Hipótese Sobre Gordura Pós-Cutting

[Vinicius C. 75]

No livro ‘The Stubborn Fat Solution”, o Lyle Mcdonald diz que a oxidação das gorduras saturadas, monosaturadas e polisaturadas são diferentes, e conseqüência disso é que as gorduras saturadas levam mais tempo para sair do corpo depois de estocadas.

Lendo isso, pensei em uma coisa:

Após um Cutting é natural que nosso corpo acumule gordura. Não seria a hora certa de diminuir a ingestão de gorduras saturadas e investir nas mono e polisaturadas? Assim em um futuro cutting a facilidade de perdê-las seria muito maior.

O que vocês acham?

[Monjoy 51]

achei interessante !

[goFran 95]

po brother agora fiquei curioso... vo esperar alguem mais experiente se pronunciar pra saber tambem !

[FRT. 87]

Olá , boa noite a todos. To me revirando inteiro aqui pra achar isso, por enquanto, vamos a alguns trechos interessantes do research do lyle,

For someone who is lean, active, eating plenty of fruits and vegetables, who is in caloric balance there appears to be no real danger (in a health context) to an increased intake of saturated fats. One study I recall in cyclists found that, as long as they were in caloric balance, an increase intake of saturated fats had no impact on blood cholesterol one way or the other.

It’s worth mentioning in this context that some research suggests that saturated fat is required for optimal hormone levels (e.g. testosterone) so trying to reduce saturated fat excessively may be a mistake for athletes in the first place.

But not all individuals are lean, active athletes who are eating lots of fruits and vegetables who are in caloric balance. For someone who is overweight (which is an inflammatory state in and of itself), inactive (which has a host of negative health effects), is under a lot of stress, not eating sufficient fruits and vegetables, etc. , saturated fats may have a very different impact on the body.

From a body fat perspective, it’s at least worth mentioning that saturated fats tend to be stored a bit more easily than polyunsaturated fats (more accurately, when polyunsaturated fats are consumed, the body tends to burn them off a bit more readily) but the effect is not massive.

Ok, até ai , vimos que a gordura saturada não é nenhuma vilã, e que seu consumo aliado a uma rotina de esportes, não causa "doenças" que tanto são temidas. Porém se for um sedentario, que não come uma boa quantidade de micronutrientes (frutas e verduras) deve-se atentar ao consumo de tal. OK, até ai acho que todo mundo ja sabia.

Logo abaixo, ele meio que confirma a hipótese do martin, aonde ele alega, que poli-insaturadas tendem a ser queimadas mais rapido/facilmente ou usadas como fonte enérgetica mais facilmente, pelo nosso corpo, PORÉM , o efeito não é algo massivo.

O artigo que vou colocar agora, é do The Arm American Journal of Nutrition,

Tissue accumulation of fatty acids

In the utilization of fats as fuel, there is selectivity in the partitioning of specific fats between oxidation and storage in adipose tissue. The fatty acid composition of adipose tissue in persons with widely varying dietary intakes is relatively similar. In studies of the influence of dietary composition on adipose fatty acids, dietary intake determined <25% of the variance in adipose fatty acid composition (47). Nevertheless, diet does influence tissue composition, and recent studies showed that certain fatty acids in adipose tissue are effective biomarkers of specific dietary fatty acid intake (48). For example, 15:0 and 17:0 in adipose reflect dairy intake, and n−3 fatty acids (18:3 and 22:6) reflect fish intake. Dietary and adipose n−6 fatty acids are correlated, and the best indicators of total transfatty acid intake are cis,trans 18:2n−6 and trans,cis 18:2n−6, whereas 18:1 and 16:1 trans fatty acids are the next best indicators. Although it is commonly believed that saturated fats and dietary cholesterol are the lipids that accumulate in arteries and that this accumulation is a further rationale for decreasing all saturated fatty acids in diets, this is not necessarily true. Excessive n−6 polyunsaturated fatty acid (PUFA) intake from refined vegetable oils has also been implicated as contributing to cancer and heart disease, and arterial plaque is primarily composed of unsaturated fats, particularly polyunsaturated fats, and not saturated fat (49). A recent study found that in healthy persons, the intake of fish oil, which contains long-chain n−3 fatty acids, decreased both fasting and postprandial triacylglycerol concentrations but increased LDL-cholesterol concentrations irrespective of whether the diet was rich in saturated fatty acids or in monounsaturated fatty acids (50). Although evidence suggests that unsaturated fatty acids may protect against atherosclerosis, the replacement of monounsaturated fatty acids with PUFAs in low-fat, high-carbohydrate diets was suggested as being premature on the basis of detrimental effects observed in animal models (51). Other investigators recommend that the daily intake of PUFAs should not be >10% of total energy (52). If balance and reason are to be applied to intakes of monounsaturated fats and PUFAs, the same cautionary perspectives should be applied to saturated fats.

Até ai, entra outra controvérsia, que o acumulo de gordura, (levando em conta o alto consumo de gordura saturada) não funciona desse jeito. Se voce exagerar no consumo de poli-insaturadas e mono, tais como óleos vegetais, o risco de doenças é o mesmo para o de um alto consumo de gordura saturadas. Ja no final, eles dizem o basico, sobre o balanço de gorduras, aonde devem ser consumidas pelo menos 10% das calorias de gorduras, poli e mono saturadas. Porém , lendo um pouco antes da ultima parte em negrito, verá que os testes foram feitos em animais, o que na minha opinião, perde um pouco de credibilidade.

HEALTH EFFECTS OF SATURATED FATTY ACIDS

The approach of many mainstream investigators in studying the effect of consuming saturated fats has been narrowly focused to produce and evaluate evidence in support of the hypothesis that dietary saturated fat elevates LDL cholesterol and thus the risk of CAD. The evidence is not strong, and, overall, dietary intervention by lowering saturated fat intake does not lower the incidence of nonfatal CAD; nor does such dietary intervention lower coronary disease or total mortality (31, 61). Unfortunately, the overwhelming emphasis on the role of saturated fats in the diet and the risk of CAD has distracted investigators from studying any other effects that individual saturated fatty acids may have on the body. If saturated fatty acids were of no value or were harmful to humans, evolution would probably not have established within the mammary gland the means to produce saturated fatty acids—butyric, caproic, caprylic, capric, lauric, myristic, palmitic, and stearic acids—that provide a source of nourishment to ensure the growth, development, and survival of mammalian offspring.

]Esta parte em especial, relata a importancia da gordura saturada na dieta, e que sem ela , provavelmente não teriamos evoluido.

Fatty acids are essential parts of all body tissues, where they are a major part of the phospholipid component of cell membranes. Saturated fatty acids have been suggested to be the preferred fuel for the heart (62). Fatty acids are used as a source of fuel during energy expenditure, and heavy exercise is associated with decreases in the plasma concentrations of all free fatty acids. In light exercise, fat metabolism may be controlled to favor adipose tissue lipolysis and extraction of free fatty acids from the circulation by muscle, whereas in heavy exercise, adipose tissue lipolysis is inhibited and hydrolysis of muscle triacylglycerols may play a more important part (63). In the absence of sufficient dietary fat, the body synthesizes the fatty acids that it needs from carbohydrates. The major fatty acid synthesized de novo via fatty acid synthase is palmitate, which undergoes elongation involving acyl-CoA and malonyl-CoA to form longer-chain saturated fatty acids. Desaturation via fatty acyl-CoA desaturases introduces unsaturation at C4, C5, C6, or C9. The lack of capability to desaturate past C9 makes dietary linoleic acid an essential fatty acid (for review see reference 64). Synthesis of palmitic acid is also increased by consumption of very-low-fat diets with a high ratio of sugar to starch (14)

Based on the controversy over the effects of fat in the diet, the question most often addressed is, What are the relative cholesterolemic effects of the major saturated fatty acids in the diet? However, the evidence suggests that caproic, caprylic, and capric acids are neutral with respect to cholesterol-increasing properties and their ability to modulate LDL metabolism; lauric, myristic, and palmitic acids are approximately equivalent in their cholesterol-increasing potential, and stearic acid appears to be neutral in its cholesterol-increasing potential (65; for review see reference 66). A limited number of controlled studies suggest that myristic acid is the most potent cholesterolemic dietary saturated fatty acid (for review see reference 67). However, there is evidence that the increase in chlolesterol is related to an increase in both LDL and HDL cholesterol (68). Aside from the reported effects on plasma cholesterol concentrations, there are other properties and functions of the individual saturated fatty acids that support beneficial roles in the body. Some of these roles are briefly discussed below

Leiam sobre tais "acidos"

Butyric acid

]Short-chain fatty acids are hydrolyzed preferentially from triacylglycerols and absorbed from the intestine to the portal circulation without resynthesis of triacylglycerols. These fatty acids serve as a ready source of energy, and there is only a low tendency for them to form adipose (69). Butyric acid (4:0) is the shortest saturated fatty acid and is present in ruminant milk fat at 2–5% by weight (70), which on a molar basis is approximately one-third the amount of palmitic acid. Human milk contains a lower percentage (≈0.4%) of butyric acid. No other common food fat contains this fatty acid.

Butyrate is a well-known modulator of genetic regulation (71, 72), and it also may play a role in cancer prevention (73). Published information thus far indicates that butyric acid exhibits contradictory and paradoxical behavior (74). Although butyric acid is an important energy source for the normal colonic epithelium, is an inducer of the growth of colonic mucosa, and is a modulator of the immune response and inflammation, it also functions as an antitumor agent by inhibiting growth and promoting differentiation and apoptosis (75).

Caproic, caprylic, and capric acids

bovine and human milk, caproic acid (6:0) is present at ≈1% and 0.1% of milk fat, respectively, and caprylic acid (8:0) and capric acid (10:0) are present at ≈0.3% and 1.2% of milk fat, respectively. Goat milk contains the highest percentage of caprylic acid, at 2.7% of milk fat. These 3 fatty acids have similar biological activities. Both caprylic acid and capric acid have antiviral activity, and when formed from capric acid in the animal body, monocaprin has antiviral activity against HIV (76, 77). Caprylic acid has also been reported to have antitumor activity in mice (78). Negative effects of these fatty acids on CAD and cholesterol have not been a dietary issue

Lauric acid

]Lauric acid (12:0) is a medium-chain fatty acid that is present in human and bovine milk at ≈5.8% and 2.2% of milk fat, respectively. This fatty acid has been recognized for its antiviral (79) and antibacterial (80, 81) functions. Recent results suggest that Helicobacter pylori present in stomach contents (but not necessarily within the mucus barrier) should be rapidly killed by the millimolar concentrations of fatty acids and monoacylglycerols that are produced by preintestinal lipases acting on suitable triacylglycerols, such as those present in milk fat (82). Lauric acid is also effective as an anticaries and antiplaque agent (83). Medium-chain saturated fatty acids and their monoacylglycerol derivatives can have adverse effects on various microorganisms, including bacteria, yeast, fungi, and enveloped viruses, by disrupting the lipid membranes of the organisms and thus inactivating them (84, 85). This deactivation process also occurs in human and bovine milk when fatty acids are added to milk (86, 87). The release of monolaurin from milk lipids by human milk lipases may be involved in the resulting antiprotozoal functions (88, 89). One study indicated that one antimicrobial effect against bacteria is related to the interference of monolaurin with signal transduction or toxin formation (90). In addition to disrupting membranes to inactivate viruses, lauric acid has an effect on virus reproduction by interfering with assembly and maturation, ie, cells make the components of the virus, but their assembly is inhibited (79).[

Myristic acid

Bovine milk fat contains 8–14% myristic acid (14:0), and in human milk, myristic acid averages 8.6% of milk fat. As stated above, myristic acid is one of the major saturated fatty acids that have been associated with an increased risk of CAD, and human epidemiologic studies have shown that myristic acid and lauric acid are the saturated fatty acids most strongly related to average serum cholesterol concentrations. However, in healthy subjects, although myristic acid is hypercholesterolemic, it increased both LDL- and HDL-cholesterol concentrations compared with oleic acid (68).

Palmitic acid

Palmitic acid (16:0) is present in human and bovine milk at 22.6% and 26.3% of milk fat, respectively. Palmitic acid in triacylglycerols in human milk is predominantly esterified in the sn-2 position of the molecule. Feeding human infants a formula containing triacylglycerols similar to those in human milk (16% palmitic acid esterified predominantly in the sn-2 position) has significant effects on fatty acid intestinal absorption (91, 92). Myristic, palmitic, and stearic acids are better absorbed from human-like milk than from standard formula, without a change in total fat fecal excretion. Mineral balance is improved in comparison with a conventional formula, as shown by lower fecal calcium excretion, higher urinary calcium, and lower urinary phosphate. The specific distribution of the fatty acids in the triacylglycerol is known to play a key role in lipid digestion and absorption. Because pancreatic lipase selectively hydrolyzes triacylglycerols at thesn-1 and sn-3 positions, free fatty acids and 2-monoacylglyceriols are produced. Free palmitic acid, but not 2-monopalmitin (which is efficiently absorbed), may be lost as a calcium-fatty acid soap in the feces. A comparison between the effects of dietary laurate-myristate and the effects of palmitic acid in normolipemic humans showed that palmitic acid lowers serum cholesterol (93). In humans, replacement of dietary laurate-myristate with palmitate-oleate has a beneficial effect on an important index of thrombogenesis, ie, the ratio of thromboxane to prostacyclin in plasma (94).

Stearic acid

Dietary stearic acid (18:0) is derived primarily from bovine meat and dairy products. Stearic acid is present in human and bovine milk at 7.7% and 13.2% of milk fat, respectively. In relation to the question of their effects on serum cholesterol, stearic acid and saturated fatty acids with <12 carbon atoms are thought not to increase cholesterol concentrations (95). Dietary stearic acid decreases plasma and liver cholesterol concentrations by reducing intestinal cholesterol absorption. Recent data from studies with hamsters, which have a lipoprotein cholesterol response to dietary saturated fat that is similar to that of humans, suggest that reduced cholesterol absorption by dietary stearic acid is due, at least in part, to reduced cholesterol solubility and further suggest that stearic acid may alter the microflora populations that synthesize secondary bile acids (96)

The absorption of stearic acid from triacylglycerols containing only oleate and stearate depends on the position of esterification. 2-Monstearin is well absorbed if the stearic acid is esterified at the sn-2 position of the triacylglycerol. If the triacylglycerol is esterified at the sn-1 or the sn-3 position, it is released as free stearic acid, and in the presence of calcium and magnesium, it is poorly absorbed (97). In a study of the effects of dietary fat on serum lipid and lipoporoteion concentrations, the absorption of dietary oleic acid, palmitic acid, and stearic acid was similar, which indicates that differential effects of these fatty acids on plasma lipoprotein cholesterol are not due to differential absorption (98). Another study in humans also indicated that, even though stearic acid appears to have different metabolic effects with respect to its effect on the risk of cardiovascular disease than do other saturated fatty acids (95), reduced stearic acid absorption does not appear to be responsible for the differences in plasma lipoprotein responses (99)

Compared with consumption of dietary palmitic acid, consumption of dietary stearic acid (19 g/d) for 4 wk by healthy males produced beneficial effects on thrombogenic and atherogenic risk factors (100). Mean platelet volume, coagulation factor VII activity, and plasma lipid concentrations decreased significantly with consumption of the stearic acid diet, whereas platelet aggregation increased significantly with consumption of the palmitic acid diet. A subsequent study showed no alteration in plasma lipids, platelet aggregation, or platelet activation in short-term (3 wk) feeding trials when stearic acid and palmitic acid were provided in commercially available foods (101). An interesting finding in a study of the association between the composition of serum free fatty acids and the risk of a first myocardial infarction was that the percentage content of both very-long-chain n−3 fatty acids and stearic acid is inversely associated with the risk of myocardial infarction. The investigators speculated that the very-long-chain n−3 fatty acids might reflect diet but also that these 2 free fatty acids might in some way be related to the pathogenetic process and not just reflect their content in adipose tissue (102).

E agora, a conclusão.

CONCLUSIONS

Twenty years ago, government guidelines recommended that all persons consume a low-fat diet, with the advice being to “avoid too much fat, saturated fat, and cholesterol” (121). Consumption of a low-fat diet (defined as one containing 20% of energy from fat) was subsequently shown to induce atherogenic dyslipidemia (122, 123). On the basis of government guidelines, the food industry was obliged to change the formulation of foods to a preponderance of low-fat and nonfat products, with calories from carbohydrates being substituted for fat. It is now known that a high-carbohydrate diet can lead to the lipoprotein pattern (124) that characterizes atherogenic dyslipidemia. At the time the 1980 guidelines were established, there was no solid basis for understanding what the consequences of such overall dietary changes would be for most persons. The recommendation to lower saturated fat intake was based on a single marker of health outcome—a correlation between dietary saturated fat and the incidence of CAD, with blood cholesterol being the indicator of potential disease. Now, the most recent published recommendations are for all persons to reduce the saturated fat content of their diet (10% of total calories), although it was stated in the Dietary Guidelines Advisory Committee report (2) that “…no lower limit of saturated fat intake has been identified.” The summary report by the Institute of Medicine (60) takes this recommendation one step further by clearly stating that “…there is no intake level of saturated fatty acids…at which there is no adverse effect.” This nutritional rhetoric is driving the food industry to respond to governmental and public demands to decrease the amounts of all saturated fats from the food supply. The agricultural enterprise will continue to lower saturated fatty acids by every means possible.

Public health recommendations for the consumption of total fat and the composition of fat in the diet are being reevaluated, and this reevaluation is projected to be finished in 2004. To meet the body’s daily energy and nutritional needs while minimizing the risk of chronic disease, the newest report on recommendations for healthy eating from the National Academies’ Institute of Medicine is that adults should get 45–65% of their calories from carbohydrates, 20–35% from fat, and 10–35% from protein. It was recently pointed out that reducing the proportion of energy from fat below 30% is not supported by experimental evidence and that advice to decrease total fat intake has failed to have any effect on the prevalence of obesity, diabetes, and cardiovascular disease (125). The recent conference summary from the Nutrition Committee of the American Heart Association emphasized that studies with cardiovascular endpoints that go beyond the measurements of plasma lipids and lipoproteins are needed to evaluate the effects of individual fatty acids in humans (126).

At this time, research on how specific saturated fatty acids contribute to CAD and on the role each specific saturated fatty acid plays in other health outcomes is not sufficient to make global recommendations for all persons to remove saturated fats from their diet. No randomized clinical trials of low-fat diets (105) or low-saturated fat diets of sufficient duration have been carried out; thus, there is a lack of knowledge of how low saturated fat intake can be without the risk of potentially deleterious health outcomes. Although the removal of particular foods from the diet can be accomplished quickly, the removal of all saturated fats or particular saturated fatty acids from foods cannot be accomplished quickly by the agricultural community. This will require modification of existing foods and changes in policies to improve health, which in turn will require integration of nutrition needs with economic growth and development; agriculture and food production, processing, and marketing; health care and education; and changing of lifestyles and food choices by individual consumers. It requires years to change the course of commodity manipulation and to make drastic changes in the food supply. Before such implementation can be achieved, all food sources of specific saturated fatty acids must be accurately identified and quantified, the core commodities will need to be changed at the level of production, agricultural processes will require new approaches and procedures, and food formulations will need to be changed. The question remains, What is an appropriate amount to which saturated fatty acids in the diet can be lowered for optimal health? Before recommendations are made to further lower the content of these components in the food supply, should we not wait until scientific evidence clearly shows that this is the healthiest direction to take?

Because of the paucity of scientific understanding of the role of specific fatty acids in humans beyond the effects on total and LDL cholesterol, research on the effects of specific fatty acids in a broader health context should be viewed as a clear research priority. Given the varying health status of much of the developed world, it would also be appropriate to explore these effects in a range of human metabolic phenotypes, including persons with various body mass index values, persons with insulin resistance, and persons with chronic inflammation. Finally, the scientific community not only is recognizing the interindividual variation in dietary response and health but is also building the tools to measure it. Therefore, the influence of varying saturated fatty acid intakes against a background of different individual lifestyles and genetic backgrounds should also be considered.

Bom, pelo o que eu entendi , seguindo o contexto da conclusão, a gordura saturada (e a gordura em geral) é benéfica, e não deve ser removida nunca de sua dieta, "low" fat diets são falhas, e gorduras parecem trazer beneficios para a regularização do colesterol e tendem a diminuir o risco de doenças cardiovasculares, a questão é, que devemos saber "dosa-las" , pois um excesso de certa fonte continuo, pode prejudicar a absorção ou ação de outra, ou seja, deve haver um equilibrio entre o consumo de gorduras, para que seu organismo saiba trabalhar com elas. Mas, no final da conclusão (parte em negrito) , é citado que, deve ser levado em conta o nivel de atividade do sujeito, sua genética, se é resistente a insulina , etc.. pois tudo isso influencia, a partir do momento em que voce é resistente a insulina, uma dieta com mais gordura é benéfica, logo, mais gordura saturada vai ser inserida no seu dia-a-dia, ou seja, depende de muita coisa, e ainda não há algo comprovado sobre uma quantidade CERTA de gordura saturada, apenas dizem para manter em 10% do valor calórico total, porém isso não tem comprovação de que é o correto, mesmo porque neste artigo, mostra que dietas com alto teor de gordura saturada melhoraram a qualidade de vida de muitas pessoas. Então, levando em conta de que somos todos ativos, e temos uma dieta saudavel e adequada aos "padrões", com uma ingestão de micronutrientes alta, PARECE que essa história de gordura saturada ser armazenada com mais facilidade não se aplica, como é citado pelo lyle no primeiro artigo que linkei, realmente, ela é mais demorada para ser usada/queimada, porém este efeito não é algo que vá fazer diferença, levando em conta que voce ingere outros acidos-graxos essenciais e ingere uma boa quantidade de micronutrientes.

Bom, é isso. Foi o que eu consegui achar para contribuir, se falei alguma asneira, me desculpem e por favor corrijam, eu ja to com um puta sono e não to nem vendo o que to escrevendo. AHAHAHAHAHAHA, no mais é isso. Espero ter ajudado.

Fontes,

http://www.bodyrecom...ats-part-2.html

http://www.ajcn.org/...ournalcode=ajcn

Editado Julho 18, 2012 às 04:19 por FRT.

[menziesjb 0]

vo esperar alguem mais experiente se pronunciar pra saber tambem !

[mpcosta82 2967]

No livro ‘The Stubborn Fat Solution”, o Lyle Mcdonald diz que a oxidação das gorduras saturadas, monosaturadas e polisaturadas são diferentes, e conseqüência disso é que as gorduras saturadas levam mais tempo para sair do corpo depois de estocadas.

Lendo isso, pensei em uma coisa:

Após um Cutting é natural que nosso corpo acumule gordura. Não seria a hora certa de diminuir a ingestão de gorduras saturadas e investir nas mono e polisaturadas? Assim em um futuro cutting a facilidade de perdê-las seria muito maior.

O que vocês acham?

Vinicius,

O que o FRT postou é muito interessante.

Veja que o Lyle está falando de oxidação. Isso é a utilização da gordura como combustível.

O Lyle não está dizendo que a gordura saturada que você acumular será mais difícil de sair do que a gordura insaturada que você acumular (se isso estiver no livro, por favor poste aqui. Estou sem o livro).

Em um bulking você praticamente não irá oxidar gordura (a não ser que a sua dieta tenha muita gordura em relação a carboidrato). A maior parte do combustível do seu corpo será glicose, já que você está em um ambiente com excesso de calorias.

Ou seja: independente da gordura que você consumir, ela será preferencialmente estocada (e será perdida em um futuro cutting da mesma forma).

Abraços

[Brunobyof 330]

mpcosta,

No caso, creio que a consequência da maior facilidade de oxidação das gorduras mono e poli INsaturadas imcplicam em uma maior facilidade em "perdê-las" durante um cutting. Aì, quando as gorduras mono e poli já foram e sobra aquela "gordura teimosa", é porque são as gorduras saturadas, em grande parte. Mas não se resume a isso, claro que tem vários fatores pra gordura teimosa ser teimosa, como o lyle descreve no livro e nos seus artigos. Os receptores, a dieta, genética, treino...tudo vai influenciar no sucesso ou não da dieta em queimar essa gordura teimosa.

Agora, voltando à pergunta do criador do tópico:

***"Não seria a hora certa de diminuir a ingestão de gorduras saturadas e investir nas mono e polisaturadas? Assim em um futuro cutting a facilidade de perdê-las seria muito maior.

O que vocês acham? "***

Acho que as gorduras poli e mono insaturadas devem fazer parte da dieta de maneira geral, sempre, assim como a gordura saturada. O problema é que as pessoas obesas, na maioria das vezes se tornaram obesas por que passaram muito tempo das suas vidas ingerindo muito mais gorduras saturadas do que qualquer outro tipo de gorduras, e aliado à uma ingestão alta de carbos em uma dieta hipercalórica, essas pessoas acabam estocando toda aquela gordura saturada, resultando em um corpo cheio de gordura saturada estocada, o que por sua vez, torna mais difícil perder essa gordura do que um fisiculturista por exemplo, que provavelmente após um bulking possui mais gorduras poli e mono insaturadas do que saturadas em seu corpo, e portanto consegue se livrar delsa mais facilmente.

Enfim, excluindo-se as gorduras TRANS, que não servem nenhum propósito saudável em nosso organismo, todas as outras gorduras devem, ou melhor, podem fazer parte da dieta saudável. Lembrando que, ácidos graxos essenciais são apenas os EHP e DHA, provenientes do óleo de peixe.

[Antony5000 9]

O que eu tenho para dizer basicamente é isso:

- fuja das gorduras poli-insaturadas (coma o mínimo que puder);

- consuma mais gorduras mono e saturadas.

Quem quiser saber por que, basta ler um pouco:

- http://chriskresser.com/heartdisease

-

http://www.westonapr...ts-introduction

- http://www.umaoutrav...aturadaboa.html

- http://www.marksdail.../#axzz20zYEOzez

- http://wholehealthso...t-increase.html

Tudo o que nos dizem que é certo, na verdade é errado!!!

Abraços

Editado Julho 18, 2012 às 16:21 por Antony5000

[mpcosta82 2967]

mpcosta,

No caso, creio que a consequência da maior facilidade de oxidação das gorduras mono e poli INsaturadas imcplicam em uma maior facilidade em "perdê-las" durante um cutting. Aì, quando as gorduras mono e poli já foram e sobra aquela "gordura teimosa", é porque são as gorduras saturadas, em grande parte. Mas não se resume a isso, claro que tem vários fatores pra gordura teimosa ser teimosa, como o lyle descreve no livro e nos seus artigos. Os receptores, a dieta, genética, treino...tudo vai influenciar no sucesso ou não da dieta em queimar essa gordura teimosa.

Agora, voltando à pergunta do criador do tópico:

***"Não seria a hora certa de diminuir a ingestão de gorduras saturadas e investir nas mono e polisaturadas? Assim em um futuro cutting a facilidade de perdê-las seria muito maior.

O que vocês acham? "***

Bruno, pelo que entendi o estudo comparou a oxidação de gorduras da dieta. Se você seguir uma dieta hipocalórica, gorduras insaturadas serão oxidadas preferencialmente em relação às gorduras saturadas (da mesma forma que gorduras de cadeia média (MCTs) serão oxidados mais facilmente).

Não tem nada a ver com as gorduras estocadas no corpo.

Quanto às gorduras teimosas serem saturadas, você leu isso no livro?

[Brunobyof 330]

@Antony: Isso inclui o que você disse? Agora fiquei confuso hauhauuah brinks. Mas eu já li por aí mesmo que tem alguns estudos relacionando excesso de poliinsaturadas com doenças cardíacas, como o ômega-6 por exemplo, mas isso ainda não é um fato consumado ao que me pareceu....ninguém também consome quantidades muito grandes de w-6 tão facilmente assim...eu espero.

@mpcosta: Não, eu apenas conclui isso apartir da informação dada sobre a maior facilidade na oxidação das mesmas. mas creio que a maior dificuldade em oxidá-las (as saturadas) também implica em uma menor taxa de mobilização e oxidação das gorduras estocadas no corpo...ou estaria eu errado?