diet and
hormones on desaturase activity is summarized in Fig. 4. It is difficult to
reconcile why the Zone Diet views carbohydrate unfavorably because it
inhibits {Delta}6, while glucagon is viewed favorably even though it too
inhibits {Delta}6. Similarly, the Zone Diet views insulin as unfavorable
because it stimulates {Delta}5, but protein is viewed as favorable even
though it too has the same effect (Fig. 4). Although carbohydrate, protein,
insulin and glucagon can impact delta destaurase enzyme activity, it is
clear that information is selectively reported by Zone Diet advocates and
contradictory facts are ignored (Fig. 4). In reality, the effects of
glucose and amino acids on the desaturase enzymes is most notable in vitro
and is likely masked in vivo by the pancreatic hormones they stimulate
[81]. However, the precise regulation of desaturase enzyme function using
dietary endocrinology in free-living people has never been demonstrated.
Fig. 4. Select nutritional and hormonal factors stimulating (+) or
inhibiting (-) desaturase enzyme activity. (* = hormone actions supersede
macronutrient actions in vivo [81]). Adapted from reference [12].
It is additionally important to recognize that desaturase enzyme activity
is influenced by a multitude of other physiological and dietary variables
including temperature, circadian oscillations, product feedback inhibition
other hormones operating through the cAMP second messenger and alcohol
consumption [45,75,81,82,84]. In fact, the conversion of DGLA to AA may
also be influenced by other factors not directly related to desaturase
activity, such as competitive deacylation-reacylation reactions [85].
Pharmaceutical interventions targeted at occupying omega-6 eicosanoid
receptor sites or decreasing the rate of omega-6, series-2/4 eicosanoid
synthesis (e.g., aspirin), coupled with dietary changes that increase
omega-3 fatty acid intakes and/or reduce omega-6 fatty acid intakes
represent the only scientifically sound approach to ameliorating many of
the chronic health disorders linked to excessive omega-6, series-2/4
eicosanoid signaling [45,65,86].
CONCLUSIONS
The biological plausibility of any diet and health relationship is crucial
when deciding whether or not it is worthy of assessment [4]. The connection
made between diet, endocrinology, eicosanoid metabolism and health [1,15]
is enticing [tentante] and indeed plausible. While there are no cross
sectional or longitudinal studies examining the potential health merit of
adopting a Zone Diet per se, closely related peer-reviewed findings from
scientific research cast strong doubt over the purported benefits of this
diet. When properly evaluated, the theories and arguments of popular low
carbohydrate diet books like the Zone rely on poorly controlled,
non-peer-reviewed studies, anecdotes and non-science rhetoric. This review
illustrates the complexity of nutrition misinformation perpetrated by some
popular press diet books. A closer look at the science behind the claims
made for the Zone Diet reveals nothing more than a modern twist on an
antique food fad.
[Si conclude in buona sostanza che in mancanza di riscontri
scientificamente verificabili sui reali effetti della dieta a Zona, l'esame
della letteratura scientifica esistente su temi vicini, passata in rassegna
dall'ariticolo, getta forti dubbi sui possibili benefici della Zona....]
ACKNOWLEDGMENTS
[...]
Received June 18, 2002. Accepted August 30, 2002.
REFERENCES
[...]
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