How to calculate your intake to lose weight?

gymrat827 said:

x2x on the replies so far.

go on a online calc, figure out your daily intake and drop it by 10-20%. Than make sure to get in 4 cardio sessions a week. You can have *cheat* meals, but when starting out you want to try to avoid them as they can hinder your progress.

post up what your doing now. There is a ton of knowledge here and we can fine tune things for you. Please remember, this isnt a fast proces, it takes time.

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jyoung8j said:

If have a smart phone try my fitness pal app.. it will guide u thru ur needs excellent for a beginner. .

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Fidelity said:

Yes the BMR way is the tried and true calculation; however, be mindful of what you are really consumming. Don't get sucked into the high protein mantra that many people preach, in the end whether it's carbs, protein, or fats they all convert to fat if you surpass your number. You could eat only protein and still get fat. Find your number and create a deficit and keep track of what your eating and you will lose. Best of luck

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Fidelity said:

I respectfully disagree; excess protein in times of energy sufficiency contributes to at storage through a metabolic pathway known as lipogenesis. All macros consumed are ultimately converted initially to glucose and via the Kreb cycle (gluconeogenesis), these glucose molecules enter the electron transport chain and are converted to adenosine triphosphate to be used as fuel to drive cellular metabolism. In the even the body has consumed sufficient nutrients to support BMR, the excess glucose (derived from protein, carbs, and fats) are converted to lipids via lipolysis. Excess protein for example (when energy requirements are met) will be broken down to their component amino acids and converted to glucose (ketones) which can be used for energy production; however, as I said earlier, when energy demands are met, glucose will undergo lipogenesis and be stored as another from of energy, fat. So directly? No there is no direct metabolic pathway that converts protein to fat; however, excess protein will ultimately become fat.

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Fidelity said:

Lyle McDonald?

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Fidelity said:

McDonald isn't credible come one. He debunks everything that doesn't subscribe to his theories.

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In conclusion, we found that that the lipogenic capacity of adipose tissue is reduced in humans compared with rats. This is not explained by differences in the CHO-to-fat ratio in the diet and appears to be related to a reduced amount of SREBP-1c protein. Differences in the expres- sion of ChREBP could also play a role. Finally, this finding of low lipogenic activity in adipose tissue in humans con- firms that most of the TGs stored in adipose tissue are pro- vided by diet and delivered to adipocytes by circulating li- poproteins.

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This paper addresses the ongoing controversy over regulation of lipogenesis in human adipose tissue. Two main questions have surrounded the issue of DNL in humans, particularly in adipose tissue: 1) does DNL occur to such a degree that it can potentially contribute to whole-body lipid balance? and 2) is DNL regulated by diet or energy restriction, as it is in rodents? Several studies determined that the amount of fat contributed by hepatic DNL ranged from 1–2 g/d for lean (34) and eucaloric men (35), <6 g/d in lean and obese men and women consuming their normal diets (36,37) or fed excessive carbohydrates (7,9), and 7 g/d in former smokers consuming their diet ad libitum (38). Even at the highest measured levels (7 g/d), the amount of fat synthesized is minor relative to the average daily adult consumption of fat, which is 50–150 g (1). These relative lipogenic rates have been accepted to be generally lower than those reported for rodents.

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In summary, the consumption of 24 g ethanol activates the lipogenic pathway in humans, but de novo synthesis of fatty acids represents a quantitatively minor fate (<5%) of ingested ethanol. The primary fate (70–80%) of ethanol is conversion to acetate by the liver, release into the circulation, and oxidation by tissues. Inhibition of lipolysis and whole-body lipid oxidation are secondary consequences of the greatly increased availability of acetate. The liver, therefore, mediates the positive whole-body lipid balance induced by ethanol by providing acetate systemically, not through the direct conversion of ethanol to lipids.

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The enzymatic pathway for converting dietary carbohydrate (CHO) into fat, or de novo lipogenesis (DNL), is present in humans, whereas the capacity to convert fats into CHO does not exist. Here, the quantitative importance of DNL in humans is reviewed, focusing on the response to increased intake of dietary CHO. Eucaloric replacement of dietary fat by CHO does not induce hepatic DNL to any substantial degree. Similarly, addition of CHO to a mixed diet does not increase hepatic DNL to quantitatively important levels, as long as CHO energy intake remains less than total energy expenditure (TEE). Instead, dietary CHO replaces fat in the whole-body fuel mixture, even in the post-absorptive state. Body fat is thereby accrued, but the pathway of DNL is not traversed; instead, a coordinated set of metabolic adaptations, including resistance of hepatic glucose production to suppression by insulin, occurs that allows CHO oxidation to increase and match CHO intake. Only when CHO energy intake exceeds TEE does DNL in liver or adipose tissue contribute signi®cantly to the whole- body energy economy.
It is concluded that DNL is not the pathway of ®rst resort for added dietary CHO, in humans. Under most dietary conditions, the two major macronutrient energy sources (CHO and fat) are therefore not interconvertible currencies; CHO and fat have independent, though interacting, economies and independent regulation. The metabolic mechanisms and physiologic implications of the functional block between CHO and fat in humans are discussed, but require further investigation.

Summary
DNL is not the pathway of ®rst resort for added dietary CHO in humans, at least on Western (high-fat) diets. DNL can occur, but it generally does not. A `functional block' therefore exists between CHO and fat in humans, analogous to the absolute biochemical block in the direction from fat to carbohydrate in all animals. Therefore, the two major macronutrient energy sources are not interconvertible currencies in the mammalian organism; they must be considered separately and are prob- ably regulated independently, by separate signals and toward separate ends. The major insight concerning DNL is therefore a negative one. Many questions related to this central observa- tion still remain unanswered: what is the functional signi®- cance of DNL in adult life (Table 9)? What are the ultimate limits of DNL in humans? Is DNL only used as a ®nal `safety- valve' for CHO in the organism? What constrains DNL in human lipogenic tissues? Are there regulatory roles played by DNL that we have not yet identi®ed? Regardless of the answers to these questions, the metabolic and clinical con- sequences of the apparent functional block between CHO and fat are profound and have only begun to be understood.

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Carbohydrate metabolism and de novo lipogenesis in human obesity.

Acheson KJ, Schutz Y, Bessard T, Flatt JP, Jéquier E.
Respiratory exchange was measured during 14 consecutive hours in six lean and six obese individuals after ingestion of 500 g of dextrin maltose to investigate and compare their capacity for net de novo lipogenesis. After ingestion of the carbohydrate load, metabolic rates rose similarly in both groups but fell earlier and more rapidly in the obese. RQs also rose rapidly and remained in the range of 0.95 to 1.00 for approximately 8 h in both groups. During this time, RQ exceeded 1.00 for only short periods of time with the result that 4 +/- 1 g and 5 +/- 3 g (NS) of fat were synthesized via de novo lipogenesis in excess of concomitant fat oxidation in the lean and obese subjects, respectively. Results demonstrate that net de novo lipid synthesis from an unusually large carbohydrate load is not greater in obese than in lean individuals.

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Jamie Hale said:

Although the rates of de novo lipogenesis in carbohydrate enriched, energy balanced diets were significantly greater in obese women. The absolute quantities of fat synthesized from carbohydrates during both phases of the diet were relatively small. That is, levels of DNL were minimal.

Hellerstein (1999) has pointed out that the de novo lipogenesis is a path of last resort in regards to carbohydrate metabolism. The pathway for converting dietary carbohydrates into fat, is present in humans, but the capacity to convert fats into CHO does not exist. Eucaloric replacement of dietary fat by CHO does not induce DNL to any significant degree. Similarly, addition of CHO to a mixed diet does not increase DNL to significant levels, as long as CHO energy intake remains less than total energy expenditure. Only when CHO intake exceeds total caloric expenditure does DNL contribute significantly to the whole-body energy balance.

In conclusion, DNL is not the pathway of first resort for added dietary CHO in humans. “Under most dietary conditions, the two major macronutrient energy sources (CHO and fat) are not interconvertible.” (Hellerstein, 1999).

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Although the glycogen stores are normally maintained within a relatively narrow range, the capacity for storing large amounts of dietary CHO by conversion to glycogen is relatively large (Acheson et al. 1982, 1984, 1985, 1988). Fig. 1 shows that a large load of CHO (500g dextrin-maltose given as three meals over 5 h) to healthy subjects induces a marked stimulation of CHO oxidation over the 14 h after the first meal (240 g oxidized, 260 g stored; Acheson et al. 1985). Net lipogenesis occurred at a low rate from 5 to 10 h after the first meal, but this lipid accumulation was offset by a greater rate of lipid oxidation over the next 4 h. The fat balance calculated over 14 h was negative, indicating that the large load of CHO did not induce a gain in fat. Cumulative dextrin-maltose oxidation over 14 h comprised 65% of total C H O oxidation, indicating that 35% of C H O oxidation resulted from endogenous CHO stores. In another study, after 3 d on a hypoenergetic low-CHO diet to deplete glycogen stores, a very large amount (740 g) of dietary CHO (with 60 g fat and 100 g protein), consumed during the 4th day by healthy young human subjects, induced an increase of 340 g in the glycogen store, without initiating de novo lipid synthesis at rates exceeding concomitant fat oxidation (Acheson et al. 1988). In this study, 400 g CHO/d were oxidized. These findings show that high amounts of dietary CHO can be accommodated by inducing a stimulation of CHO oxidation and an increase in glycogen stores. The important point is that there was no gain of fat by de novo lipogenesis, as a small amount of net lipid oxidation was observed.
What happens when CHO overfeeding lasts several days? Acheson et al. (1988) showed in young men that glycogen stores must increase by about 500 g before net conversion of CHO into fat occurs. When the glycogen stores become saturated, the only way of disposing of additional excess CHO intake is by fat synthesis. This phenomenon can be demonstrated under artificial conditions of overfeeding. In everyday life, a high intake of CHO elicits an increase of satiety, and subsequently food intake is decreased (Blundell et al. 1993). These results support the concept that dietary CHO does not increase an individual’sfat content by de novo lipogenesis under normal conditions.
There are large species differences in lipogenic capacity (Masoro, 1962). In rodents the conversion of CHO to fat is an important pathway in liver and adipose tissues (Assimacopoulos-Jeannet & Jeanrenaud, 1976). In humans, de novo lipogenesis from CHO is mainly a hepatic process, since fat synthesis from CHO in adipose tissue is negligible (Bjorntorp & Sjostrom, 1978). In addition, lipogenic enzyme activities are much lower in human liver than in livers of rats or birds (Zelewski & Swierczynki,1990). By using a non-invasive stable-isotope method, Hellerstein et al. (1991) showed in humans that the fraction of very-low-density-lipoprotein-palmitate derived from de novo lipogenesis was only 0.9% in the fasted state and 2% in the fed state after a high-CHO breakfast. These results support the concept that de novo lipogenesis is not an important pathway in humans.

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The regulation of adipose tissue lipogenesis therefore appears to be different in human beings compared with some other mammalian species. In rats, for example, adipose tissue lipogenesis is more active and is, as is liver lipogenesis, responsive to high insulin/glucose levels and to variations of carbohydrate intake (35, 36). SREBP-1c plays a major role in the regulation of lipogenic genes expression, at least in their response to insulin (18, 37, 38). This transcription factor is a major determinant of the lipogenic capacity of mammalian and avian tissues (39). Therefore, it is possible that SREBP-1c expression is low in human adipose tissue compared with other species, but such a comparison between human beings and other species has not been performed to our knowledge. The lack of response in our study of adipose tissue FAS and ACC1 expression and lipogenesis to acute or chronic carbohydrate overfeeding could be related to the lack of increase of SREBP-1c mRNA. Since SREBP-1c expression is stimulated in rats by dietary carbohydrates and/or insulin (18, 40, 41), it remains to be determined why this stimulation is absent in human adipose tissue.

The comparison of the quantitative estimate of hepatic and adipose lipogenesis during Study 2 with the amount of glucose ingested (less than 1 g vs. 250–270 g) shows that the contribution of this metabolic pathway to the disposal of ingested glucose was minimal. The increase of hepatic and adipose lipogenesis after a hypercaloric HC diet (1–1.5 g/day) was also moderate, and can thus explain only a minimal part of the weight gain of the subjects (1,500 g on average during the 2 weeks of controlled diet). Since liver biopsies for measurement of tracer incorporation in liver TAG were not performed for obvious ethical reasons, we cannot exclude the possibility that some newly synthesized FAs remained within liver TAG stores. However, it seems very unlikely that an increase in liver TAG stores could explain a large part of the disposal of ingested glucose in Study 2 and of the weight gain observed during the HC diet. An increase in lipogenesis in another tissue is unlikely. Therefore, the most probable explanations for the observed body weight increase are merely a repletion of muscles and liver glycogen stores, along with the simultaneous storage of water and the suppression of fat oxidation leading to the deposition of ingested fat. Moreover, although the contribution of fat to total energy intake was decreased during the HC diet, the total amount ingested was increased.

In conclusion, our results show that in normal humans, adipose tissue lipogenesis, although active, is quantitatively a minor pathway and is less responsive than hepatic lipogensis to acute or prolonged carbohydrate overfeeding. The picture could be different in obesity, but the recent finding that lipogenic gene expression is decreased in the adipose tissue of obese subjects (11) makes this possibility improbable. Thus, DNL in adipose tissue is an unlikely contributor to the development of dietary-induced obesity in humans.

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Thus, de novo hepatic lipogenesis is a quantitatively minor pathway, consistent with gas exchange estimates; fatty acid futile cycling (oxidation/resynthesis) is not thermogenically significant; and synthesis rates of different nonessential fatty acids by human liver are not identical in nonoverfed normal men. The contribution and regulation of de novo lipogenesis in other settings can be studied using this technique.

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The energy cost of synthesizing fat from glucose and depositing it in adipose tissue is considerable, but ATP expenditures are substantially lower during fat than during glucose oxidation (Flatt & Tremblay, 1997). If synthesis of fat from glucose and the oxidation of an equivalent amount of fat are considered together, the substrate handling costs are in effect hardly greater than those incurred during the direct oxidation of glucose (Flatt & Tremblay, 1997). Thus one can expect that energy expenditure is raised appreciably by de novo lipogenesis only when lipid is being synthesized from carbohydrate and retained. In subjects eating ad libitum, however, the synthesis of fat, which may be initiated by the occasional consumption of even uncommonly large amounts of carbohydrate, is not sufficient to offset the amounts of fat oxidized during the rest of the day (Acheson et al. 1982). Under conditions of approximate energy balance, de novo lipogenesis is thus very unlikely to have a demonstrable effect in raising 24 h energy expenditure.
As Chwalibog and Thorbek point out, de novo lipogenesis may be an important consideration for animal husbandry, where feed efficiency is an important consideration. However, feed efficiency is hardly an important issue in man and de novo lipogenesis a rather limited process. Thus, one might indeed wonder how important it may be to know the exact impact of de novo lipogenesis on energy expenditure in man.

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The implications of not having a single interconvertible energy currency, but instead having 2 independent, although interacting, macronutrient economies (8), remain intriguing and incompletely explored. Does the rule that carbohydrate avail- ability to tissues controls whole-body fuel selection also apply to endogenous glucose production by the liver (9)? It might then be concluded that hepatic metabolism and hepatic genes are more likely to contribute to obesity through effects on glucose pro- duction than through effects on fat synthesis (11). Also, are there regulatory, as opposed to quantitative, functions of the de novo lipogenesis pathway? Certainly, malonyl-CoA, the first commit- ted metabolite in the de novo lipogenesis pathway, has several known regulatory actions. In addition to well-established antike- togenic actions in liver, malonyl-CoA concentrations are believed to influence fuel selection in muscle, fuel sensing and insulin secre- tion in the pancreatic ﰋ cell, and perhaps fuel sensing and appetite regulation by the brain (12). The fate of tissue malonyl-CoA gen- erated for regulatory functions is a related, unanswered question (eg, is disposal of regulatory malonyl-CoA an unrecognized function of the de novo lipogenesis pathway?).
Finally, what is the role of de novo lipogenesis in human dis- ease? Recent studies (13) have identified different insulin signal- ing pathways for de novo lipogenesis and cholesterol synthesis, on the one hand, and carbohydrate metabolism, on the other, as well as co-induction of de novo lipogenesis with cholesterogen- esis by overexpression of the sterol response element binding protein. Thus, is de novo lipogenesis involved in the pathogenesis of insulin resistance or hypercholesterolemic syndromes? Or does de novo lipogenesis influence intracellular signaling pathways involving myristoylation, palmitoylation, or membrane fatty acids? These questions and more arise from the observation that de novo lipogenesis is the pathway of last resort and that, at least regarding converting carbohydrates to fats, humans are neither bees nor pigs.

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