Novità sulla Zona in massa!

[nicodipietro]

Ciao a tutti, mi è appena arrivata la risposta da Dr. Sears (o qualche suo vice):

Gli avevo chiesto conferma per questa questione ancora irrisolta:

Benchè credo profondamente nel potere degli ormoni, benchè ho trovato altri studi dove l'assunzione di igf-1 negli uomini allenati ma in regime molto ipocalorico favorisca comunque sintesi proteica e aumento di massa muscolare e ritenzione di azoto, benchè ci sono studi che me lo dimostrino, un piccolo dubbio ogni tanto si insinuava in me:

circa il problema delle calorie!!

Gli ho chiesto, in sintesi:

"Ma se io rispetto la zona, però l'apporto calorico totale della dieta non raggiunge quello mio di mantenimento, come faccio ad aumentare di massa muscolare, cioè NEL LUNGO TERMINE la carenza di calorie, specie per chi è già molto magro e quindi non attinge al grasso corporeo, può sopraffare l'ambiente anabolico anticatabolico della Zona?

Inoltre ho avuto una idea, ispirato da una frase detta dallo stesso Sears che dice che negli atleti che si impegnano ad alta intensità i grassi possono essere anche raddoppiati:
La chiave per la zona è il rapporto proteine/carboidrati per il controllo ormonale, di insulina/glucagone e degli eicosanoidi. Aumentare i grassi si deve per DIMAGRIRE e perchè vanno ridotti i carbo e l'organismo da qualche parte l'energia la deve prendere! anzi i grassi abbassano ulteriormente l'indice glicemico dei pasti già ad ig medio-basso della zona, contribuendo a contenere l'insulina (e il suo effetto antidimagrante ed ingrassante).

Inoltre i grassi, puri, NON CAUSANO ALCUN RILASCIO DI INSULINA dopo essere stati ingeriti, ZERO!

Allora ho pensato: in un individuo magro, che non ha ciccia dalla quale attingere eventuali calorie extra, può mangiare molti più grassi monoinsaturi fermo restando il rapporto prot./carbo = 0,75 ?

In questo modo si superano facilmente le calorie del metabolismo basale + attività psicofisiche!"

ECCO LA LORO RISPOSTA, TRADOTTA E SINTETIZZATA:

"ancora guardi le calorie? la zona mira all'aspetto ormonale! specialmente per chi si allena con i pesi l'importante non sono le calorie, ma la quantità di ormoni anabolici e di ATP che permette la contrazione e il recupero muscolare (e la sintesi proteica), e TUTTE LE ALTRE ATTIVITA' METABOLICHE E NON DELL'ORGANISMO!
La zona col controllo dell'insulina, l'utilizzo dei grassi e il controllo degli ormoni e degli eicosanoidi aumenta pure la produzione di ATP e quindi il fabbisogno calorico, a parità di condizioni, è minore rispetto a chi sta "fuori zona";"

Inoltre mi dicono che l'idea di aumentare l'apporto di grassi monoinsaturi è ottima, a patto di tenere sotto dovuto controllo l'insulina!

[max_power]

Sarò tradizionale e non voglio mettermi nella polemica, ma le calorie io le guardo eccome al momento in cui faccio una dieta che sia per massa o per definizione.

max_power

[nicodipietro]

Si ma al fattore ATP non ci avevo mai pensato!

Cioè qual'è la fonte di energia del corpo per fare TUTTO (termogenesi, muscoli involontari, attività celebrale, muscoli volontari, digestione, respirazione, attività di secrezione, eccetera = RICHIESTA ENERGETICA)?

L'ATP!

E se troppi carbo inducono insulina che poi fa usare gli zuccheri NON come energia ma come accumulo di grasso (che poi in un SECONDO momento EVENTUALMENTE e se non c'è insulina in giro potranno essere convertiti, ma per il momento SI ACCUMULANO E TUTTE QUELLE CALORIE IN PIU' NON LE USI), NON RICAVI ATP UTILE!!!

Con la zona invece i livelli di energia e di utilizzazione di carbo e grassi per ricavare energia (ATP) sono al massimo e molto più efficienti! quindi....

Inoltre c'è la possibilità di aumentare l'apporto di grassi monoinsaturi:

30 g. a pasto per 6 pasti sono 1800 kcal. solo dai grassi, NON SONO MICA POCHE! aggiungici le kcal. di prot. e carbo e vedi come puoi fare massa!

Poi c'è la questione degli ormoni anabolici che abbiamo già appurato sono in grado di AUMENTARE MASSA MUSCOLARE E SINTESI PROTEICA ANCHE IN REGIMI FORTEMENTE IPOCALORICI.

[max_power]

Guarda che tu lo sai meglio di me che l'ATP si può ripristinare in molte vie. Una di questa è la glicolisi ossidativa e non ossidativa. Quella ossidativa utilizza appunto gli acidi grassi che vengono scomposti per ricreare APT. Quella non ossidativa utilizza il glucosio scindendolo in due molecole più piccole sempre per ripristinare ATP.
Quindi con una dieta ricca di carboidrati si tengono piene le riserve di glicogeno che serviranno poi alla glicolisi anaerobica per ripristinare l'ATP.

max_power

[nicodipietro]

1) Sai perchè nessun bbder pro usa la zona? perchè usa i farmaci


2)non cita studi? eccoti servito (e vedi quanti numeretti ci sono nelle risposte di Sears verso il centro, e alla fine ALCUNI studi che CONFERMANO le sue tesi) :

The San Antonio Study Results

This data was presented at the 58th annual American Diabetes Association convention in Chicago.

A Nutrition Intervention Program to Improve Glycemia, Lipid Profiles, and Hyperinsulinemia in Patients with Type 2 Diabetes

BARRY SEARS, PAUL KAHL, GEORGE RAPIER, Marblehead, MA and San Antonio, Tx, USA.


Introduction

It is believed that Type 2 diabetes can be primarily controlled by diet. However, diets routinely prescribed to these patients have less than expected clinical benefits despite intensive education programs and materials.

We designed a clinical trial using similar calorie ranges used by the American Diabetes Association but with a macronutrient ratio consisting of 40% carbohydrate, 30% protein and 30% fat to determine whether clinically significant improvement in blood parameters can be achieved in free-living Type 2 diabetics.
Methods
Subjects

Seventy patients with Type 2 diabetes greater than one-year duration were recruited from Princeton Medical Management Resources (PMMR) in San Antonio, TX. During the previous year, all had undergone intensive individual nutrition counseling according to American Diabetes Association guidelines. Each subject signed a consent form provided by PMMR.

Trial Design

The diet consisted of three meals and two snacks daily. The amount of dietary protein was individualized to maintain the subject's lean body mass (LBM). The average protein amount for males was approximately 100 grams/day and for females, 75 grams/day. The minimal protein for any subject was 75 grams/day, divided between 3 meals and 2 snacks.

The protein-to-carbohydrate ratio for each meal and snack was approximately 0.75. The fat content for each meal/snack was adjusted to provide 30% of the total calories. Any added fat was primarily monounsaturated. The five meals per day consisted of breakfast, lunch, late afternoon snack, dinner and a late evening snack. Each snack was approximately 100 calories. The total caloric intake varied from 1,100 (minimal allowed) to 2,000 calories daily depending on individual protein requirements.

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Nutrition bars consisting of 20 grams carbohydrate, 14 grams protein, and 7 grams fat equaling 190 calories provided breakfast and the two snacks. The snacks used one-half bar. The bars provided 40 mg. eicosapentaenoic acid (EPA) and 0.5 mg gamma linolenic acid (GLA) and were fortified with 19 vitamins and minerals. The RDA for these vitamins and minerals was met or exceeded by the ingestion of two bars/day.

Additionally, molecularly distilled fish oil containing 1080 mg of EPA were supplied in six soft gelatin capsules to be taken with meals. Eicotech Corporation, Marblehead, MA, supplied both the nutrition bars and capsules.

All subjects were required to attend four one-hour weekly group sessions. During this period, they received information on food composition, meal preparation, and food shopping according to the above dietary guidelines. Dietary meal plans for each subject based on their protein requirements and meal preferences were provided.

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Results

The results after six weeks in subjects with Type 2 diabetes are shown in Table 1.
Table 1.
Six Week Results with Type 2 Diabetics (n=68)
Parameter 0 Wks 6 Wks % Diff p value
Insulin 28 21 -23 p<0.0001
FBS 167 153 -8 p=0.03
HbA1c 7.8 7.3 -7 p<0.0001
Tot. Chol 203 202 0 n.s.
LDL Chol 123 122 0 n.s.
HDL Chol 45 49 8 p<0.0001
TG 189 162 -14 p=0.002
TC/HDL 4.7 4.3 -9 p<0.0001
TG/HDL 4.2 3.1 -26 p<0.0001
Weight 188 188 0 n.s.
Fat Mass 72 70 -3 p<0.0001
Even though there was no loss in body weight (although there was a decrease in fat mass), statistically significant improvements were observed in glycemic control, lipid profiles and fasting insulin ratios. Additional blood chemistry was done at 12 weeks. The results are shown in Table 2.

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Table 2
12-Week Results with Type 2 Diabetics (n=56)

Parameter 0 Wks 12 Wks % Diff p value
HbA1c 7.7 7.3 -6 p<0.0001
FBS 164.4 158 -5 n.s.
Total Chol 200 200 0 n.s
LDL Chol 121.8 123.7 +2 n.s.
HDL Chol 45.8 50.2 +9 p<0.0001
TG 170 130 -20 p<0.0004
TC/HDL 4.4 4 -9 p<0.0001
TG/HDL 3.7 2.7 -27 p<0.0001
Weight 191 184 -4 p<0.0001
Only 1 out of 34 patients in this second group using insulin at the start of the study required insulin at the twelve week time point. Unlike the six week point, there was now statistically significant weight loss at the twelve week period. All other lipid parameters were basically unchanged from the six-week mark.

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Discussion

The benefits of any dietary intervention require long-term compliance. Although this was a calorie restricted diet, compliance was good during the 12-week period (79% completed the clinical trial). Part of this compliance may have been that they were responsible for only two meals per day. Fewer than 10% of the subjects complained of hunger.

As seen from the 12-week data points, the benefits achieved at six weeks were maintained. Although there was a slight increase in patient's fasting blood sugar, we believe this reflects the large reduction in glycemic lowering medication during the course of the trial. Of 34 patients using exogenous insulin at the start of the study, only one patient continued insulin injections by week 12.

Lipid profiles, in particular triglycerides and HDL cholesterol, improved significantly. Recent studies have indicated that an elevated triglyceride to HDL cholesterol ratio is strongly associated with both an increase in the amounts of atherogenic small, dense LDL particles and increased myocardial infarction risk (Gaziano et al. Circulation 96: 2520-2525, 1997). Reduction of the triglyceride/HDL cholesterol ratio illustrates significant improvement in this cardiovascular risk parameter with this nutritional intervention used in this study.

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We believe that many of the clinical improvements ultimately may be explained by the reduction of insulin levels on eicosanoid formation. Hyperinsulinemia is known to activate the delta-5-desaturase enzyme that increases the formation of arachidonic acid (AA) from dihomo gamma linolenic acid (DGLA) [Pelikanova et al. Clinica Chimica Acta 203: 329-338, 1993]. Thus, lowering insulin levels should reduce AA production with a corresponding increase in DGLA.

Supplementation with combinations of EPA and GLA can promote further improvement in the DGLA/AA ratio. EPA acts as a feedback inhibitor of delta-5-desaturase, while supplementation with GLA ensures an adequate substrate for the formation of DGLA. Changing the ratio of DGLA to AA in target tissues, especially in the vascular bed, increases the likelihood of generating eicosanoids that are vasodilatory, anti-inflammatory and anti-thrombotic. Simultaneously, there will be less production of eicosanoids that are vasoconstrictive, pro-inflammatory and pro-thrombotic. This change in eicosanoid balance would have a significant effect on endothelial cell function.

Endothelial cell dysfunction is known to be present in Type 2 diabetics (Pinkney et al. Diabetes 46: S9-S13, 1997). We believe endothelial cell dysfunction may be an underlying cause of insulin resistance by limiting insulin access to its target tissues. A favorable eicosanoid balance may enhance endothelial cell function providing insulin access to the target cell receptors. Better glucose homeostasis would be achieved with lower insulin levels under this hypothesis. Our results are consistent with recently published studies using calorie restricted formula diets consisting of 38% carbohydrates, 33% protein, and 29% fat (Markovic et al. Diabetes Care 21: 695-700, 1998) which demonstrated reduced insulin levels and improved insulin sensitivity within four days after institution of a similar dietary program.

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Conclusions

A protein-adequate, carbohydrate-moderate, low-fat, calorie-restricted diet can be integrated readily into the lifestyle of patients with Type 2 diabetes, providing highly significant clinical improvements within six weeks in hyperinsulinemia, glycemia, and lipid profiles as shown below:.
Insulin 23% decrease
HbA1c 7% decrease
TG 14% decrease
TG/HDL 26% decrease

The decrease in each of the risk factors indicates the Zone Nutritional Program has significant potential in reducing the cardiovascular risk that is elevated in Type 2 diabetics.

Dr. Sears' comments: This study was the first to demonstrate that the Zone Diet can lower insulin levels, decrease the ratio of triglycerides to HDL cholesterol, and reduce glycosylated hemoglobin levels in short period of time in Type 2 diabetics.
The changes in these clinical parameters are not only important in the treatment of Type 2 diabetics, but also are paramount for reversing the aging process.



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The Journal of the American Dietetic Association 1998;98(9):s1,a43

(Dr. Sears' comments are at the end of the abstract.)

TITLE: A COMPREHENSIVE STUDY OF A 1500 CALORIE 40/30/30 DIET VS. 1500-CALORIE STEP 1 DIET ON BODY COMPOSITION AND BLOOD PARAMETERS IN OVERWEIGHT ADULTS.

AUTHORS: D. Kalman MS, RD, Peak Wellness. Greenwich, CT; C.M. Colker, M.D., Greenwich Hospital. Greenwich, CT; J. Roufs MS, RD, NVI. Phoenix, AZ; I. Wilets, Ph.D., Beth Israel Medical Center. New York, NY; J. Antonio, Ph.D., University of Texas. Arlington, TX.

LEARNING OUTCOME: To determine, what effects if any, macronutrient manipulation would have on body composition, energy levels and blood parameters.

ABSTRACT: Twenty-nine overweight men and women (body mass >25) participated in this six-week outpatient study. The participants were randomized to either a 1500 calorie 40/30/30 diet [40% CHO] (n=14) or a 1500 calorie Step 1 diet [60% CHO] (n=15). The 40/30/30 diet consisted of 40% CHO, 30% protein, 30% fat, the Step 1 diet consisted of 60% CHO, 15% protein, and 25% fat. All subjects participated in Universal Circuit Training ™, one hour, three times per week supervised by an exercise physiologist. All subjects met two to four times (avg.=3) over six weeks with a registered dietitian for review and analysis of compliance to the study diets. Both groups lost a significant amount of weight (p<0.05) after 6 weeks of treatment (40% CHO, -2.8kg; 60% CHO, -1.2kg). However, the 40% CHO group lost more weight and a greater amount of body fat (-2.6kg; p<0.05), while the 60% CHO (-1.0kg) group did not achieve significant fat loss. There were no significant changes for both groups in serum glucose, HgBA1C, total cholesterol, HDL, LDL, or triglycerides during the study. Profile of Mood States (POMS) for fatigue and vigor was also analyzed in both study groups with the following results: 44% reduction in fatigue (p<0.05) for the 40% CHO group with a corresponding 15.7% increase in vigor (non-significant; p>0.05). The changes within the 60% CHO group did not achieve significance in either fatigue or vigor. In conclusion, the 1500 calorie 40/30/30 diet resulted in a significantly greater fat and weight loss compared with the 1500 calorie Step 1 diet over 6 weeks.

Dr. Sears' comments: This abstract is a very compelling argument against the common nutritional mantra that "a calorie is a calorie." Both diets tested were isocaloric, differing only in the macronutrient composition. The protein-to-carbohydrate ratio in the Zone Diet was 0.75, whereas in the American Heart Association Diet the protein-to-carbohydrate ratio was 0.25. The fact that exercise was part of the study also eliminated that factor in analyzing the data on weight loss and reduction of body fat. The fat loss in the participants following the Zone Diet was 260 percent greater than those following the American Heart Association Step 1 diet. This difference is even more impressive since participants following the Zone Diet consumed 20 percent more fat than the participants on the Step 1 diet. Furthermore, the fat loss in the Zone Diet was statistically significant (meaning it was reproducible) whereas the in the Step 1 group it was not. In terms of subjective measurements of fatigue reduction and increased vigor, the Zone Diet was again superior to the Step 1 diet. The lack of effect of the Zone Diet on triglyceride levels was probably due to inadequate levels of Omega-3 fatty acids in the diet. Unfortunately, fasting insulin levels were not analyzed in this study (as with other Zone studies) to correlate insulin reduction with loss of body fat. Other than those two items, this study is a very important step forward in the validation of the Zone Diet by other researchers.

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Diabetes Care 21: 687-694 (1998)

(Dr. Sears' comments are at the end of the abstract.)

Title: The Determinants of Glycemic Response to Diet Restriction and Weight Loss in Obesity and NIDDM.

Authors: Markovic TP, Jenkins AB, Campbell LV, Furler SM, Kraegen EW, and Chisholm DJ.

Abstract:
Objectives: To examine the mechanisms by which weight loss improves glycemic control in overweight subjects with NIDDM, particularly the relationships between energy restriction, improvements in insulin sensitivity, and regional and overall adipose tissue loss.

Research Design and Methods: Hyperinsulinemic glucose clamps were performed in 20 subjects (BMI=32 kg/m2, age=48) with normal glucose tolerance (n=10) or mild NIDDM (n=10) before and on the 4th and 28th days of a reduced-energy (1,100 kcal) formula diet. Body composition changes were assessed by dual x-ray absorptionmetry and insulin secretory changes were measured by insulin response to intravenous glucose before and after weight loss.

Results: In both groups, energy restriction at the 4th day reduced fasting plasma glucose, which was independently related to reduced carbohydrate intake. There was a marked increase by the 4th day in percent insulin suppression of hepatic glucose output in both groups. By the 28th day with 6.3 kg weight loss, plasma glucose was further reduced in the NIDDM group only, and insulin sensitivity increased in both groups. Only loss of abdominal fat related to improvements of plasma glucose and insulin sensitivity after weight loss. In contrast to insulin action, there were only small changes in insulin secretion.

Conclusions: Both energy restriction and weight loss have beneficial effects on insulin action and glycemic control in obesity and mild NIDDM. The effect of energy restriction is related to changes in individual macronutrients, whereas weight loss effects relate to changes in abdominal fat.

Dr. Sears Comments: This study appeared the same month that I presented our Type 2 data at the American Diabetes Association. The balance of macronutrients and amount of calorie restriction in this study was virtually identical to the Zone Diet. Not surprisingly, the clinical results were also virtually identical to our results. The most striking observation was that insulin resistance and fasting insulin levels were dramatically reduced within four days, and in the absence of any significant weight loss. This study also answers the chicken and the egg question: does weight gain cause increased insulin or does increased insulin levels precede weight gain? The answer is the latter since insulin levels and insulin resistance are lowered prior to any weight loss. This study demonstrates that others can replicate the effects of the Zone Diet, and that the hormonal changes are seen within days.

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Pediatrics 103: E26 (1999)

Title: High Glycemic Index Foods, Overeating, and Obesity

Authors: Ludwig DS, Majzoub JA, Al-Zahrani A, Dallal GE, Blanco I, and Roberts SB.

Abstract:
Objective: The prevalence of obesity has increased dramatically in recent years. However, the role of dietary composition in body weight regulation remains unclear. The purpose of this work was to investigate the acute effects of dietary glycemic index (GI) on energy metabolism and voluntary food intake in obese subjects.

Methods: Twelve obese teenage boys were evaluated on three separate occasions using a crossover study protocol. During each evaluation, subjects consumed identical test meals at breakfast and lunch that had a low, medium or high GI. The high- and medium-GI meals were designed to have similar macronutrient composition, fiber content, and palatability, and all meals for each subject had equal energy content. After breakfast, plasma and serum concentrations of metabolic fuels and hormones were measured. Ad libitum food intake was determined in the 5-hour period after lunch.

Results: Voluntary energy intake after the high-GI meal was 53% greater than after the medium-GI meal, and 81% greater than the low-GI meal. In addition, compared with the low-GI meal, the high-GI meal resulted in higher serum insulin levels, lower plasma glucagon levels, lower post-absorptive plasma glucose and serum fatty acid levels, and elevation in plasma epinephrine. The are under the glycemic response curve for each test meal accounted for 54% of the variance in the food intake within subjects.

Conclusions: The rapid absorption of glucose after consumption of high-GI meals induces a sequence of hormonal and metabolic changes that promote excessive food intake in obese subjects. Additional studies are needed to examine the relationship between dietary GI and long-term body weight regulation.

Dr. Sears Comments: The low-GI meal used in this study was a Zone meal. This study demonstrated that a slight change in the balance of macronutrients in an isocaloric meal generate dramatic changes in the hormonal output by a single meal. In particular, only in the Zone meal were glucagon levels increased. In the other meals (high-GI and medium-GI), glucagon levels were depressed. The increased glucagon output would maintain adequate blood sugar levels thus explaining why the children consumed 81% fewer calories with their next meal. You simply don't eat as much if you aren't hungry. This study indicates that the effect of the Zone Diet can be observed with a single meal.

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International Journal of Obesity 23: 528-536 (1999)

Title: Randomized trial on protein vs carbohydrate in ad libitum fat reduced diet for the treatment of obesity.

Authors: Skov AR, Toubro S, Ronn B, Holm L, and Astrup A.

Abstract:
Objective: To study the effect of weight loss in obese subjects by replacement of carbohydrate by protein in ad libitum consumed fat-reduced diets.

Design: Randomized dietary intervention study over six months comparing two ad libitum fat reduced diets (30% of total energy) strictly controlled in composition. High-carbohydrate (HC, protein 12% of total energy) or high-protein (HP, protein 25% of total energy).

Setting and Participants: Subjects were 65 healthy, overweigh and obese subjects (50 women, 15 men, aged 18-65) randomly assigned to HC (n=25) HP (n=25) or a control group (C, n=15). All food was provided by self-selection in a shop at the department, and compliance to the diet composition was evaluated by urinary nitrogen excretion.

Main Outcome Measure: Change in body weight, body composition and blood lipids.

Results: More than 90% completed the trial. Weight loss after six months as 5.1 kg in the HC group and 8.9 kg in the HP group (p < 0.0001), and fat loss was 4.3 kg and 7.6 kg respectively (p < 0.0001), whereas no changes occurred in the control group. More subjects lost > 10 kg in the HP group (35%) than in the HC group (9%). The HP diet only decreased fasting plasma triglycerides and free fatty acids respectively.

Conclusions: Replacement of some dietary carbohydrate by protein in an ad libitum fat-reduced diet, improves weight loss and increases the proportion of subjects achieving a clinically relevant weight loss. More freedom to choose between protein-rich and complex carbohydrate-rich foods may allow obese subjects t choose more lean meat and dairy products, and hence improve adherence to low-fat diets in weight reduction programs.

Dr. Sears Comments: 25% of calories as protein is not a high-protein diet since under the conditions of this study the amount of calories from carbohydrate was 45%. This means you are eating almost twice as many carbohydrates as protein. Nonetheless, the ratio of protein-to-carbohydrate in the HP diet was 0.6, which is right at the edge of the Zone (0.6 to 1.0). The HC diet had a protein-to-carbohydrate ratio of 0.2. The greater weight loss, body fat loss, and the lowering of triglyceride levels indicated that HP diet caused a significant lowering of insulin levels.
This study demonstrates following the Zone Diet over an extended period of time leads to much greater fat loss than expected.

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Am J Clin Nutr 70: 221-227 (1999)

Title: Dietary Protein and the Risk of Ischemic Heart Disease in Women.

Authors: Hu FB, Stampfer MJ, Manson JE, Rimm E, Colditz GA, Speizer FE, Hennekens CH, and Willett WC.

Abstract:
Background: Ingestion of animal protein raises serum cholesterol in some experimental models but not in others, and ecologic studies have suggested a positive association between animal protein intake and risk of ischemic heart disease. Prospective data on the relation of protein intake to risk of ischemic heart disease is sparse.

Objective: The objective was to examine the relation between protein intake and risk of ischemic heart disease.

Design: The study was a prospective cohort study.

Results: We examined the association between dietary protein intake and incidence of ischemic heart disease in a cohort of 80,082 women aged 34-57 y and without a previous diagnosis of ischemic heart disease, stroke, cancer, hypercholesterolemia, or diabetes in 1980. Intakes of protein and other nutrients were assessed with validated dietary questionnaires. We documented 939 major instances of ischemic heart disease during the 14 y of follow-up. After age, smoking, total energy intake, percentages of energy from specific types of fat, and other ischemic heart disease risk factors were controlled for, high protein intakes were associated with a low risk of ischemic heart disease: when extreme quintiles of total protein intake were compared, the relative risk was 0.74. Both animal and vegetable proteins contributed to the lower risk. The inverse association was similar in women with low-or high-fat diets.

Conclusions: Our data does not support the hypothesis that a high protein intake increases the risk of ischemic heart disease. In contrast, our findings suggest that replacing carbohydrates with protein may be associated with a lower risk of ischemic heart disease. Because a high dietary protein intake is often accompanied by increases in saturated fat and cholesterol intakes, application of these findings to public dietary advice should be cautious.

Dr. Sears Comments: The women with the lowest incidence of heart disease followed a Zone Diet with a protein-to-carbohydrate ratio of 0.7 (near the center of the Zone). They also consumed less bread, less starch, and consumed more protein, fruits and vegetables than the other women. These modifications (which are exactly those recommended on the Zone Diet) resulted in a 24% reduction in heart disease.
This study represents a long-term consequence of following the Zone Diet is the reduction of heart disease. This is the reason I developed the Zone Diet many years ago.

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Am J Clin Nutr 70: 1009-1015 (1999)

(Dr. Sears' comments are at the end of the abstract.)

Title: High-monounsaturated fatty acid diets lower both plasma cholesterol and triacylglycerol concentrations.

Authors: Kris-Etherton PM, Pearson TA, Wan Y, Hargrove RL, Moriarty K, Fishell V, and Etherton TD.

Abstract:
Background: Low-fat diets increase plasma triacylglycerol and decrease HDL-cholesterol concentrations, thereby potentially adversely affecting cardiovascular disease (CVD) risk. High-monounsaturated fatty acid (MUFA), cholesterol-lowering diets do not raise triacylglycerol or lower HDL cholesterol, but little is known about how peanut products, a rich source of MUFAs, affect CVD risk.

Objective: The present study compared the CVD risk profile of an Average American diet (AAD) with those of 4 cholesterol-lowering diets: an American Heart Association/National Cholesterol Education Program Step II diet and high-MUFA diets [olive oil (OO), peanut oil (PO), and peanuts and peanut butter (PPB)].

Design: A randomized, double-blind, 5-period crossover study design (n=22) was used to examine the effects of the diets on serum lipids and lipoproteins: AAD [34% fat; 16% saturated fatty acids (SFAs), 11% MUFAs], Step II (25% fat; 7% SFAs, 12% MUFAs), OO (34% fat; 7% SFAs, 21% MUFAs), PO (34% fat; 7% SFAs, 17% MUFAs), and PPB (36% fat; 8% SFAs, 18% MUFAs).

Results: The high-MUFA diets lowered total cholesterol by 10% and LDL cholesterol by 14%. This response was comparable with that observed for the Step II diet. Triacylglycerol concentrations were 13% lower in subjects consuming the high-MUFA diets and were 11% higher with the Step II diet than with the AAD. The high-MUFA diets did not lower HDL cholesterol whereas the Step II diet lowered it by 4% compared with the AAD. The OO, PO, and PPB diets decreased CVD risk by an estimated 25%, 16%, and 21% respectively, whereas the Step II diet lowered CVD risk by 12%.

Conclusion: A high-MUFA, cholesterol-lowering diet may be preferable to a low-fat diet because of more favorable effects on the CVD risk profile.

Dr. Sears Comments: This article has tremendous implications (and potential warnings) for cardiovascular patients. The American Heart Association (AHA) Step II diet rarely works, thus forcing cardiovascular patients to use life-long cholesterol-lowering drug therapies. Now we know why. The AHA Step II diet increases triglycerides and lowers HDL cholesterol. The increase in the TG/HDL ratio has been shown by Harvard Medical School to be a powerful risk factor for the development of heart disease. On the other hand, diets with higher levels of monounsaturated fat decrease the TG/HDL ratio. This is why the Zone Diet primarily uses monounsaturated fat is its primary fat source and is not afraid to recommend fat. Hidden within the article is another reason for the poor results of the AHA Step II diet: the protein-to-carbohydrate ratio. The protein-to-carbohydrate ratio of the AHA Step II diet was 0.27, whereas the protein-to-carbohydrate ratios in each of the monounsaturated fat diets was 0.32. It is known that the lower the protein-to-carbohydrate ratio of a diet, the higher the higher the fasting insulin levels. Since fasting insulin is greatest predictor of future heart disease, any increase in insulin levels doesn't bode well for cardiovascular patients. If the study had used the Zone Diet (which has a protein-carbohydrate ratio of about 0.7), I believe the results would even better because a higher protein-to-carbohydrate ratio reduces insulin levels. Nonetheless, this study implies that the diets recommended by the AHA for the past 20 years may have been driving cardiovascular patients to be more likely to have a heart attack.

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Am J Clin Nutr 71: 901-907 (2000)

Title: Dietary composition and physiologic adaptations to energy restriction.

Authors: Michael SD Agus, Janis F Swain, Courtney L Larson, Elizabeth A Eckert, and David S Ludwig.

Abstract:
Background: The concept of a body weight set point, determined predominantly by genetic mechanisms, has been proposed to explain the poor long-term results of conventional energy-restricted diets in the treatment of obesity.

Objective: The objective of this study was to examine whether dietary composition affects hormonal and metabolic adaptations to energy restriction.

Design: A randomized, crossover design was used to compare the effects of a high-glycemic-index (high-GI) and a low-glycemic-index (low-GI) energy-restricted diet. The macronutrient composition of the high-GI diet was (as percent of energy) 67% carbohydrate, 15% protein, and 18% fat and that of the low-GI diet was 43% carbohydrate, 27% protein, and 30% fat; the diets had similar total energy, energy density, and fiber contents. The subjects, 10 moderately overweight young men, were studied for 9 days on 2 separate occasions. On days -1 to 0, they consumed self-selected foods ad libitum. On days 1-6, they received an energy-restricted high- or low-GI diet. On days 7-8, the high- or low-GI diets were consumed ad libitum.

Results: Serum leptin decreased to a lesser extent from day 0 to day 6 with the high-GI diet than with the low-GI diet. Resting energy expenditure declined by 10.5% during the high-GI diet but by only 4.6% during the low-GI diet (7.38 +/- 0.39 and 7.78 +/- 0.36 MJ/d, respectively, on days 5-6; P = 0.04). Nitrogen balance tended to be more negative, and energy intake from snacks was on days 7-8 was greater with the high-GI than the low-GI diet.

Conclusions: Diets with identical energy contents can have different effects on leptin concentrations, energy expenditure, voluntary food intake, and nitrogen balance, suggesting that the physiologic adaptations to energy restriction can be modified by dietary composition.

Dr. Sears Comments: The article from Harvard Medical School provides strong supporting evidence that the Zone Diet (with a protein-to-carbohydrate ratio of 0.6) is superior to commonly recommended high-carbohydrate diets (with a protein-to-carbohydrate ratio of 0.2). In this crossover experiment, the weight loss was greater on the Zone Diet even though the calories consumed on both diets were identical. The statistically significant lower levels of insulin secretion can explain this unexpected result following the Zone Diet compared to the standard high-carbohydrate diet. In addition, patients on the Zone Diet maintained a positive nitrogen balance, whereas those consuming the high-carbohydrate diet were in a negative nitrogen balance indicating loss of muscle mass. Most important for long-term weight loss, when patients were given the opportunity to eat without any restriction on calories after six days, they ate 25% fewer calories after following the Zone Diet compared to when they consumed a high-carbohydrate diet.

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Clin Invest Med 1999 Aug;22(4): 140-148

Title: Replacement of carbohydrate by protein in a conventional-fat diet reduces cholesterol and triglyceride concentrations in healthy normolipidemic subjects.

Authors: Wolfe BM; Piche LA.

Abstract:
Objective: To determine the effect on plasma lipid profiles of replacement of dietary carbohydrate by low-fat, high-protein foods.

Design: Cross-over randomized controlled trial

Participants: Ten healthy, normolipidemic subjects (8 women and 2 men).

Interventions: Subjects were randomly allocated to either a low-protein (12%) or high-protein (22%) weight-maintaining diet for 4 weeks and then switched to the alternate diet for 4 more weeks. The first 2 weeks of each diet served as an adjustment/washout period. Fat was maintained at 35% of energy, mean cholesterol intake at 230 mg per day and mean fibre intake at 24 g per day. Compliance was promoted by the use of written dietary protocols based on the food preferences of the subjects and weekly dietary consultation as required.

Results: Consumption of the high- versus low-protein diet resulted in significant reductions in mean plasma levels of total cholesterol (3.8 v. 4.1 mmol/L, p < 0.05), VLDL cholesterol (0.20 v. 0.26 mmol/L, p < 0.02), LDL cholesterol (2.4 v. 2.6 mmol/L, p < 0.05), total triglycerides (0.69 v. 0.95 mmol/L, p < 0.005) and VLDL triglycerides (0.35 v. 0.57 mmol/L, p < 0.001), as well as in the ratio of total cholesterol to HDL cholesterol (3.1 v. 3.5, p <0.01). A trend towards an increase in HDL cholesterol (1.26 v. 1.21 mmol/L, p = 0.30) was observed but was not statistically significant. Satiety levels tended to be higher among those eating the high-protein diet (6.1 v. 5.4, p = 0.073).

Conclusions: Moderate replacement of dietary carbohydrate with low-fat, high-protein foods in a diet containing a conventional level of fat significantly improved plasma lipoprotein cardiovascular risk profiles in healthy normolipidemic subjects.

Dr. Sears Comments: This is another crossover study comparing the Zone Diet to a high-carbohydrate diet while containing equal amounts of calories and fat using healthy volunteers with normal lipid levels. The Zone Diet (with a protein-to-carbohydrate ratio of .5) showed statistically significant improvements in lipid parameters after only four weeks. Compared to the high-carbohydrate diet (with a protein-to-carbohydrate ratio of 0.3), the individuals following the Zone Diet had a 7% decrease in total cholesterol, an 8% decrease in LDL cholesterol, and a 27% decrease in triglycerides along with a 4% increase in HDL cholesterol. These same improvements in lipid levels for the Zone Diet have already been reported for hypercholesterolemic and postmenopausal women and male elite distance runners. It appears that everyone would benefit from following the Zone Diet.

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Good Morning America Challenge
June 9, 2000

ELIZABETH VARGAS, co-host: Now to the controversial but extremely popular diet known as "The Zone." The man behind it, diet Dr. Barry Sears claims you can lose weight, gain energy and even slow the aging process with it. And in "The Soy Zone" and "A Week in the Zone," he says you can even begin to get results in just a week. It's a diet that may seem complicated, so Dr. Barry Sears is joining us this morning to explain it all. And we've decided to see for ourselves how it works by following your four volunteers through their own week in The Zone. We'll get to that in just a second, but...Dr. Sears, good morning. Good to have you here.

Dr. BARRY SEARS: Well, thank you very much.

VARGAS: Let's talk about The Zone. First of all, this is not about counting calories per se, it's about hormone levels.

Dr. SEARS: Exactly. It's keeping the hormone insulin in zone, not too high, but not too low. Now, why do you want to do that? Because the only way you can lose excess body fat on a permanent basis is to enter that zone. The only way you can reduce the likelihood of heart disease is to enter that zone. And the only way to live longer is to enter that zone.

VARGAS: Now, millions of people are fans of your diet. Many others have not even tried it because they perceive it as being far too difficult. How--how do you get that diet, that right combination of foods so you can get hormonally in that, quote-unquote, "Zone."

Dr. SEARS: It turns out that your hand gives you all the rules you need. You never consume any more low-fat protein at a meal than you can fit on the palm of your hand.

VARGAS: Mm-hmm.

Dr. SEARS: You take your plate, divide it into three sectors. On one third of the plate, you put some low-fat protein, no bigger and no thicker than the palm of your hand. The other two thirds of the plate, you fill till it's overflowing with fruits and vegetables. You add a dash, that's a small amount, a dash of heart-healthy, monounsaturated fat, like olive oil, slivered almonds, or guacamole. And there you have it.

VARGAS: You diet is different from others in that you're not so bad on fat, as you just said, some like healthy fat is actually good for you. But you're definitely down on carbohydrates. In your diet, we really eliminate most of bread, rice and pasta.

Dr. SEARS: Right. The starchy carbohydrates. We use them as moderation,as condiments. You're using now primarily fruits and vegetables. Most Americans don't realize their fruits and vegetables are also carbohydrates.

VARGAS: So no bread at all?

Dr. SEARS: No. We use them as condiments, as, you know, touch-ups.

VARGAS: When you say condiments, what are we talking about? Can I have one mouthful of bread, but not a whole roll?

Dr. SEARS: Treat it like a piece of seven-layer cake. Savor it but, basically, use it in moderation.

VARGAS: OK. Now, your second book--your first book deals with a week in the zone, which we'll get to in a second...

Dr. SEARS: Yes.

VARGAS: ...with your volunteers. But your second book out right now deals
with soy, which has become huge. I was reading a statistic that said Okinawans, people who live in Okinawa, live longer than anyone else in the world, and they consume 25 times more soy than Americans do.

Dr. SEARS: That's correct.

VARGAS: What does that tell you about soy?

Dr. SEARS: Well, it tells us soy is pretty close to a miracle food, if you use it in the construct of The Zone diet, which is all based upon a balance and moderation. Now, when we think of soy, most people think of things like tofu.

VARGAS: Right. That's this over here, which...

Dr. SEARS: Frankly...

VARGAS: ...is this kind of white spongy thing, which doesn't, I admit even though I like tofu, doesn't look too appetizing.

Dr. SEARS: And most Americans are not going to eat tofu. But what Americans will eat are things that look like and taste like hot dogs, hamburgers, and sausages.

VARGAS: Like this here. And these are all--this is not meat, this is all made with soy?

Dr. SEARS: Exactly. Our technology is now basically so advanced we can make good-tasting soy imitation meat products that most Americans say, 'I could eat that.' And that-- that's the secret.

VARGAS: Now here's a question I've always wondered, with things like tofu, tofu, that sort of thing. We know it's got lots of protein in there, but what about the fat content? Is it high in fat?

Dr. SEARS: Well, not really. But keep in mind, dietary fat doesn't make you fat. What makes you fat and keeps you fat is excess insulin, and how do you control that? You balance the protein and carbohydrate at every meal, like you balance a carburetor of a car, to get the right hormonal cluck for the buck for the next four to six hours.

VARGAS: So would you eat as much soy as you would regular animal or fish protein?

Dr. SEARS: Yes.

VARGAS: And would this, eating this with your fruits and vegetables, make you a vegetarian, out of curiosity?

Dr. SEARS: It would, but it would make you a very healthy vegetarian. And a vegetarian that you could say, for most Americans, 'I don't mind being a vegetarian if I'm eating hamburgers and hot dogs and sausages.'

VARGAS: Right. Getting all that. Now here, you've got here a typical Zone breakfast. Explain what that is.

Dr. SEARS: Well, we're looking to see, we want to have our protein and carbohydrate. So here's our protein, we take a three egg-white omelet...

VARGAS: Mm-hmm.

Dr. SEARS: Add a touch of feta cheese to it, some sun-dried tomatoes. Added two soy sausage links.

VARGAS: Mm-hmm.

Dr. SEARS: There's our protein.

VARGAS: And if you don't want that, you can just put some soy protein in say a bowl of oatmeal?

Dr. SEARS: Well, that's it. Now we have carbohydrate, we have oatmeal.

VARGAS: Mm-hmm.

Dr. SEARS: And now the strawberries. Or, if this is too difficult to make, we could add soy protein just directly into the oatmeal.

VARGAS: But why do you need--you have to have the protein with it?

Dr. SEARS: A balancing. You can never--always have carbohydrate and protein together at the same time.

VARGAS: Your other book is "A Week in The Zone." Now this is a whole plan to do this for one week, and you swear that somebody will feel different after doing this for just seven days?

Dr. SEARS: That's correct. What can they expect? Within two to three days, all of a sudden, they're thinking more clearly. Why? You're stabilizing blood sugars levels. Within three to four days, all your carbohydrate cravings are gone, and there is unlimited surge of energy...

VARGAS: Mm-hmm.

Dr. SEARS: ...again, because they're stabilizing blood sugar and now being able to access your own stored body fat. And by the end of seven days, you haven't lost a lot of weight, but your clothes are fitting better.

VARGAS: But you feel better.

Dr. SEARS: Your clothes are fitting better because you're losing only pure fat.

VARGAS: All right. We have four volunteers here. Come on in, folks. What's your name?

JEROME: Jerome.

VARGAS: Jerome.

NARIA: Maria.

KATE: Kate.

JERRI: Jerri.

VARGAS: Sorry for my reach. Now, all four of you are going to put this to the test.

Dr. SEARS: That's correct.

VARGAS: They're going to try your week--weeklong program. Have you ever tried anything like this or tried anything like a zone before?

JEROME: I've tried--sorry about...

VARGAS: Hello.

JEROME: ...I've tried other diets before but I figure summer's here and it's time to lose some excess baggage and not offend anybody on the beach. And so, hopefully--hopefully, I'll lose some weight on it.

VARGAS: A lot of folks have felt that maybe The Zone might be too difficult. Are you a little nervous about trying to stick to this?

MARIA: No. I mean, the process of the hand thing seems to keep things in balance, and I'm trying to incorporate more soy into my diet now anyway.

VARGAS: Right. And I don't know about you, but bread for me is a huge—like I love it.

KATE: Right, true.

VARGAS: Are you going to have problems giving that up?

KATE: Yeah. Carbohydrates.

VARGAS: Can you pass that down to her.

MARIA: Sure.

KATE: Bread and candy seems to be a large part of my diet, so I'm looking for more balance, more of a balanced one.

VARGAS: OK, great. And you're looking forward to it, too?

JERRI: Oh, yes. I'm looking forward to getting more energy and, hopefully, losing some weight.

VARGAS: All right. We're going to check in with the four of you in a week, and, hopefully, your book will prove true, and they'll feel and look healthier and better. Thanks, Dr. Barry Sears.

Dr. SEARS: Thank you.

VARGAS: And our four volunteers, we'll check in with you next week.

And, as I say, we'll follow their progress, and meanwhile, you can chat About The Zone online with Dr. Barry Sears. You can visit our Web site, gma.abcnews.com today at noon Eastern time.

PART 2
Good Morning America
June 15, 2000

The man behind the popular and controversial Zone diet says it will help you lose weight, gain energy, and increase mental alertness. And in Barry Sears' two books, "The Soy Zone" and "A Week in the Zone," he says you can begin to see results within a week. And so, we put all this to the test. Last Friday, if you were watching, we met four volunteers who agreed to try the diet out, spend a week in the zone. And here's what they had to say about their expectations.

Unidentified Man: I've tried other diets before, but I figure summer is here, and it's time to lose some excess baggage and not offend anybody on the beach.

Ms. MYREAH MOORE ("Zone" Volunteer): Now that I'm in the process of handling things and keeping it in balance, I'm trying to incorporate more soy into my diet now anyway.

Unidentified Woman #1: Bread and candy seems to be a large part of my diet so I'm looking for more balance.

Unidentified Woman #2: I'm looking forward to getting more energy and hopefully losing some weight.

GIBSON: OK. So joining us now, Barry Sears and the four volunteers, Yuron Nhaissi (ph), Myreah Moore, Kate Dooley (ph), and Jerry Lee (ph). And we'll find out how they did in just a moment. But for those who didn't see this a week ago, and for those who want aren't familiar with "The Zone," essentially what have they been doing for a week?

Dr. BARRY SEARS ("The Zone"): What they have been doing is using food almost as if it was a drug, to keep insulin in a zone, not too high but not
too low.

GIBSON: Yes. What you're basically worried about is insulin levels...

Dr. SEARS: Exactly.

GIBSON: ...in the body. But how do they do that with diet? What kinds of things have they been eating?

Dr. SEARS: Simply, basic--the foods they already like to eat but a better balance. Balancing protein and carbohydrates at every meal. And how to do this? Simply using your hand and your eye. Never eating anymore low-fat protein than you can fit on the palm of your hand. Taking a plate at each meal, dividing the three sectors. On one third of the plate, you can put some low-fat protein. No bigger and no thicker than the palm of your hand. The other two thirds of the plate, you fill it until it's overflowing with fruits and vegetables. You add a dash, that's a small amount, a dash of heart-healthy mono-unsaturated fat. That can be olive oil, slivered almonds, or guacamole and that's it.

GIBSON: I was kidding with Elizabeth, last week, about the fact that there's a lot of soy in this diet. I said--and I said, 'Boy, I just can't wait to sit down to a plate of soy every day.' But--but you should explain what that—what that's involved with.

Dr. SEARS: Well, when we talk about--and soy actually gives you a lot of--protein it gives better hormonal control than animal protein, but most American's are not going to eat tofu. They will eat soybean hamburgers, soybean hot dogs, and soybean sausages. It's much easier, now than any time in our history, to now incorporate more soy into the zone diet.

GIBSON: Now, when you all came down we weighed you and measured you this morning, is that right? OK. Yuron, what were the results with you?

YURON: Well, I--I lost about an inch off my waist and four pounds and I feel great. I feel wonderful after every meal, and it's just very easy to do and I'm going to be doing this for a long time.

GIBSON: Was it an easy diet to stay on?

YURON: Yeah, absolutely.

GIBSON: It was?

YURON: Absolutely.

GIBSON: All right. I want to ask you some more about that, or all of you
about that in a moment. Myreah, how did you do?

Ms. MYREAH MOORE: Well, I lost three pounds and I lost five inches off my waist.

GIBSON: Five inches off your waist? Well, you're a mere slip of a girl. You're disappearing right in front of my eyes.

Ms. MOORE: Yes, indeed. I--I followed the soy plan, more so than the regular week on The Zone.

GIBSON: Right.

Ms. MOORE: And--because I wanted to incorporate more soy, because I have diabetes on both sides of my family.

GIBSON: So what kinds of things did you eat that incorporated soy?

Ms. MOORE: I ate more, like, soy hot dogs. There's a hamburger-type soy product that I incorporated.

GIBSON: You both cited hamburgers and hot dogs. Anything else?

Ms. MOORE: Soy cheese. I already drank soy milk but more soy.

GIBSON: OK. Kate, how did you do?

KATE: I lost an inch and a half around my waist?

GIBSON: And pounds?

KATE: I actually didn't weigh myself. But I...

GIBSON: You didn't weigh yourself? Were you scared to do this? But—but you did lose some off the waist.

KATE: I definitely felt results, yeah.

GIBSON: OK. And, Jerry, how about you?

JERRY: Well, I lost five pounds and I lost over two inches off my waist.

GIBSON: You did?

JERRY: Yes.

GIBSON: All right. Now--but a couple of things. For instance, when you go to a restaurant, or when you're eating out, did anybody go to a barbecue, for instance, this week? A lot of people do that--OK, you went to a barbecue this week?

JERRY: My barbecue.

GIBSON: You gave the barbecue. What do you do at a thing like that?

JERRY: Well, it's difficult. The temptation is certainly there. But I did buy, again, soy products so--to incorporate soy burgers and a soy hot dog and...

GIBSON: Burgers and hot dogs.

JERRY: And grilled chicken. I eat a lot of chicken now.

GIBSON: You did do a lot of chicken?

JERRY: Yes.

GIBSON: All right. And how about restaurants? Is it--is it relatively easy to do in restaurants?

Ms. MOORE: Well, if you--I eat a lot of Asian-type food anyway, so it much--was much easier incorporating the Asian-type of diet into it.

GIBSON: My gut feeling is what they've done in the first week is lose a lot of water weight.

Dr. SEARS: No. They have lost a little bit of water weight. You can lose only maybe one to one-half pounds of fat per week. That's the maximum you can lose. But you can lose this now on a consistent basis. That's why there are very large changes in the waist size, because excess fat is accumulating in the visceral area. And that's really the most dangerous part of fat. So, in fact, they are losing weight but more importantly, they're improving their health status.

GIBSON: Yuron says he's going to stay on it. Myreah?

Ms. MOORE: Yes, definitely.

GIBSON: You're going to stay on it? Kate?

KATE: Yes, definitely.

GIBSON: Jerry?

JERRY: I'm going to try to stay on it.

GIBSON: That's the spirit. That's the way I approach these things. OK. Good luck to all of you. Thanks very much.

Dr. SEARS: Thank you.
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Reply to USDA Executive Summary, January 2001

This is a note I wrote to the USDA protesting their potential exclusion of the Zone Diet in testing various diet plans. As I point out in the letter, every time the USDA dietary recommendations have been tested against those of the Zone, the Zone has won every time. No matter, they want to exclude testing the Zone Diet because it would again be the obvious winner.

January 12, 2001

Dr. Shanthy A. Bowman
USDA
Agricultural Research Service
BHNRC/CNRG
10300 Baltimore Blvd.
Building 005
Room 125
BARC-West
Beltsville, MD 20705-2350

Dear Dr. Bowman:

Although I applaud your desire for developing a scientific consensus on appropriate diets for weight loss, your Executive Summary from the USDA Coordinated Research Program on Health and Nutrition Effects of Popular Weight Loss Diets was sadly lacking a fourth dietary program.

You discuss, a high-fat, low-carbohydrate diet (i.e. Atkins diet), a moderate-fat, high-carbohydrate diet (i.e. USDA Food Pyramid), and low-fat very-high carbohydrate (i.e. Ornish diet). However, nowhere in your discussion did you mention a moderate-fat, moderate-carbohydrate diet, which would include the Zone Diet. I feel that omission of this component diet makes any proposed research program meaningless. In Table 1, I have followed your example in your White Paper, and have characterized each of these diets:
Table 1. Characterization of Diets as Percentage of Calories

Type of Diet % Fat % Carbs % Protein
High-fat, low carb 55-65 <20 25-35
Moderate-fat, moderate carb 30 40 30
Moderate-fat, high carb 20-30 55-60 15-20
Very low-fat, very high carb 10-20 >65 10-20

Continuing as you did in your White Paper, I have also characterized each of these diets in absolute grams assuming an intake of 1,450 calories.
Table 2. Characterization of Diets as Absolute Grams Assuming a Total Dietary Intake of 1,450 calories

Type of Diet g. Fat g. Carbs g. Protein
High-fat, low carb 97 (60) 36 (10) 109 (30)
Moderate-fat, moderate carb 48 (30) 145 (40) 109 (30)
Moderate-fat, high carb 40 (25) 218 (60) 54 (15)
Very low-fat, very high carb 16 (10) 271 (75) 54 (15)

You can also classify each diet by its protein-to-carbohydrate ratio as shown in Table 3.
Table 3. Characterization of Diets as Protein-to-Carbohydrate Ratio

Type of Diet Protein to Carb Ratio
High-fat, low carb 3.0:1
Moderate-fat, moderate carb 0.75:1
Moderate-fat, high carb 0.25:1
Very low-fat, very high carb 0.20:1

The reason that Table 3 is important is that every clinical study conducted with isocaloric diets has consistently demonstrated that the protein-to-carbohydrate ratio found in moderate-fat, moderate carbohydrate diet (i.e. Zone Diet) was superior from hormonal (1,2), satiety (1,2), metabolic (3), and fat loss perspectives (4) when compared to a moderate-fat, high-carbohydrate diet (i.e. USDA Food Pyramid). The failure to include a moderate-fat, moderate carbohydrate diet such as the Zone Diet in any proposed USDA research would be irresponsible as it ignores the peer-reviewed research demonstrating the superiority of moderate-fat, moderate carbohydrate diets.

I look forward to your response.

Respectively yours,

Barry Sears, Ph.D.
President

References

References:

1. Ludwig DS, Majzoub JA, Al-Zahrani A, Dallal GE, Blanco I, and Roberts SB. "High glycemic index foods, overeating, and obesity." Pediatrics 103: E26 (1999)
2. Agus MSD, Swain JF, Larson CL, Eckert EA, and Ludwig DS. "Dietary composition and physiologic adaptations to energy restriction." Am J Clin Nutr 71: 901-907 (2000)
3. Wolfe BMJ and Piche LA. "Replacement of carbohydrate by protein in a conventional-fat diet reduces cholesterol and triglyceride concentrations in healthy normolipidemic subjects." Clin Invest Med 22: 140-148 (1999)
4. Skov AR, Toubro S, Ronn B, Holm L, and Astrup A. "Randomized trial on protein vs carbohydrate in ad libitum fat reduced diet for the treatment of obesity." International Journal of Obesity 23: 528-536 (1999)

Ms. Barbara Harris
Editor-in-Chief
Shape
One Park Avenue
New York, NY 10016

Dear Ms. Harris:

I have just read the article entitled "Protein Propaganda" by Ms. Colleen Bates in your April 1997 issue of Shape. I am astounded by the misinformation provided to your readers about the hormonal control technology set forward in my books, "The Zone" and "Mastering the Zone," and I would like to take this opportunity to set the record straight for your readers.

To begin with, the critics of my work continually use the tired argument that my dietary program is a high-protein diet, thereby trying to lump me in with the ketogenic diets of the 1970s. It should be clear to anyone who has read my books that the Zone Diet is a protein-adequate diet based on each person's unique protein requirements. I agree that metabolic complications can arise from high-protein, low-carbohydrate diets, and therefore ketogenic diets should not be recommended for anyone. However, the Zone Diet is a protein-adequate diet that contains more carbohydrates than protein thus making it metabolically impossible to become ketogenic.

I give Ms. Bates credit as she correctly points out that "even The Zone recommends" less than the average of 80-120 grams of protein per day that Americans currently eat. Then Ms. Bates turns to quote one critic (Ms. Ellen Coleman) as saying that the average active 130-pound women should eat 78 grams of protein per day (seems pretty close to what The Zone recommends), with the implication that I recommend more than twice that amount. A little logical proofreading should have been done by Ms. Bates.

Ms. Bates should have gone one step further and reported that I have never advocated taking in more protein than a person requires, but only the amount of protein necessary to maintain lean body mass. That amount of protein is unique to an individual. Furthermore, this total amount of protein should be spread evenly throughout the day so that the actual amount of protein consumed at any one meal is very small (usually 3 oz. of lean protein for females and 4 oz. of lean protein for males).

The critics mentioned in Ms. Bates' article strongly believe that "a calorie is a calorie," and that fat gain and fat loss is simply a matter of calories regardless of their macronutrient composition. As Dr. Alice Lichtenstein states, "it's the first law of thermodynamics. If you take in more calories than you expend, you'll gain weight."

Perhaps these "experts" can explain to your readers a recent study that was published in Medicine and Science in Sports and Exercise (1). In this study the following question was asked: "What would the effect be of adding extra fat calories to the diet of active runners?" This study used athletes running more than 35 miles per week on a standard diet that contained 16 percent of their calories as fat. For eight weeks the researchers added additional dietary fat to the overall diet of the runners but with no change in their exercise habits. The total amount of extra fat added over this eight-week period was an astounding 45,000 calories. If "a calorie is a calorie," then after two months of consuming this massive increase in fat calories, some change should have been observed in their weight or per cent body fat. However, no such changes were observed. How does consuming an extra 45,000 calories of fat over an eight-week period not increase the weight or per cent body fat in these athletes if "a calorie is a calorie?" Perhaps because dietary fat has no effect on insulin, and fat gain is a consequence of elevated insulin levels.

However, I should point out that the change worth noting in these runners was that their blood lipid profiles were significantly improved by consuming higher levels of fat. This led the authors of the study to state that the "the cardiovascular benefits of exercising by athletes may be negated by consuming a low-fat diet (1)."

As I try to make clear in "The Zone," it is excess insulin that makes you fat. If insulin levels are constantly elevated, this indicates a medical condition known as hyperinsulinemia. Hyperinsulinemia is now known to be a primary risk factor in predicting the occurrence of coronary heart disease (2). It is likely that individuals with hyperinsulinemia have come from a pool of those who are genetically predisposed to over-producing insulin in response to excess dietary carbohydrate. These individuals are termed insulin resistant.

However, there is a major difference between being hyperinsulinemic and being simply insulin resistant. Being insulin resistant indicates that you are genetically predisposed to becoming hyperinsulinemic. Here Ms. Bates makes a major mistake when she states that sometimes insulin resistance can develop into diabetes because "the pancreas no longer can produce enough insulin to remove excess glucose." The form of diabetes that strikes insulin-resistant individuals is called Type II diabetes. This type of diabetes is characterized by an over-production of insulin (i.e. hyperinsulinemia) coupled with a corresponding decrease in the removal of glucose at the cellular level. 95% of all diabetics are Type II diabetics. If Ms. Bates had read Dr. Gerald Reaven's work more carefully, she would not have made this scientifically incorrect statement to your readers.

Ms. Bates indicates clearly that she isn't familiar with my work when she implies that the Zone Diet "discourages people from eating fruits and vegetables." Nothing could be further from the truth. The Zone Diet is primarily a fruit and vegetable diet because they have very low carbohydrate densities, thus making it very difficult to over-consume them. The so-called "bad" carbohydrates are those that either enter the blood stream very quickly and/or have a very high carbohydrate density. Both of these factors will give rise to an exaggerated insulin response. You never avoid "bad" carbohydrates on the Zone Diet, just use them in moderation.

The article also questions my scientific credibility when Dr. Lichtenstein is quoted as saying that she can't find any of the studies cited in my book. A simple toll-free call to the number is listed in the back of both "The Zone" and "Mastering the Zone," would have been sufficient to allow Dr. Lichtenstein to receive a complete 45-page bibliography saving her valuable hours on her computer. Then a person calls our office asking for a bibliography, his or her name is entered on our computer. No listing for Lichtenstein is in our data base. Furthermore, a complete listing of the bibliography is also found at our web site (www.eicotech.com). Apparently Dr. Lichtenstein's difficulty in accessing these studies via Medline would have been solved if she called our laboratory or visited our web site as thousands of other investigators have done. I have never received word from these investigators that the studies cited in the bibliography do not exist, but far be it from me to question Dr. Lichtenstein's ability to conduct computer searches.

I am also amazed by Ms. Liebman's response to Ms. Bates' question: "How does all this explain the Zonies' claims of "never feeling better." Ms. Liebman contends it is only because they are losing weight (something that is becoming increasingly rare in America). Apparently it never crossed her mind that people feel better because the Zone Diet is hormonally correct, and that feeling good is the way you are supposed to feel all the time.

And finally even the layout of the article is highly misleading to your readers. The first page of the article features the cover of my first book, The Zone. The second page of the article implies that The Zone recommends a daily diet that includes salami, cheddar cheese, pork chops and butter. Even a cursory reading of the book would have given you the information that the Zone Diet certainly does not recommend these foods.

Sincerely yours,

Barry Sears, Ph.D.

References

1. Leddy J, Horvath P, Rowland J, and Pendergast D. "Effect of a high fat or low fat diet on cardiovascular risk factors in male and female runners." Med Sci Sport Exercise 29: 17-25 (1997)

2. Depress JP, Lamarche B, Mauriege P, Cantin B, Dagenais GR, Moorjani S, and Lupien PJ. "Hyperinsulinemia as an independent risk factor for ischemic heart disease." N Engl J Med 334: 952-957 (1996)
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July 19, 1999

Dr. Richard French
Editor
Sports Medicine

Dear Dr. French:

I am somewhat puzzled whether or not the article entitled "The Zone Diet and Athletic Performance" by Samuel Cheuvront was ever reviewed by anyone at your journal before being published, as it appears to be more of a diatribe than a review. If it was reviewed, then your reviewers are guilty of a very lax approach by overlooking Mr. Cheuvront's many erroneous statements.

For example, in the abstract of his review Mr. Cheuvront mistakenly refers to the Zone Diet used for elite athletes as a "40/30/30" diet. If he had closely read my book, he would have realized that I recommend a much higher fat content for athletic performance (1). Furthermore, his statement that a mixed diet will have no effect on pancreatic hormone release is also incorrect. Work by Westphal et al (2) and more recently by Ludwig et al (3) have shown that changing the protein-to-carbohydrate ratio in a single meal will have a significant impact on the release of insulin and glucagon during the postprandial period. Also in Mr. Cheuvront's abstract, he mistakenly states that glucagon has lipolytic actions. It is also well known that at physiological concentrations, glucagon has no lipolytic action. And nowhere in any of my writings have I ever stated that glucagon has any lipolytic action.

Now for the main body of Mr. Cheuvront's "review". I have made it clear in both my first book, The Zone, and in a subsequent book, Mastering the Zone, (4) that elite athletes must add significant amounts of extra fat (and primarily monounsaturated fat) to their diet. This is to maintain their percent body fat in an appropriate range suitable for the needs of their particular sport. Therefore the Zone Diet for elite athletes is not a calorie-restricted program as Mr. Cheuvront implies, nor are his calculations for the calories required for a typical male marathon runner remotely close to those that I would recommend for an elite athlete.

Many of Mr. Cheuvront's arguments are based on the importance of muscle glycogen levels. He ignores the results of one of the very few long-term (greater than 7 days) dietary studies done at Ohio State, which indicated that a higher-carbohydrate diet produces a 33-percent increase in muscle glycogen compared to a lower-carbohydrate diet for the same individual. Yet even with significant increase in muscle glycogen levels, there was no improvement in endurance (5). If muscle glycogen levels were overwhelmingly important in athletic performance, I would expect that a 33-percent increase in their levels should manifest itself in some type of performance increases. Earlier studies at Ohio State showed that swimmers following a higher-carbohydrate diet had statistically significant increases in their lactic acid formation under performance conditions when compared to swimmers following a lower-carbohydrate diet (6). One might assume that this increase in lactic acid formation on a higher-carbohydrate diet comes from less efficient oxygen transfer. Since the dietary protocols were the same in both Ohio State studies, one can assume that the swimmers on the high-carbohydrate diet also had significantly increased muscle glycogen compared swimmers to following a lower- carbohydrate diet. Thus it would appear that research at Ohio State indicates that a higher-carbohydrate diet will produce more muscle glycogen, decrease oxygen transfer, and provide no improvement in performance. Perhaps there is some magical threshold, above which increased muscle glycogen has no role in athletic performance. If so, it is obvious that Mr. Cheuvront has not found it in his extensive research.

This paradoxical relationship between muscle glycogen levels and performance is also indicated in a study conducted with the Navy SEALS, who one might assume maintain high levels of fitness (7). This study indicates that the amount of carbohydrate consumed by these highly trained athletes ranged from 42-51 percent of their total calories with an average of 230 grams per day. It should be noted that this is more than 50 percent lower in absolute amount in grams of carbohydrate than was used in the "moderate"-carbohydrate diet employed by the Ohio State researchers with their swimmers and runners. Using the dietary guidelines of the Zone Diet for an 80 kg SEAL (assuming 10 percent body fat), such an individual would require 210 grams of carbohydrates per day. That amount is similar to the self-selected intake by these highly trained individuals. Furthermore, dietary records indicate that these highly trained individuals were consuming approximately 1730 calories per day. If these individuals were following the formulas described in The Zone for elite athletes, their caloric intake would be more than 2,700 calories. I find it interesting that such trained individuals are not demonstrating a drop-off in performance even though their diet contains approximately the same amount of carbohydrate as recommended by the Zone Diet, but with 1,000 calories less energy than recommended by the Zone Diet.

Mr. Cheuvront further calls the study done by Munio et al as "scant evidence" that high-fat (and thus a lower-carbohydrate) diet improves performance even though both endurance and VO2 max were improved with a high degree of statistical significance (8). A 10-percent improvement of VO2 max in highly trained distance runners should be cause for further exercise physiology research as opposed to a simple dismissal by Mr. Cheuvront. Mr. Cheuvront also seems to be unaware of subsequent work by Leddy et al that shows a high-carbohydrate diet has adverse effects on the cardiovascular risk profile of elite athletes when compared to a lower-carbohydrate, higher-fat diet (9). Exactly the same conclusions are reached with Type 2 diabetic patients (10).

Mr. Cheuvront continues to demonstrate his "objective" review of my work by stating: "the bottom line message of the Zone diet, which is clearly to avoid insulin production." That statement is an outright falsehood. Other statements that he makes, such as "the Zone generally regards insulin as the enemy," are equally outrageous. No where are such statements or even the implication of such statements ever made in any of my works. In fact, it is an absurd statement. The goal of the Zone Diet is to maintain an appropriate zone of insulin. That means maintaining adequate insulin levels, but not excessive insulin levels (hyperinsulinemia). I hope that even Mr. Cheuvront would recognize that hyperinsulinemia is detrimental to physiological performance.

Once Mr. Cheuvront ventures into the realm of eicosanoids, he seems to be like a deer caught in the headlights, as he makes one contradictory statement after another relative to his premise that the Zone Diet cannot affect performance. For example, he makes statements such as "it appears then that an undefined critical balance rather than an absolute quantity of exogenous eicosanoid precursors may determine the degree of potential prostaglandin synthesis." That is a rather obtuse description of the goal of the Zone Diet. Statements Mr. Cheuvront makes that seem to support the Zone Diet include:

1. "it is therefore a reasonable postulation that vasoactive prostaglandins could act as one class of metabolites responsible for regulating muscle blood flow";
2. "changes in the production of vasoactive prostaglandins from series 2 to series 1 prostaglandins could theoretically improve performance"; and

3. "the lipid biochemistry related to the Zone diet is factual"

Mr. Cheuvront overlooks the points that blood flow and therefore oxygen transfer can be reduced by excess production of both thromboxane A2 and PGE2 because of their adverse effects on platelet aggregation. The conflicting effects of PGE2 (i.e. acting as vasodilator in certain tissues, but increasing platelet aggregation) are due to the differential effects of various eicosanoid receptors (11, 12). For example, there are four discrete receptors for prostaglandins of the E series, each of them using a different set of second messengers. A molecular definition of a "bad" eicosanoid is one that operates through the IP3/DAG pathway, whereas the definition of a "good" eicosanoid is one that operates through the cyclic AMP pathway. PGE1 appears to bind only to the EP2 receptor that mediates its message by increasing cyclic AMP levels. One the other hand, PGE2 binds to all four EP receptors, including the EP3 receptor that decreases cyclic AMP levels. Thus depending on the concentration of EP receptors and types in a specific tissue, PGE2 can have diametrically opposite physiological effects. This has been demonstrated in a recent study with various rat liver fractions (13). It should also be noted that thromboxane A2 operates through the IP3/DAG second messenger pathway via its TP receptor, and that insulin also acts via the same second messenger. Hyperinsulinemia and overproduction of "bad" eicosanoids are synergistic in producing adverse physiological responses because of the positive feedback loops of increased insulin on increasing arachidonic acid production and the effect of leukotrienes derived from arachidonic acid causing an increase in insulin production (14).

Finally, Mr. Cheuvront seems to have trouble doing simple mathematics and understanding plain English when it comes to estimating protein requirements. He quotes Lemon (15) in stating that endurance athletes require 1.2 to 1.4 grams of protein per kg of total body weight and neglects to report that strength athletes would require 1.4 to 1.8 grams per kg of total body weight. If Mr. Cheuvront had read The Zone carefully, he would have known that the protein requirements for the Zone Diet are based on lean body mass, not total body weight. Assuming an athlete has 10 percent body fat, then his or her lean body mass will be 90 percent of total body weight. Therefore for a strength athlete, my upper limit for protein recommendations for the Zone Diet would be 2.2 grams of protein per kg of lean body mass. If I use Lemon's upper estimate of 1.8 grams of protein per kg of total body weight, then I would have to divide his estimate by 0.9 to compare the two numbers directly. This would correspond to 2.0 grams of protein per kg of lean body mass, which is pretty close to my stated upper limit. An endurance athlete who does no strength training would only require a maximum of 1.8 grams of protein per kg of lean body mass according to the calculations I put forward in The Zone. Again converting Lemon's estimates (assuming 10 percent body fat), then the upper limit would be approximately 1.6 grams of protein per kg of lean body mass. For both endurance and strength athletes, my estimates of protein requirements are within 10 percent of Lemon's estimates. A surprisingly good convergence from two different sources.

I certainly hope that before Mr. Cheuvront gets a graduate degree from Florida State University, he is required to actually do some real research in exercise physiology. Until that time, his "colleagues and mentors" who read his manuscript should be ashamed of themselves for their "expert advice and guidance."


Respectfully yours,


Barry Sears, Ph.D.

References
1. Sears B. The Zone. Regan Books. pp. 88. New York, NY (1995)
2. Westphal SA, Gannon MC, and Nutrall FQ. "Metabolic response to glucose ingested with various amounts of protein." Am J Clin Nutr 62: 267-272 (1990)
3. Ludwig DS, Majzoub JA, Al-Zahrani A, Dallal GE, Blanco I, and Roberts SB. "High glycemic index foods, overeating, and obesity." Pediatrics 103: E26 (1999)
4. Sears B. Mastering the Zone. pp. 58. Regan Books. New York, NY (1997)
5. Sherman WM, Doyle JA, Lamb DR, and Strauss RH. "Dietary carbohydrate, muscle glycogen, and exercise performance during 7 d of training." Am J Clin Nutr 57: 27-31 (1993)
6. Lamb DR, Finehardt KF, Bartels RL, Sherman WM, and Snook JT. "Dietary carbohydrate and intensity of interval swim training." Am J Clin Nutr 52: 1058-1063 (1990)
7. Jacobs I, Prusaczyk WK, and Goforth HW. "Muscle glycogen, fiber type, aerobic fitness, and anaerobic capacity of west coast U.S. Navy Sea-Air-Land Personnel (SEALS)." Report 92-10, Naval Medical Research and Development Command. Bethesda, MD (1992)
8. Munio DH, Leddy JJ, Horvath PJ, Awad AB, and Pendergast DR. "Effect of dietary fat on metabolic adjustments to maximal VO2 and endurance in runners." Med Sci Sports Exerc 26: 81-88 (1994)
9. Leddy J, Horvath P, Rowland J, and Pendergast D. "Effect of a high or a low fat diet on cardiovascular risk factors in male and female runners." Med Sci Sports Exerc 29: 17-25 (1997)
10. Garg A, Bonanome A, Grundy SM, Zhang ZJ, and Unger RH. "Comparison of a high carbohydrate diet with a high-monounsaturated fat diet in patients with non-insulin –dependent diabetes mellitus." N Engl J Med 319: 829-834 (1988)
11. Coleman RA, Eglen RM, Jones RL, Narumiya S, Shimizu T, Smith WL, Dahlen S-E, Drazen JM, Gardiner PJ, Jackson WT, Jones TR, Krell RD, and Nicosia S. "Prostanoid and leukotriene receptors: a progress report from the IUPHAR working parties on classification and nomenclature. Adv Prostaglandin Thromboxane Leukot Res 23: 283-285 (1995)
12. Colman RA, Smith WL, and Narumiya S. "International union of pharmacology classification of prostanoid receptors: properties, distribution, and structure of the receptors and their subtypes." Pharmacol Rev 46: 205-229 (1994)
13. Fennekohl A, Schieferdecker HL, Jungermann K, and Puschel GP. "Differential expression of prostanoid receptors in hepatocytes, Kupffer cells, sinusoidal endothelial cells and stellate cells of rat liver." J Hepatalogy 30: 38-47 (1999)
14. Pek SB and Nathan MH. "Role of eicosanoids in biosynthesis and secretion of insulin." Diabetes Metab 20: 146-149 (1994)
15. Lemon P. "Do athletes need more dietary protein and amino acids?" Int J Sports Nutr 5: S39-61 (1995)
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High glycemic index foods, overeating, and obesity.

Ludwig DS, Majzoub JA, Al-Zahrani A, Dallal GE, Blanco I, Roberts SB.

Division of Endocrinology, Department of Medicine, Children's Hospital,Boston, 300 Longwood Ave, Boston, MA 02115, USA.

OBJECTIVE: The prevalence of obesity has increased dramatically in recent years. However, the role of dietary composition in body weight regulation remains unclear. The purpose of this work was to investigate the acute effects of dietary glycemic index (GI) on energy metabolism and voluntary food intake in obese subjects. METHODS: Twelve obese teenage boys were evaluated on three separate occasions using a crossover study protocol. During each evaluation, subjects consumed identical test meals at breakfast and lunch that had a low, medium, or high GI. The high- and medium-GI meals were designed to have similar macronutrient composition, fiber content, and palatability, and all meals for each subject had equal energy content. After breakfast, plasma and serum concentrations of metabolic fuels and hormones were measured. Ad libitum food intake was determined in the 5-hour period after lunch. RESULTS: Voluntary energy intake after the high-GI meal (5.8 megajoule [mJ]) was 53% greater than after the medium-GI meal (3.8 mJ), and 81% greater than after the low-GI meal (3.2 mJ). In addition, compared with the low-GI meal, the high-GI meal resulted in higher serum insulin levels, lower plasma glucagon levels, lower postabsorptive plasma glucose and serum fatty acids levels, and elevation in plasma epinephrine. The area under the glycemic response curve for each test meal accounted for 53% of the variance in food intake within subjects. CONCLUSIONS: The rapid absorption of glucose after consumption of high-GI meals induces a sequence of hormonal and metabolic changes that promote excessive food intake in obese subjects. Additional studies are needed to examine the relationship between dietary GI and long-term body weight regulation.

Publication Types:
· Clinical trial
· Controlled clinical trial
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Dietary composition and physiologic adaptations to energy restriction.

Agus MS, Swain JF, Larson CL, Eckert EA, Ludwig DS.

Division of Endocrinology, Department of Medicine, Children's Hospital, Boston, and the General Clinical Research Center, Brigham and Women's Hospital, Boston, MA 02115, USA.

BACKGROUND: The concept of a body weight set point, determined predominantly by genetic mechanisms, has been proposed to explain the poor long-term results of conventional energy-restricted diets in the treatment of obesity. OBJECTIVE: The objective of this study was to examine whether dietary composition affects hormonal and metabolic adaptations to energy restriction. DESIGN: A randomized, crossover design was used to compare the effects of a high-glycemic-index (high-GI) and a low-glycemic-index (low-GI) energy-restricted diet. The macronutrient composition of the high-GI diet was (as percent of energy) 67% carbohydrate, 15% protein, and 18% fat and that of the low-GI diet was 43% carbohydrate, 27% protein, and 30% fat; the diets had similar total energy, energy density, and fiber contents. The subjects, 10 moderately overweight young men, were studied for 9 d on 2 separate occasions. On days -1 to 0, they consumed self-selected foods ad libitum. On days 1-6, they received an energy-restricted high- or low-GI diet. On days 7-8, the high- or low-GI diets were consumed ad libitum. RESULTS: Serum leptin decreased to a lesser extent from day 0 to day 6 with the high-GI diet than with the low-GI diet. Resting energy expenditure declined by 10.5% during the high-GI diet but by only 4.6% during the low-GI diet (7.38 +/- 0.39 and 7.78 +/- 0.36 MJ/d, respectively, on days 5-6; P = 0.04). Nitrogen balance tended to be more negative, and energy intake from snacks on days 7-8 was greater, with the high-GI than the low-GI diet. CONCLUSION: Diets with identical energy contents can have different effects on leptin concentrations, energy expenditure, voluntary food intake, and nitrogen balance, suggesting that the physiologic adaptations to energy restriction can be modified by dietary composition.

Publication Types:
· Clinical trial
· Randomized controlled trial
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Replacement of carbohydrate by protein in a conventional-fat diet reduces cholesterol and triglyceride concentrations in healthy normolipidemic subjects.

Wolfe BM, Piche LA.

Department of Medicine, University of Western Ontario, London. bernard.wolfe@lhsc.on.ca

OBJECTIVE: To determine the effect on plasma lipid profiles of replacement of dietary carbohydrate by low-fat, high-protein foods. DESIGN: Cross-over randomized controlled trial. PARTICIPANTS: Ten healthy, normolipidemic subjects (8 women and 2 men). INTERVENTIONS: Subjects were randomly allocated to either a low-protein (12%) or high-protein (22%) weight-maintaining diet for 4 weeks and then switched to the alternate diet for 4 more weeks. The first 2 weeks of each diet served as an adjustment/washout period. Fat was maintained at 35% of energy, mean cholesterol intake at 230 mg per day and mean fibre intake at 24 g per day. Compliance was promoted by the use of written dietary protocols based on the food preferences of the subjects and weekly dietary consultation as required. OUTCOME MEASURES: Mean plasma levels of total, very-low-density-lipoprotein (VLDL), low-density-lipoprotein (LDL), and high-density-lipoprotein (HDL) cholesterol, and of total and very-low-density-lipoprotein (VLDL) triglycerides. Satiety levels were self-rated on a 10-point scale. RESULTS: Consumption of the high- versus the low-protein diet resulted in significant reductions in mean plasma levels of total cholesterol (3.8 v. 4.1 mmol/L, p < 0.05), VLDL cholesterol (0.20 v. 0.26 mmol/L, p < 0.02), LDL cholesterol (2.4 v. 2.6 mmol/L, p < 0.05), total triglycerides (0.69 v. 0.95 mmol/L, p < 0.005) and VLDL triglycerides (0.35 v. 0.57 mmol/L, p < 0.001), as well as in the ratio of total cholesterol to HDL cholesterol (3.1 v. 3.5, p < 0.01). A trend towards an increase in HDL cholesterol (1.26 v. 1.21 mmol/L, p = 0.30) was observed but was not statistically significant. Satiety levels tended to be higher among those eating the high-protein diet (6.1 v. 5.4, p = 0.073). CONCLUSIONS: Moderate replacement of dietary carbohydrate with low-fat, high-protein foods in a diet containing a conventional level of fat significantly improved plasma lipoprotein cardiovascular risk profiles in healthy normolipidemic subjects.

Publication Types:
· Clinical trial
· Randomized controlled trial
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Randomized trial on protein vs carbohydrate in ad libitum fat reduced diet for the treatment of obesity.

Skov AR, Toubro S, Ronn B, Holm L, Astrup A.

Research Department of Human Nutrition, The Royal Veterinary and Agricultural University, Copenhagen, Denmark.

OBJECTIVE: To study the effect on weight loss in obese subjects by replacement of carbohydrate by protein in ad libitum consumed fat-reduced diets. DESIGN: Randomized dietary intervention study over six months comparing two ad libitum fat reduced diets (30% of total energy) strictly controlled in composition: High-carbohydrate (HC, protein 12% of total energy) or high-protein (HP, protein 25% of total energy). SETTING AND PARTICIPANTS: Subjects were 65 healthy, overweight and obese subjects (50 women, 15 men, aged 18-55 y) randomly assigned to HC (n = 25), HP (n = 25) or a control group (C, n = 15). All food was provided by self-selection in a shop at the department, and compliance to the diet composition was evaluated by urinary nitrogen excretion. MAIN OUTCOME MEASURE: Change in body weight, body composition and blood lipids. RESULTS: More than 90% completed the trial. Weight loss after six months was 5.1 kg in the HC group and 8.9 kg in the HP group (difference 3.7 kg, 95% confidence interval (CI)(1.3-6.2 kg) P < 0.001), and fat loss was 4.3 kg and 7.6 kg, respectively (difference 3.3 kg (1.1-5.5 kg) P < 0.0001), whereas no changes occurred in the control group. More subjects lost > 10 kg in the HP group (35%) than in the HC group (9%). The HP diet only decreased fasting plasma triglycerides and free fatty acids significantly. CONCLUSIONS: Replacement of some dietary carbohydrate by protein in an ad libitum fat-reduced diet, improves weight loss and increases the proportion of subjects achieving a clinically relevant weight loss. More freedom to choose between protein-rich and complex carbohydrate-rich foods may allow obese subjects to choose more lean meat and dairy products, and hence improve adherence to low-fat diets in weight reduction programs.

Publication Types:
· Clinical trial
· Randomized controlled trial
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Effect of a high or a low fat diet on cardiovascular risk factors in male and female runners.

Leddy J, Horvath P, Rowland J, Pendergast D.

Department of Physiology, School of Medicine, State University of New York at Buffalo 14214, USA. jleddy@ubmede.buffalo.edu

Dietary fat may be associated with coronary heart disease (CHD). Studies suggest that restricting fat intake may compromise endurance performance and that increasing fat intake may improve endurance performance. We studied the effects of varying dietary fat intake on CHD risk factors in runners. Twelve male and 13 female runners increased fat from 16% to 30% of daily calories (4 wk each). Of this group, six males and six females increased fat to 42% of daily calories (4 wk). Physiological and lipoprotein risk factors were measured after each diet. Results were analyzed by repeated measures ANOVA. Increasing dietary fat from 16% to 42% of daily calories did not change adiposity, weight, heart rate, blood pressure, serum triglycerides, total cholesterol, LDL cholesterol. Apolipoprotein B, or the Apo A1/Apo B ratio. Compared with those eating higher fat, subjects eating 16% fat had lower HDL cholesterol (50 +/- 3 vs 62 +/- 3 mg.dl-1, P < 0.0001) and Apolipoprotein A1 (111 +/- 6 v. 134 +/- 6 mg/dl, P < 0.0005) and a higher TC/HDL-C ratio (4.05 +/- 0.27 vs 3.42 +/- 0.24, P < 0.0005). Runners who increased fat intake to 42% further raised HDL cholesterol (64 +/- 6 to 69 +/- 5 mg.dl-1, P < 0.04) without adversely affecting other lipoproteins. In conclusion, a 42% fat diet maintained favorable CHD risk factors in female and male runners whereas a 16% fat diet lowered Apo A1 and HDL-C and raised the TC/HDL-C ratio.
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Hyperinsulinemia as an independent risk factor for ischemic heart disease.

Despres JP, Lamarche B, Mauriege P, Cantin B, Dagenais GR, Moorjani S, Lupien PJ.

Lipid Research Center, Laval University Hospital Research Center, Quebec, Canada.

BACKGROUND. Prospective studies suggest that hyperinsulinemia may be an important risk factor for ischemic heart disease. However, it has not been determined whether plasma insulin levels are independently related to ischemic heart disease after adjustment for other risk factors, including plasma lipoprotein levels. METHODS. In 1985 we collected blood samples from 2103 men from suburbs of Quebec City, Canada, who were 45 to 76 years of age and who did not have ischemic heart disease. A first ischemic event (angina pectoris, acute myocardial infarction or death from coronary heart disease) occurred in 114 men (case patients) between 1985 and 1990. Each case patient was matched for age, body-mass index, smoking habits, and alcohol consumption with a control selected from among the 1989 men who remained free of ischemic heart disease during follow-up. After excluding men with diabetes, we compared fasting plasma insulin and lipoprotein concentrations at base line in 91 case patients and 105 controls. RESULTS. Fasting insulin concentrations at base line were 18 percent higher in the case patients than in the controls (P<0.001). Logistic-regression analysis showed that the insulin concentration remained associated with ischemic heart disease (odds ratio for ischemic heart disease with each increase of 1 SD in the insulin concentration, 1.7; 95 percent confidence interval, 1.3 to 2.4) after adjustment for systolic blood pressure, use of medications, and family history of ischemic heart disease. Further adjustment by multivariate analysis for plasma triglyceride, apolipoprotein B, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol concentrations did not significantly diminish the association between the insulin concentration and the risk of ischemic heart disease (odds ratio, 1.6; 95 percent confidence interval, 1.1 to 2.3). CONCLUSIONS. High fasting insulin concentrations appear to be an independent predictor of ischemic heart disease in men.
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Acute metabolic response to high-carbohydrate, high-starch meals compared with moderate-carbohydrate, low-starch meals in subjects with type 2 diabetes.

Gannon MC, Nuttall FQ, Westphal SA, Fang S, Ercan-Fang N.

Veterans Affairs Medical Center, and the Department of Food Science and Nutrition, University of Minnesota, Minneapolis 55417, USA. ganno004@maroon.tc.umn.edu

OBJECTIVE: The monosaccharides resulting from the digestion of ingested carbohydrates are glucose, fructose, and galactose. Of these three monosaccharides, only ingested glucose resulted in a large increase in the plasma glucose concentration. Fructose (Metabolism 41:510-517, 1992) and galactose (Metabolism 42:1560-1567, 1993) had only a minor effect. Therefore, we were interested in determining whether we could design a mixed meal, using foods of known monosaccharide, disaccharide, and starch composition, the ingestion of which would result in only a small rise in plasma glucose concentration. RESEARCH DESIGN AND METHODS: The experimental meal was composed of very little readily digestible starch but rather large amounts of fruits and vegetables. It contained 43% carbohydrate, 22% protein, and 34% fat. The results were compared with a second type of meal that contained 55% carbohydrate, 15% protein, and 30% fat, with an emphasis on complex carbohydrates (starch). It also was compared with a third meal that contained 40% carbohydrate, 20% protein, and 40% fat, typical of that consumed by the average American. The test meals were ingested in random order by people with type 2 diabetes who were not treated with oral hypoglycemic agents or insulin. Each subject ingested each type of meal. The same identical meal was ingested at 0800, 1200, and 1700. RESULTS: The integrated 24-h plasma glucose area response was statistically significantly smaller (P < 0.05) after ingestion of the low-starch meals compared with the high-starch, high-carbohydrate meals or the typical American meals. The 24-h integrated serum insulin area response also was statistically significantly less (P < 0.05) after ingestion of the low-starch meals compared with the high-starch meals or the typical American meals. The serum triglyceride area response was similar after ingestion of all three test diets. CONCLUSIONS: A diet in which fruits, nonstarch vegetables, and dairy products are emphasized may be useful for people with type 2 diabetes.

Publication Types:
· Clinical trial
· Randomized controlled trial
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Metabolic response to glucose ingested with various amounts of protein.

Westphal SA, Gannon MC, Nuttall FQ.

Section of Endocrinology, Metabolism, and Nutrition, VA Medical Center, Minneapolis, MN 55417.

Seven healthy, normal-weight subjects were fed breakfasts of 50 g protein, 50 g glucose, and 10, 30, or 50 g protein plus 50 g glucose in random sequence. Plasma glucose, insulin, C peptide, glucagon, nonesterified fatty acids, and alpha-amino nitrogen were then measured from samples obtained over 4 h. The postmeal net area of each response curve was calculated. Ingestion of 50 g protein alone did not change the serum glucose concentration. The various amounts of protein ingested with 50 g glucose also did not alter the serum glucose response compared with that observed with 50 g glucose alone. Ingestion of the various amounts of protein also did not result in a further increase in insulin concentration when ingested with glucose, except with the 50-g-protein dose. This increase was modest. Ingestion of glucose resulted in a decrease in alpha-amino nitrogen and glucagon concentrations whereas ingestion of protein increased them as expected. Additions of progressively larger amounts of protein to the glucose meal resulted in a progressive increase in the alpha-amino-nitrogen- and glucagon-area responses. The relationship was curvilinear for both the alpha-amino-nitrogen response and the glucagon response. The null point, that is, the protein dose ingested with 50 g glucose at which there would be no change in area response, was estimated to be 9 g protein for alpha-amino nitrogen and 5 g protein for glucagon.
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High glycemic index foods, overeating, and obesity.

Ludwig DS, Majzoub JA, Al-Zahrani A, Dallal GE, Blanco I, Roberts SB.

Division of Endocrinology, Department of Medicine, Children's Hospital,Boston, 300 Longwood Ave, Boston, MA 02115, USA.

OBJECTIVE: The prevalence of obesity has increased dramatically in recent years. However, the role of dietary composition in body weight regulation remains unclear. The purpose of this work was to investigate the acute effects of dietary glycemic index (GI) on energy metabolism and voluntary food intake in obese subjects. METHODS: Twelve obese teenage boys were evaluated on three separate occasions using a crossover study protocol. During each evaluation, subjects consumed identical test meals at breakfast and lunch that had a low, medium, or high GI. The high- and medium-GI meals were designed to have similar macronutrient composition, fiber content, and palatability, and all meals for each subject had equal energy content. After breakfast, plasma and serum concentrations of metabolic fuels and hormones were measured. Ad libitum food intake was determined in the 5-hour period after lunch. RESULTS: Voluntary energy intake after the high-GI meal (5.8 megajoule [mJ]) was 53% greater than after the medium-GI meal (3.8 mJ), and 81% greater than after the low-GI meal (3.2 mJ). In addition, compared with the low-GI meal, the high-GI meal resulted in higher serum insulin levels, lower plasma glucagon levels, lower postabsorptive plasma glucose and serum fatty acids levels, and elevation in plasma epinephrine. The area under the glycemic response curve for each test meal accounted for 53% of the variance in food intake within subjects. CONCLUSIONS: The rapid absorption of glucose after consumption of high-GI meals induces a sequence of hormonal and metabolic changes that promote excessive food intake in obese subjects. Additional studies are needed to examine the relationship between dietary GI and long-term body weight regulation.

Publication Types:
· Clinical trial
· Controlled clinical trial
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Dietary carbohydrate, muscle glycogen, and exercise performance during 7 d of training.

Sherman WM, Doyle JA, Lamb DR, Strauss RH.

Exercise Physiology Laboratory, School of Health, Physical Education, and Recreation, Ohio State University, Columbus 43210.

The effects of moderate- or high-carbohydrate diets on muscle glycogen and performance in runners and cyclists over 7 consecutive days of training were determined. Muscle biopsies were performed on 4 separate days before exercise for 1 h at 75% peak oxygen consumption (VO2) followed by five, 1-min sprints. After the training session on day 7, subjects ran or cycled to exhaustion at 80% peak VO2. Muscle glycogen for cyclists and runners was maintained with the high-carbohydrate diet but was reduced 30-36% (P < 0.05) with the moderate-carbohydrate diet. All subjects completed all training sessions, and there were no differences in times to exhaustion on day 7. For cyclists and runners, consuming a moderate-carbohydrate diet over 7 d of intense training reduces muscle glycogen but has no apparent deleterious effect on training capability or high-intensity exercise performance. A high-carbohydrate diet maintains muscle glycogen, but this has no apparent benefit on training capability or high-intensity exercise performance.
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Dietary carbohydrate and intensity of interval swim training.

Lamb DR, Rinehardt KF, Bartels RL, Sherman WM, Snook JT.

Exercise Physiology Laboratory, School of Health, Ohio State University, Columbus 43210.

We tested the effects of 9 d of a high-carbohydrate diet (80% of calories as CHO, 80% CHO diet) vs. a moderate-CHO diet (43% of calories as CHO, 43% CHO diet) on the abilities of collegiate swimmers to maintain a high intensity of interval swim training. Interval swim times and other physiological indices were recorded the last 5 d of each diet. Swim-interval distances ranged from 50-m interval sets to continuous 3000-m swims. There were no diet effects on mean swim velocities for any interval distance, and mean (+/- SEM) velocities for all swims were identical for both diets. There were no diet effects on the physiological indices; however, postswim blood lactate concentrations were higher after the 80% CHO diet. When mean +/- SEM daily caloric intake is 19.56 +/- 2.16 MJ (4675 +/- 516 kcal) for swimmers undertaking swim training to develop aerobic capacity, an 80% CHO diet provides no advantage over a 43% CHO diet for maintaining interval-swim-training intensity.
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Comparison of a high-carbohydrate diet with a high-monounsaturated-fat diet in patients with non-insulin-dependent diabetes mellitus.

Garg A, Bonanome A, Grundy SM, Zhang ZJ, Unger RH.

Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas 75235-9052.

We compared a high-carbohydrate diet with a high-fat diet (specifically, a diet high in monounsaturated fatty acids) for effects on glycemic control and plasma lipoproteins in 10 patients with non-insulin-dependent diabetes mellitus (NIDDM) receiving insulin therapy. The patients were randomly assigned to receive first one diet and then the other, each for 28 days, in a metabolic ward. In the high-carbohydrate diet, 25 percent of the energy was in the form of fat and 60 percent in the form of carbohydrates (47 percent of the total energy was in the form of complex carbohydrates); the high-monounsaturated-fat diet was 50 percent fat (33 percent of the total energy in the form of monounsaturated fatty acids) and 35 percent carbohydrates. The two diets had the same amounts of simple carbohydrates and fiber. As compared with the high-carbohydrate diet, the high-monounsaturated-fat diet resulted in lower mean plasma glucose levels and reduced insulin requirements, lower levels of plasma triglycerides and very-low-density lipoprotein cholesterol (lower by 25 and 35 percent, respectively; P less than 0.01), and higher levels of high-density lipoprotein (HDL) cholesterol (higher by 13 percent; P less than 0.005). Levels of total cholesterol and low-density lipoprotein (LDL) cholesterol did not differ significantly in patients on the two diets. These preliminary results suggest that partial replacement of complex carbohydrates with monounsaturated fatty acids in the diets of patients with NIDDM does not increase the level of LDL cholesterol and may improve glycemic control and the levels of plasma triglycerides and HDL cholesterol.

Publication Types:
· Clinical trial
· Randomized controlled trial
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Prostanoid and leukotriene receptors: a progress report from the IUPHAR working parties on classification and nomenclature.

Coleman RA, Eglen RM, Jones RL, Narumiya S, Shimizu T, Smith WL, Dahlen SE, Drazen JM, Gardiner PJ, Jackson WT, et al.

Glaxo Research and Development, Ware, Hertfordshire, U.K.
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International Union of Pharmacology classification of prostanoid receptors: properties, distribution, and structure of the receptors and their subtypes.

Coleman RA, Smith WL, Narumiya S.

Glaxo Research and Development, Ltd., Ware, Hertfordshire, England.

Publication Types:
· Review
· Review, academic
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Differential expression of prostanoid receptors in hepatocytes, Kupffer cells, sinusoidal endothelial cells and stellate cells of rat liver.

Fennekohl A, Schieferdecker HL, Jungermann K, Puschel GP.

Institut fur Biochemie und Molekulare Zellbiologie, Gottingen, Germany.

BACKGROUND/AIMS: Prostanoids produced by nonparenchymal cells modulate the function of parenchymal and nonparenchymal liver cells during homeostasis and inflammation via eight classes of prostanoid receptors coupled to different G-proteins. Prostanoid receptor expression in parenchymal and nonparenchymal cells was studied in order to get a better insight into the complex prostanoid-mediated intrahepatic signaling network. METHODS: RNA was isolated from freshly purified parenchymal and nonparenchymal rat liver cells and the mRNA level of all eight prostanoid receptor classes was determined by newly developed semiquantitative reverse transcription-polymerase chain reaction protocols. RESULTS: The mRNAs for the prostanoid receptors were differentially expressed. Hepatocytes were the only cell type which contained the mRNA of the Gq-linked prostaglandin F2alpha receptor; they were devoid of any mRNA for the Gs-linked prostanoid receptors. Kupffer cells possessed the largest amount of mRNA for the Gs-linked prostaglandin E2 receptor subtype 2. Endothelial cells expressed high levels of mRNA for the Gq-linked thromboxane receptor and medium levels of mRNA for the Gs-linked prostacyclin receptor, while stellate cells had the highest levels of mRNA for the prostacyclin receptor. The mRNAs for the Gq-linked prostaglandin E2 receptor subtype 1 and the Gi-linked prostaglandin E2 receptor subtype 3 were expressed in hepatocytes and all nonparenchymal cell types at similar high levels, whereas the mRNA of the Gs-linked prostaglandin D2 receptor was expressed in all nonparenchymal cells at very low levels. CONCLUSIONS: In hepatocytes the prostaglandin F2alpha receptor can mediate an increase in glucose output via an increase of intracellular InsP3 while cAMP-dependent glucose output can be inhibited via the subtype 3 prostaglandin E2 receptor. The subtype 2 prostaglandin E2 receptor can restrain the inflammatory response of Kupffer cells via an increase in intracellular cAMP The thromboxane receptor and the prostacyclin receptor in sinusoidal endothelial and the prostacyclin receptor in stellate cells may be involved in the regulation of sinusoidal blood flow and filtration.
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Role of eicosanoids in biosynthesis and secretion of insulin.

Pek SB, Nathan MH.

Department of Internal Medicine (Division of Endocrinology and Metabolism), University of Michigan, Ann Arbor 48109.

PURPOSE: The role of icosanoids, which are products formed from the metabolism of arachidonic acid, in pancreatic islet-cell function was investigated. PROCEDURES: Secretion and biosynthesis of insulin and glucagon, biosynthesis of icosanoids, and biosynthesis of enzymes and proteins necessary for icosanoid synthesis were studied in vitro, using perfused rat pancreas, isolated and incubated islets, and insulin-secreting islet-cell lines. FINDINGS: Certain exogenous prostaglandins stimulated the secretion of insulin and glucagon; leukotrienes stimulated insulin but not glucagon release. Leukotrienes inhibited glucose-induced insulin release, but promoted insulin biosynthesis. Islet cells produced prostaglandins. Although the production of leukotrienes in islet cells could not be demonstrated conclusively, glucose-responsive biosynthesis of 5-lipoxygenase and 5-lipoxygenase-activating protein was considered evidence for leukotriene synthesis. Inhibitors of prostaglandin or leukotriene biosynthesis attenuated hormone secretion. CONCLUSION: Icosanoids produced in islet cells are involved in signal-transduction, in the form of a fine-tuning amplification of biosynthesis or secretion of insulin and glucagon in response to nutrient stimuli.

Publication Types:
· Review
· Review, tutorial
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Insulin-like growth factors counteract the effect of interleukin 1 beta on type II phospholipase A2 expression and arachidonic acid release by rabbit articular chondrocytes.

Berenbaum F, Thomas G, Poiraudeau S, Bereziat G, Corvol MT, Masliah J.

URA CNRS 1283, Faculte de Medecine Saint Antoine, Paris, France.

Interleukin 1 beta was found to stimulate arachidonic acid release, and the synthesis and secretion of type II phospholipase A2 by rabbit articular chondrocytes in vitro. Interleukin 1 beta had no effect on the level of cytosolic phospholipase A2 mRNA. Insulin-like growth factors, which help stabilize the cartilage matrix, reduced the effect of interleukin 1 beta on type II phospholipase A2 activity and mRNA level, and decreased the Interleukin 1 beta-stimulated arachidonic acid release to the basal values. This suggests that type II phospholipase A2 plays a key role in arachidonic acid release from rabbit articular chondrocytes and that insulin-like growth factors counteract the effect of interleukin 1 beta. They may therefore be considered as potential antiinflammatory agents.
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[max_power]

Minchia....si !Addio...


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[bombolo74]

Perchè la prossima volta non mandi un documento PDF?

[nicodipietro]

up

[Animal]

Ma quelli erano sul libro???Giuro che non li avevo visti!!(infatti non so a cosa sono riferiti).
Poi ci sono alcune domande per le quali non trovo risposta.
Ad esempio:tu con la trovata di alzare i grassi praticamente esci dal rapporto 40-30-30:quindi chi ti dice che il rapporto ottimale sia proprio quello?Inoltre non tutti reagiscono in modo diverso.
Ah per i culturisti che gareggiano:chiedi a Body80 o sauron o Niko se fanno la zona(loro sono natural).
Poi:non mi pare dimostrato(o mi è sfuggito)che in dieta ipocalorica si possa accrescere di massa muscolare.Infatti non si realizza un anabolismo.Per vedere ciò basta che fai una dieta ipocalorica e vai a vedere i tuoi livelli sierici di IGF-1 rispetto a quando sei in dieta ipercalorica.tra l'altro bisogna ricordare che l'IGF-1 pare venga prodotto solo in dieta ipercalorica.Anche il gh esogeno sembra funzionare incredibilmete di meno in fase di dieta ipocalorica.Poi spero che sarai alla fiera così ne parliamo a 4 occhi!!
Cmq io non ho niente contro la zona,ma non la condivido per il BB;la ritengo invcece molto valida per chi deve perdere un po' di peso o tanto peso e rientrare nel peso forma o quasi.Insomma è un'ottima dieta per le persone normali!

[max_power]

Cmq io non ho niente contro la zona,ma non la condivido per il BB;la ritengo invcece molto valida per chi deve perdere un po' di peso o tanto peso e rientrare nel peso forma o quasi.Insomma è un'ottima dieta per le persone normali![/QB][/QUOTE]

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[nicodipietro]

No non sono sul libro, su questo ti do ragione, li poteva pure mettere (SONO SOLO ALCUNI QUELLI CHE TI HO POSTATO!!) così anche il libro ne acquistava in credibilità! fatti suoi.

comunque innanzi tutto ai natural che gareggiano che hai citato faccio questa domanda: AVETE MAI PROVATO A SEGUIRLA SERIAMENTE PER ALMENO 2-3 MESI?

Per quanto riguarda le proporzioni ormai non è neanche più solo Sears, un sacco di medici anche per radio e in TV imputano la colpa del grasso all'insulina: è proprio così, è l'insulina l'"ormone dell'accumulo", come ti ho già postato tratti di libri di biochimica medica che con sears e la zona non centrano niente: POTENTE AZIONE INIBITRICE SUL DIMAGRIMENTO, POTENTE AZIONE LIPOGENETICA: ti fa ingrassare e ti impedisce di dimagrire! ogni giorno trovo nuovi studi che confermano che il pasto ad alta produzione di insulina (alto ig) impedisce l'ossidazione dei grassi e favorisce l'accumulo di glucosio come grasso (e qualcuno di questi studi li ho anche postati qui sul forum), studi che con la zona non c'entrano niente!

E questo è il bello: per mantenere l'equilibrio dell'insulina devi rispettare il rapporto proteine/carboidrati. I grassi servono per dare effettivamente l'avvio alla loro "combustione", senza l'insulina che li immagazzina e li protegge come un magnaccio protegge le proprie puttane, i grassi vengono letteralmente utilizzati come energia, perchè è l'insulina che l'impedisce! e, cosa ancor più bella, i grassi che mangi NON CAUSANO NEANCHE UN MINIMO AUMENTO DI INSULINA! ZERO! ZERO! anzi rallentano l'assorbimento dei carboidrati abbassando leggermente l'ig di un alimento, immagina se questo è già un alimento a basso ig...

Infatti numerosi studi ormai hanno concluso: se non mangi cibi iperinsulinici è letteralmente IMPOSSIBILE INGRASSARE MANGIANDO GRASSI! puoi fare una dieta 90% delle kcal. provenienti dai grassi, se non alzi l'insulina NON INGRASSI ASSOLUTAMENTE! perdi muscolo perchè comunque i carbo sono troppo pochi e anche le proteine (se il 90% sono grassi!) ma NON INGRASSI anzi DIMAGRISCI, perchè quando non c'è l'insulina non solo non ti fa ingrassare, ma non ti impedisce nemmeno di dimagrire. E di studi ce ne sono tanti, se non ci credi te li posso postare!

Ecco perchè un atleta ad alto fabbisogno può mangiare più grassi (OVVIAMENTE MONO-INSATURI): non influenzerai l'equilibrio degli eicosanoidi e del controllo dell'insulina, fattori CHIAVE della zona.

Per quanto riguarda l'igf-1 e l'anabolismo, lo so che diete ipocaloriche ne causano una diminuzione, ma per il controllo ormonale della zona succede proprio il contrario! dire che non è vero che in zona aumenta il gh, l'igf-1 e il testosterone è come dire che non è vero che se si "adagia" Manuela Arcuri su di un uomo sano, gli si alza!

E gli studi che dimostrano che IN REGIME IPOCALORICO l'organismo E' IN GRADO DI SINTETIZZARE NUOVO MUSCOLO (figuriamoci in regime MEDIOcalorico della zona o IPERCALORICO della zona se ti alleni pesante e quindi aumenti i grassi) NE HO POSTATI, SE VUOI TE LI RIPOSTO.

[swanz]

Purtoppo su di me la zona (a livello di massa) non ha funzionato.
DEVO AMMETTERE CHE STAVO REALMENTE MEGLIO: MAGGIORE ATTENZIONE, MAI UN CENNO DI SONNOLENZA, OTTIMO UMORE......MA PER LA MASSA "LA ZONA" E' IN DEBITO CON ME DI 1KG!

[nicodipietro]

Swanz, scusa ma quando te l'ho fatta ancora non avevo pensato al fatto dei grassi! ora come hai visto dal post ho nuove acquisizioni, se vuoi te la rifaccio;

Comunque, sei sicuro che quel kg sia di muscolo? e la forza com'era? e mica ti sovrallenavi?

[Body80]

Il mio preparatore mi ha sempre fatto una dieta per definirmi che si avvicina più alla CHETO piuttosto che alla ZONA.
In massa poi una dieta + tradizionale, diciamo una cronodieta leggermente modificata (sono cresciuto sempre tanto).
Cmq condivido ANIMAL, alla fine occorre guardare il proprio metabolismo e le calorie assunte.

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Uptaded ----> http://digilander.iol.it/bodystrong/index.htm

[nicodipietro]