Dieta low carb é realmente necessária?

[krebz 3646]

1 hora atrás, Thorun disse:

 

Não deixa de ser mas a premissa é q se ela se sacia comendo 4000 kcal, na lowcarb se saciaria com menos. Ja segui a estratégia low carb e me dou bem, pois fico de boa fazendo 2 ou no maximo 3 refeições / dia, o que me agrada. Com uma dieta de mais carbs acabo tendo que fracionar muito pois sempre estou com fome, posso comer 900 g de comida no almoço, sendo 450g de arroz e feijão e 450g de carne, q de 2 a 3h depois estarei morrendo de fome, então acho melhor trabalhar a saciedade nessa dieta comendo 500g no almoço e fazendo esse lanche da tarde. Mas gordo q não conta calorias e sai comendo tudo a vê pela frente, acho q é uma boa opção.

Só q claro, como falaram aí em cima, num contexto de dieta e treino sério, performance, o melhor é contar as kcal independente da dieta, ter um controle mais justo sobre oq tá comendo.

 

Exatamente.

 

Duro é ler as merdas que o Norton insiste em postar fazem anos no fórum e já provadas serem meia-verdades ou pura bobagens.

As "centenas de pesquisas" não existem, quase todas as pesquisas igualando calorias entre diferentes dietas mostram que a médio/longo prazo DA NO MESMO o resultado de perda de peso/gordura? a curto prazo sim, low-carbo e keto perde mais peso inicialmente (supostamente uma grande quantidade de água).

 

Mas sim, quando não há controle algum (isocalórico), low-carb e keto faz perder mais peso que outras dietas por aos poucos reduzir o apetite.

 

https://jissn.biomedcentral.com/articles/10.1186/s12970-017-0174-y

 

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Low-carbohydrate diets

Similar to LFD, low-carbohydrate diets (LCD) are a broad category lacking an objective definition. There is no universal agreement on what quantitatively characterizes an LCD. The AMDR lists 45–65% of total energy as the appropriate carbohydrate intake for adults [33]. Therefore, diets with intakes below 45% fall short of the ‘official’ guidelines and can be viewed as LCD. However, other published definitions of LCD disregard the limits set in the AMDR. LCD have been defined as having an upper limit of 40% of total energy from carbohydrate [43, 44]. In absolute rather than proportional terms, LCD have been defined as having less than 200 g of carbohydrate [43]. Some investigators have taken issue with this liberal definition of LCD, preferring to delineate non-ketogenic LCD as containing 50–150 g, and KD as having a maximum of 50 g [45].

Meta-analyses comparing the effects of LFD with LCD have yielded mixed results across a wide range of parameters. Liberal operational definitions of LCD (e.g., ≤45%) have led to a lack of significant differences in body weight and waist circumference [46], while lower carbohydrate classification thresholds (<20%) have favored LCD for weight loss and other cardiovascular risk factors [47]. Recently, Hashimoto et al. [48] conducted the first-ever meta-analysis on the effect of LCD on fat mass (FM) and body weight. The analysis, limited to trials involving overweight/obese subjects, had a total of 1416 subjects, stratifying the diets as “mild LCD” (~40% CHO) or “very LCD” (~50 g CHO or 10% of total energy). Eight RCTs included a very LCD treatment, and 7 RCTs included a mild LCD treatment. With all groups considered, FM decrease was significantly greater in the LCD than the control diets. However, sub-analysis showed that fat mass decrease in very LCD was greater than the controls, while the difference in FM decrease between mild LCD and controls was not significant. A separate sub-analysis of short- versus long-term effects found that both types of LCD yielded significantly greater fat loss than controls in trials less than, as well as longer than 12 months. A further sub-analysis of found that BIA failed to detect significant between-group differences in FM reduction, while DXA showed significantly greater decreases in LCD than controls. It should be noted that despite reaching statistical significance, mean differences in FM reduction between LCD and control groups were small (range = 0.57–1.46 kg). Practical relevance is questionable given the obese nature of the subjects. The authors speculated that the advantage of the LCD over the control diets could have been due to their higher protein content.

Ketogenic diets

Despite being a subtype of LCD, the ketogenic diet (KD) deserves a separate discussion. Whereas non-ketogenic LCD is subjectively defined, KD is objectively defined by its ability to elevate circulating ketone bodies measurably – a state called ketosis, also known as physiological or nutritional ketosis. Aside from completely fasting, this condition is attained by restricting carbohydrate to a maximum of ~50 g or ~10% of total energy [45], while keeping protein moderate (1.2–1.5 g/kg/d) [49], with the remaining predominance of energy intake from fat (~60–80% or more, depending on degree protein and carbohydrate displacement). Ketosis is a relatively benign state not to be confused with ketoacidosis, which is a pathological state seen in type 1 diabetics, where a dangerous overproduction of ketones occurs in the absence of exogenous insulin. The primary ketone produced hepatically is acetoacetate, and the primary circulating ketone is β-hydroxybutyrate [50]. Under normal, non-dieting conditions, circulating ketone levels are low (<3 mmol/l). Depending on the degree of restriction of carbohydrate or total energy, KD can raise circulating ketone levels to a range of ~0.5–3 mmol/l, with physiological ketosis levels reaching a maximum of 7–8 mmol/l [49].

The proposed fat loss advantage of carbohydrate reduction beyond a mere reduction in total energy is based largely on insulin-mediated inhibition of lipolysis and presumably enhanced fat oxidation. However, a single-arm study by Hall et al. [51] examined the effect of 4 weeks on a low fat diet (300 g CHO) followed by 4 weeks on a KD (31 g CHO). Blood ketone levels plateaued at ~1.5 mmol/l within two weeks into the KD. A transient increase in energy expenditure (~100 kcal/day) lasting a little over a week occurred upon switching to the KD. This was accompanied by a transient increase in nitrogen loss, potentially suggesting a stress response including the ramping up of gluconeogenesis. Although insulin levels dropped rapidly and substantially during the KD (consisting of 80% fat, 5% CHO), an actual slowing of body fat loss was seen during the first half of the KD phase.

It has been postulated that the production and utilization of ketone bodies impart a unique metabolic state that, in theory, should outperform non-ketogenic conditions for the goal of fat loss [45]. However, this claim is largely based on research involving higher protein intakes in the LCD/KD groups. Even small differences in protein can result in significant advantages to the higher intake. A meta-analysis by Clifton et al. [52] found that a 5% or greater protein intake difference between diets at 12 months was associated with a threefold greater effect size for fat loss. Soenen et al. [53] systematically demonstrated that the higher protein content of low-carbohydrate diets, rather than their lower CHO content, was the crucial factor in promoting greater weight loss during controlled hypocaloric conditions. This is not too surprising, considering that protein is known to be the most satiating macronutrient [54]. A prime example of protein’s satiating effect is a study by Weigle et al. [55] showing that in ad libitum conditions, increasing protein intake from 15 to 30% of total energy resulted in a spontaneous drop in energy intake by 441 kcal/day. This led to a body weight decrease of 4.9 kg in 12 weeks.

With scant exception [56], all controlled interventions to date that matched protein and energy intake between KD and non-KD conditions have failed to show a fat loss advantage of the KD [51, 53, 57,58,59,60]. A recent review by Hall [61] states, “There has never been an inpatient controlled feeding study testing the effects of isocaloric diets with equal protein that has reported significantly increased energy expenditure or greater loss of body fat with lower carbohydrate diets.” In light of this and the previously discussed research, the ‘special effects’ of LCD and KD are not due to their alleged metabolic advantage, but their higher protein content. Perhaps the strongest evidence against the alleged metabolic advantage of carbohydrate restriction is a recent pair of meta-analyses by Hall and Guo [60], which included only isocaloric, protein-matched controlled feeding studies where all food intake was provided to the subjects (as opposed to self-selected and self-reported intake). A total of 32 studies were included in the analysis. Carbohydrate ranged from 1 to 83% and dietary fat ranged from 4 to 84% of total energy. No thermic or fat loss advantage was seen in the lower-CHO conditions. In fact, the opposite was revealed. Both energy expenditure (EE) and fat loss were slightly greater in the higher-CHO/lower-fat conditions (EE by 26 kcal/day, fat loss by 16 g/d); however, the authors conceded that these differences were too small to be considered practically meaningful.

A common criticism of the existing literature is that trials need to run longer (several months instead of several weeks) to allow sufficient “ketoadaptation,” which is a physiological shift toward increased fat oxidation and decreased glycogen utilization [62]. The problem with this claim is that the rise in fat oxidation – objectively measured via decreased respiratory quotient – reaches a plateau within the first week of a KD [51]. Increased oxidation of free fatty acids, plasma triacylglycerol, and intramuscular triacylglycerol during exercise is a well-established response to fat-rich diets [63]. However, this rise in fat oxidation is often misconstrued as a greater rate of net FM reduction. This assumption ignores the concomitant increase in fat intake and storage. As a result of fat-adaptation, increased intramuscular triacylglycerol levels indicate increased fat synthesis over degradation during the rest periods between exercise bouts [64]. To reiterate a previous point, rigorously controlled isocaloric, protein-matched studies have consistently demonstrated that ketoadaptation does not necessarily amount to a net decrease in fat balance, which is ultimately what matters.

If there is any advantage to KD over non-KD for fat loss, it is potentially in the realm of appetite regulation. Under non-calorically restricted conditions, KD has consistently resulted in body fat and/or body weight reduction [65,66,67,68,69]. This occurs via spontaneous energy intake reduction, which could be due to increased satiety through a suppression of ghrelin production [70]. Moreover, KD has demonstrated hunger-suppressive effects independent of protein content. In a 4-week crossover design, Johnstone et al. [66] found that a KD consumed ad libitum (without purposeful caloric restriction) resulted in an energy intake reduction of 294 kcal/day. The latter results were seen despite a relatively high protein intake (30% of energy) matched between KD (4% CHO) and non-KD (35% CHO) conditions. In further support of this idea, a meta-analysis by Gibson et al. [71] found that KD suppresses appetite more than VLED. However, it remains unclear whether the appetite suppression is due to ketosis or other factors such as an increased protein or fat intake, or restriction of carbohydrate.

An area of growing interest is the effect of KD on athletic performance. Since training capacity has the potential to affect body composition, the effect of KD on exercise performance warrants discussion. Carbohydrate restriction combined with high fat intake to become fat-adapted (or ketoadapted) is a tactic that attempts to improve performance by increasing the body’s reliance on fat as fuel, thereby sparing/decreasing glycogen use, which ostensibly could improve athletic performance. However, in contrast to the proposed benefits of fat-adaptation on performance, Havemann et al. [72] found that 7 days of a high-fat diet (68%) followed by 1 day of high-CHO diet (90%) expectedly increased fat oxidation, but decreased 1-km sprint power output in well-trained cyclists. Stellingwerff et al. [73] compared substrate utilization, glycogenolysis, and enzymatic activity from either 5 days of a high-fat diet (67%) or high-CHO (70%) followed by one day of high-CHO with no training, followed by experimental trials on the seventh day. The high-fat diet increased fat oxidation, but also lowered pyruvate dehydrogenase activity and decreased glycogenolysis. These results provide a mechanistic explanation for the impairment in high-intensity work output as a result of high-fat, CHO-restricted diets [62, 65, 67]. Recently, an ergolytic effect from ketoadaptation has been observed at lower intensities as well. Burke et al. [74] reported that after 3 weeks on a KD at a slight energy deficit, elite race walkers showed increased fat oxidation and aerobic capacity. However, this was accompanied by a reduction in exercise economy (increased oxygen demand for a given speed). The linear and non-linear high-CHO diets in the comparison both caused significant performance improvements, while no significant improvement was seen in the KD (there was a nonsignificant performance decrease). It is notable that Paoli et al. [75] found no decrease in bodyweight-based strength performance in elite artistic gymnasts during 30 days of KD. Furthermore, the KD resulted in significant loss of FM (1.9 kg) and non-significant gain of LM (0.3 kg). However, unlike Burke et al.’s study, which equated protein between groups (~2.2 g/kg), Paoli et al.’s protein intakes were skewed in favor of the KD (2.9 vs. 1.2 g/kg). Wilson et al. [56] recently reported similar increases in strength and power in a protein and calorie-matched comparison of a KD and a Western diet model, suggesting that KD might have less ergolytic potential for strength training than it does for endurance training.

 

 

Ou se preferir uma meta analise de 2019 sobre o assunto:

https://www.sciencedirect.com/science/article/pii/S1933287419302673

 

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Evidence for the effect of low-CHO and very-low-CHO diets on weight loss

Weight loss in adults with overweight or obesity

Despite favorable effects of low-CHO and very-low-CHO diets on EE and intake, long-term effects on weight loss may not be superior to more conventional strategies. According to the 2013 American Heart Association/American Cardiology/The Obesity Society (AHA/ACC/TOS) Guideline for the Management of Overweight and Obesity in Adults,³⁴ research has not demonstrated any advantage of a very-low-CHO diet on weight loss at 6 months compared with a calorie-restricted, low-fat diet. More recently, several systematic reviews and meta-analyses of RCTs have examined the effectiveness of low-CHO, high-fat (LCHF) (>30% TDE fat) vs high-CHO, low-fat (HCLF) diets (<30% TDE fat) for weight loss in individuals with overweight or obesity at 3 to 6 months⁵⁷ or 1 to 2 years.57, 58, 59, 60 Participants assigned to both LCHF and HCLF diets achieved clinically meaningful weight loss (Table 2, Fig. 1). However, weight loss was significantly greater with LCHF diets vs HCLF diets when the prescribed diets were hypocaloric,⁵⁹ when the prescribed ad libitum LCHF diets were hypocaloric (even though not required or encouraged),⁶⁰ and the study duration was less than 2 years.⁵⁸

Table 2. Effect of low-CHO and very-low-CHO diets compared with HCLF diets on weight, lipids, HbA1c, and blood pressures at 1–2 years follow-up reported in meta-analyses

Author	# of RCTs	Weight WMD (95% CI), kg	LDL-C, WMD (95% CI), mg/dL	HDL-C, WMD (95% CI), mg/dL	TG, WMD (95% CI), mg/dL	HbA1c WMD (95% CI), %	SBP, WMD (95% CI), mm/Hg	DBP, WMD (95% CI), mm/Hg
Meta-analyses of studies of adults with overweight and/or obesity
Naude et al. 201457	14	−0.48 (−1.44 to 0.49)	2.71 (−0.39 to 6.19)	1.55 (0.39 to 3.09)	−5.31 (−12.4 to 2.66)	NR	−2.00 (−5.00 to 1.00)	−0.03 (−1.68 to 1.62)
Bueno et al. 201358	13	−0.91 (−1.65 to −0.17)	4.64 (1.55 to 7.73)	3.48 (2.32 to 4.64)	−15.9 (−23.9 to −7.09)	−0.24 (−0.55 to 0.06)	−1.47 (−3.44 to 0.50)	−1.43 (−2.49 to −0.37)
Schwingshackl & Hoffmann 201359	32	0.15 (−0.50 to 0.80); −0.59∗ (−1.04 to −0.15)	3.11 (1.71 to 4.51)	2.35 (1.29 to 3.42)	−8.38 (−13.5 to −3.25)	NR	NR	NR
Mansoor et al. 201660	11	−2.17 (−3.36 to −0.99)	6.19 (0.12 to 12.8)	5.41 (3.48 to 7.35)	−23.0 (−32.8 to −13.3)	NR	−1.02 (−2.98 to 0.94)	−1.01 (−2.75 to 0.74)
Gjuladin-Hellon et al. 201961	5†	NR	1.55 (−1.55 to 4.64)	3.48 (0.77 to 5.80)	−9.74 (−15.9 to −2.66)	NR	NR	NR
Sackner-Bernstein et al. 201662	17	−2.04‡ (−3.15, −0.93)	8.6‡ (3.6 to 13.7)	5.1‡ (3.5 to 6.7)	−28.8‡ (−39.1 to −18.5)	NR	−1.7‡ (−3.5 to 0.2)	NR
Meta-analyses of studies of adults with overweight and/or obesity with pre-diabetes and/or type 2 diabetes
Naude et al. 201457	5	0.91 (−2.08 to 3.89)	3.87 (−2.32 to 10.44)	0.00 (−3.48 to 3.09)	−7.09 (−43.4 to 23.0)	0.01 (−0.28 to 0.30)	0.31 (−3.1 to 3.72)	0.09 (−1.95 to 2.13)
Schwingshackl & Hoffmann 201463	14§	−0.47 (−1.85 to 0.92)	1.55 (−5.41 to 8.89)	1.55 (0.00 to 3.09)	−15.9 (−21.3 to −11.5)	−0.17 (−0.39 to 0.06)	−1.35 (0.35 to 2.35)	−1.35 (−1.79 to −0.92)
Meng et al. 201764	9	−0.24 (−2.18 to 1.70)	1.55 (−3.09 to 6.19)	2.71 (1.16 to 4.25)	−29.2 (−39.9 to −18.6)	−0.44 (−0.61 to −0.26)	NR	NR
Snorgaard et al. 201765	10	0.20 (−0.97 to 1.36)	−0.39 (−3.87 to 2.71)	NR	NR	0.04 (−0.04 to 0.13)	NR	NR
Huntriss et al. 201866	5–7‖	0.28 (−1.37 to 1.92)	1.93 (−3.87 to 7.35)	2.32 (1.55 to 3.48)	−21.3 (−31.0 to −11.5)	−0.28 (−0.53 to −0.02)	−2.74 (−5.27 to −0.20)	−0.99 (−2.24 to 0.25)
Korsmo-Haugen et al. 201967	7–10¶	0.14 (−0.29 to 0.57)	1.16 (−3.87 to 6.19)	2.32 (−0.39 to 5.03)	−8.86 (−20.4 to 2.66)	0.00 (−0.10 to 0.09)	−1.39 (−3.20 to 0.43)	−0.55 (−2.17 to 1.06)
Sainsbury et al. 201868	25	−0.43 (−0.93 to 0.07)	NR	NR	NR	−0.09 (−0.21 to 0.03)	NR	NR
van Zuuren et al. 201869	2–3∗∗	−0.14 (−1.64 to 1.35)	2.32 (−3.09 to 8.12)	4.64 (2.71 to 6.57)	−16.8 (−28.3 to −4.43)	−0.02 (−0.37 to 0.41)	1.60 (−1.50 to 4.70)	0.88 (−1.25 to 3.02)

 

HCLF, high-carbohydrate, low-fat; RCT, randomized control trials; WMD, weight mean difference; LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol; TG, triglycerides; HbA1c, hemoglobin A1c; SBP, systolic blood pressure; DBP, diastolic blood pressure; NR, not reported.

If all values in the confidence interval are on the same side of zero (either all positive or all negative), the findings are significant.

In this meta-analysis, 14 RCTs were included in the full meta-analysis, but the number of RCTs varied in the analyses involving only participants with T2D: 5 RCTs were included for SBP, 6 RCTs were included for DBP, 7 RCTs were included for LDL-C, 8 RCTs were included for weight, 9 RCTs were included for HDL-C, and 10 RCTs were included for TG and HbA1c.

∗

For hypocaloric diet comparisons only.

†

In the Gjuladin-Hellon et al.⁶¹ meta-analysis, 8 RCTs were included in the full meta-analysis, but only 5 RCTs were included in the 12 mo + meta-analysis for LDL-C, HDL-C, and TG.

‡

The decimal places reported reflect those reported in the published article.

§

In the Schwingshackl & Hoffmann⁶³ meta-analysis, the authors included RCTs of high-fat diets (>30% TDE total fat) of which 6 studies were classified as low-CHO and 4 were classified as moderate-CHO.

‖

In the Huntriss et al.⁶⁶ meta-analysis, 18 RCTs were included in the full meta-analysis, but only 7 RCTs were included in the 12 mo + meta-analysis for HDL-C, TG, HbA1c, SBP, and DBP, 6 RCTs were included for weight, and 5 RCTs were included for LDL-C.

¶

In the Korsmo-Haugen et al.⁶⁷ meta-analysis, 23 RCTs were included in the full meta-analysis, but the number of RCTs varied in the 12 mo + meta-analyses, which is what is reported in Table 2: 7 RCTs were included for DBP, 8 RCTs were included for SBP, 9 RCTs were included for LDL-C and TG, and 10 were included for weight, HDL-C, and HbA1c.

∗∗

In the van Zuuren et al.⁶⁹ meta-analysis, 33 RCTs and 3 clinical control trials were included in the full meta-analysis, but the number of RCTs varied in the 12 mo + meta-analyses, which is what is reported in Table 2: 2 RCTs were included for weight, LDL-C, HDL-C, TG, SBP, and DBP, and 3 RCTs were included for HbA1c.

Table 3. 2015 ACC/AHA clinical practice guideline recommendation classification system⁷⁴

 

Modified from the 2015 ACC/AHA Clinical Practice Guideline Recommendation Classification System

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Figure 1. Effects of low-CHO and very-low-CHO diets vs high-CHO, low-fat diets on cardiometabolic risk markers at 1–2 years follow-up.57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69 LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol; T2D, type II diabetes; TG, triglycerides; HbA1c, hemoglobin A1c; SBP, systolic blood pressure; DBP, diastolic blood pressure. *No significant difference between diet groups. **Mixed results on significant difference between diet groups—some meta-analyses found a significant difference between diet groups, while others did not. ***Significant difference between diet groups.

Results for patients with prediabetes⁶³ and T2D57, 64, 65, 66, 67 were similar, with no significant difference for weight loss between the low-CHO and HCLF diet groups in long-term studies (Table 2, Fig. 1). Sainsbury et al.⁶⁸ found a significant decrease in weight with low-CHO vs HCLF diets at 3 months (weighted mean difference [WMD] −1.08 kg, 95% CI: −1.93, −0.23, n = 12 studies), but no difference at >6 months (WMD −0.14 kg, 95% CI: −0.94, 0.65, n = 9 studies). van Zuuren et al.⁶⁹ reported a significantly greater weight loss at 8–16 weeks (WMD −2.04 kg, 95% CI: −3.23, −0.85; P = .0008; n = 4 studies) with low-CHO vs HCLF diets, but no difference at any other time. In addition, Snorgaard et al.⁶⁵ reported no difference in BMI and waist circumference in their meta-analysis.

Points to consider regarding the effects of low-CHO and very-low-CHO diets on weight loss

The results from the meta-analyses discussed previously support the view that low- and very-low-CHO diets are not superior for weight loss compared with diets with a higher quantity of CHO and are difficult to maintain in clinical trials of adults with overweight and obesity, with or without prediabetes or diabetes.57, 58, 59, 60, 63, 65, 66, 67, 68, 69 In the studies included in the meta-analyses, mean CHO intake in the low- and very-low-CHO diet groups at the end of follow-up exceeded 50 g/d in all except one study.⁷⁰ Mean CHO intake in the remaining studies was between 33–47% TDE by study end.58, 59, 60 Attrition was ∼30% for both the LCHF and HCLF diet groups in some studies.⁶⁰

Gardner et al.⁷¹ found that when individuals are educated to consume foods with high dietary quality for both low-fat and low-CHO diets, weight loss was similar in both groups. Sacks et al.⁷² found that satisfaction was similar among study completers assigned to four different hypocaloric diets (n = 645): low-fat, average-protein; low-fat, high-protein; high-fat, average-protein; and high-fat, high-protein. However, there was substantial variation in weight loss achieved with each of the diet conditions with some individuals in each showing well-above-average weight loss, suggesting that personal preference in the selection of a weight loss diet is important and should be considered.

Key points

 

•

Short-term (≤6 months) hypocaloric low-CHO and very-low-CHO diets may result in greater weight loss than hypocaloric high-CHO, low-fat (HCLF) diets.

•

Longer-term (>6 months) results suggest that low-CHO and very-low-CHO diets may result in weight loss that is equivalent to that of HCLF diets.

•

Very-low-CHO diets are difficult to maintain and are not clearly superior for weight loss compared with diets that allow a higher amount of CHO in adults with overweight and obesity with or without diabetes.

•

Long-term participation in any weight loss intervention is difficult, but adherence to the assigned macronutrient distribution (ie, CHO, protein, and fat) is lower with low-CHO and, especially, very-low-CHO diets.

•

Personal preference should be considered when selecting a weight loss diet.

 

[Thorun 289]

Agora, Norton disse:

 

Felizmente existem centenas de estudos comparando dietas baseadas em contagem de calorias com as lowcarb ad libitum, e adivinha quais ganham em perda de peso e manutenção da massa magra, estatisticamente as lowcarb e cetogênica. Pois é, não é só empirismo não. Se alguém consegue comer 4000 kcal majoritariamente de proteína seguindo a saciedade não conseguirá manter o hábito por um longo período de tempo. Além das proteínas estimularem bem pouco a insulina, e este é um dos fatores já demonstrados que mais vale a qualidade do alimento que a quantidade para a perda ou manutenção do peso. Se eu for num churrasco posso até passar dessa quantia, mas afinal quem se importa em contar, garanto que no dia posterior terei bem menos fome e irei ingerir naturalmente menos comida.

 

Acredito q esses estudos devem considerar o público em geral. Num contexto de construção de massa muscular, por exemplo, contar calorias te permite fazer um ajuste fino de poder colocar 100, 200 kcal a mais do que vc consome em um dia, proporcionando ganhos mais secos e mais constantes, do que um cara q não contou nada no dia, q pode por exemplo comer em um dia um déficit de 400, no outro um superavit de 300, e q não tem a mínima ideia de q isso tá ocorrendo.

E falo isso independente da dieta. Nada impede alguém na lowcarb de contar os macros. 

[Norton 3556]

1 hora atrás, Thorun disse:

 

Acredito q esses estudos devem considerar o público em geral. Num contexto de construção de massa muscular, por exemplo, contar calorias te permite fazer um ajuste fino de poder colocar 100, 200 kcal a mais do que vc consome em um dia, proporcionando ganhos mais secos e mais constantes, do que um cara q não contou nada no dia, q pode por exemplo comer em um dia um déficit de 400, no outro um superavit de 300, e q não tem a mínima ideia de q isso tá ocorrendo.

E falo isso independente da dieta. Nada impede alguém na lowcarb de contar os macros. 

 

Sim e nada impede alguém de ganhar músculo limpo sem contar também. E era o que faziam os atletas antes dos esteróides, quer ganhar mais massa magra, apenas coma mais proteína. Já com dietas high carb o sujeito é obrigado a contar mesmo, por causa da fome. Desde que se coma certo não há necessidade de cálculos. A questão ao meu ver é que pegaram o estilo de vida dos bb's, de cálculos sobre dosagem de esteroides, e de comida, com objetivo de apresentação em palco. E extrapolaram para amadores, naturais e reproduziram isso ao longo de décadas como o único caminho, mesmo não funcionando para a maioria da população, e não dando certo porque o método é difícil de ser aplicado, anti natural para quem não vive disso.    

[Thorun 289]

Agora, Norton disse:

 

Sim e nada impede alguém de ganhar músculo limpo sem contar também. E era o que faziam os atletas antes dos esteróides, quer ganhar mais massa magra, apenas coma mais proteína. Já com dietas high carb o sujeito é obrigado a contar mesmo, por causa da fome. Desde que se coma certo não há necessidade de cálculos. A questão ao meu ver é que pegaram o estilo de vida dos bb's, de cálculos sobre dosagem de esteroides, e de comida, com objetivo de apresentação em palco. E extrapolaram para amadores, naturais e reproduziram isso ao longo de décadas como o único caminho, mesmo não funcionando para a maioria da população, e não dando certo porque o método é difícil de ser aplicado, anti natural para quem não vive disso.    

 

O que eu disse: acredito que a pessoa que conta os macros tenha um resultado melhor ( mais constante e ajustado, possibilita ganhos "secos" ) em relação a construção muscular, do que quem não conta.

O que eu não disse: acredito que é impossível alguém que não conta macros ter resultado em construção muscular.

 

 

[Norton 3556]

Em 01/02/2020 em 19:48, Thorun disse:

 

O que eu disse: acredito que a pessoa que conta os macros tenha um resultado melhor ( mais constante e ajustado, possibilita ganhos "secos" ) em relação a construção muscular, do que quem não conta.

O que eu não disse: acredito que é impossível alguém que não conta macros ter resultado em construção muscular.

 

 

 

Sim, eu defendo exatamente o contrário do que você defende. 

[Meu Amigo Fit 5]

Em 26/01/2020 em 11:49, Norton disse:

 

Pode ser zero carb também não há nenhum problema nisso, vide dieta cetogênica e dietas de nossos ancestrais e povos primitivos.  

Verdade! O que eu quis dizer é que no caso da low carb, é LOW, e não NO.

 

Mas se for na cetogênica aí é diferente mesmo.

[Monstro monstruoso 9]

Em 25/01/2020 em 21:20, heisenleo disse:

 

Tem um médico "famoso" que eu seguia, não vou citar o nome e tudo, inclusive é presidente da Associação Brasileira LC. Ele prega isso. Comer LowCarb até a saciedade.

 

Em 25/01/2020 em 23:30, heisenleo disse:

 

É, porque eu me lembro que tinha essa questão dos macros, o jeito deles fazer LCHF era comer mesmo até a saciedade e deixar o corpo regular o apetite, que você acabaria ficando em deficit sem perceber. Era bem embasado nos estudos e tal, mas pra quem treinava era meio genérico, o que era mais falado é que a massa magra era preservada pela quantidade de proteínas que você acabava comendo. Mas no escuro, sem contar as Kcal. Pra mim funcionou no começo (a parte de perca de peso porque a massa magra deve ter ido boa parte embora sim), só que em 2 ou 3 meses já tava insustentável. Antes era só sábado a noite, depois domingo, depois sexta... quando eu vi, tava comendo por pura compulsão. Mas como eu disse, pode ser que pra alguns dê certo, aliás, acho que dá né, porque uma consulta em SP com esse profissional, custa R$800,00. Foi numa dessas que resolvi mudar.

 

Antes disso até perguntei sobre carbs serem essenciais pra quem treina e tal, pra energia. Foi me respondido que isso era "Bro Science" .

Esse médico é um ex participante de reality show?