ARTICLE: I want to transform my body (w/o scientific babble) - HELP!

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I want to transform my body (w/o scientific babble) - HELP!

You Must Learn to Control Appetitie

Appetite needs to be controlled. You do not follow the principle of "eat when you are hungry" because that seems to lead to more eating. Eating and enjoying processed carbs can lead to craving and eating more processed carbs. Appetite needs to be something you can control. Appetite will change as you change the type of food you eat and the intake pattern.

Reducing the amount of calories you eat over time will have the effect of reducing your appetite. Reducing the amount of high caloric carbs and replacing them with healthy fats will also reduce your cravings.

If you use the fiber to reduce hunger and you reduce food intake over the course of two weeks you will end up at a lower overall hunger level. This will occur naturally unless you screw it up.

What the body wants to do

Toggling is a method that will help as well. By toggling I mean periods when you live with a caloric deficit and lower carbs followed by a period of higher caloric intake and managed carb intake. The body doesn't mind such swings and it will not punish you with intense uncontrollable cravings like it will if you go on a prolonged period of caloric deficit and complete banishment of carbs. Toggling also seems to allow the body to seek a different balance between those things/ factors which bring about hunger and those which signal satiety. Energy surplus and energy deficit signaling is the most fundamental system our body maintains and this signaling ties into our reproductive system and into the length of our lifespan.

We are reproductive machines. The most fundamental machinery governing our bodies (the binary code so to speak) cares only about reproducing the basic unit we house (our genes). Nothing else is important. To that end, energy input and energy output are closely monitored. Sufficient availability of food and subsequent intake puts our bodies in a state where we can reproduce. Surplus intake is stored so that we have sufficient energy to maintain future reproduction. However insufficient availability of food and subsequent failure to ingest at the level the body has previously experienced signals a need for dramatic change. That change comes in many forms and all of these forms are designed to keep and acquire more energy inputs so as to maintain the ability to reproduce. The body can become more insistent that we cease the loss of accumulated energy resources. This is why periodically we must give in and allow the body to see that food scarcity is no more. The body will cease being insistent and a balance will be able to be regained. This is a comfortable state and allows us to rechallenge yet again. As we reach states where bodyfat stores become significantly reduced the body sends additional signals. These signals can reduce reproductive hormones & states. The body becomes more efficient in the usage of energy inputs and reprioritizes their usage. The cell begins to live in a state where it is effected by caloric deficit/fast and thus undergoes mild stresses. These mild stresses actually serve to strengthen the cell and make it more resistant to disease and environmental hindrances.

You reach a state where the body realizes that there is insufficient energy available for you to reproduce today. So the cumulative result begins to be a delay in aging. The most fundamental aspect of your being, the gene wants to replicate, and if it can not do so today it wants to give itself a chance to do so tomorrow, a month from now, a year from now...

Lifespan is increased because the level of the genes needs it to increase to maximize the opportunity for self-replication.

The "We" that wants body transformation

The "we" that rides atop this genetic machinery, concerned with higher thoughts and base needs, is able with considerable effort, to effect body transformation. To the extent that we work with the body things are easy. To the extent that we work against the body things are difficult. The longer we work against the body the more difficult things become.

It is so much easier to take in caloric surpluses and expand our girth because that is what our selfish genes desire as a means to their replicative end. Eat, be happy, reproduce to the sounds of Barry White...

So understanding the end-game of our genes allows us to diet/recomp -> eat, be happy, have sexual intercourse -> diet/recomp -> eat, be happy, have sexual intercourse -> etc.

The duties assigned to us when we are Dieting/recomping are fairly clear. We are to eat less. We are to keep insulin quiet. We are to be active. However what duties are assigned to us in the eat, be happy, sex phase? During this phase you want to be anabolic. There is a likelihood that you lost a little muscle when you were in a caloric deficit. You want to regain that muscle and more. In addition you want to eat properly. Eating properly will vary depending on what you do in the diet/recomp phase.

If you fasted in that phase you need to take in a lot of calories and you do need to take in what you would consider sinful carbs. If you did not really fast, but took in primarily protein and some fats then what you eat will depend on the depth of your caloric deficit and the length of the diet phase. You will need to take in carbs but they should not be so sinful nor so abundant.

The carbless PWO discussed throughout is a good example of a toggle approach. In fact there are many toggling approaches. A Carbless PWO is but one approach.

During the eat/be happy phase muscles should be refilled with energy stores and a weight-lifting workout should be undertaken. Anabolic factors that accrue to your advantage can be used around this weight-lifting workout because you will depend on it to gain muscle. Your only genuine measuring stick is workout to workout strength. If it is increasing you are likely in the correct anabolic state. If you are losing strength you are not.

The length of time that you are in the eat/be happy & anabolic state will vary and depend on the length of the diet phase. If you did not use an absolute fast the ratio of time spent in each phase should be 2 to 1. That is 2 days of fatloss versus 1 day of attempted anabolism. So 6 days of caloric deficit will bring 2 days of surplus and attempted anabolism.

The word "attempted" is used because often there will not be much anabolism, rather you are stopping the increasing tendency for the body to catabloize muscle and you hope to restore what has been lost. If the overall goal is loss of considerable fat loss then anabolism will be minimal. If the overall goal is loss of a little fat (i.e. recomping) then the anabolism may be considerable, This latter goal fits well with the Carbless PWO because the anabolism spills into and runs concurrent with much of the fatloss. With the carbless PWO there is not a demarcation between the two phases.

So to reiterate:

- We will get control of our appetite because food intake will be continually changed and cravings need to be limited.
- We work with the body as much as we can and limit time spent working against it
- We limit the body's continued concern that nonreproductive states are approaching by limiting periods of caloric deficit
- We introduce a toggling approach or back and forth approach between a state of fatloss/caloric deficit/lower carbs and a state of tissue accrual/caloric surplus/managed carbs.
- During the fatloss phase we will attempt to reduce catabolism and during the tissue accrual phase we will attempt anabolism.

Adiposity Hormones

Food intake and energy balance are controlled by the neuronal interactions of a wide variety of gastrointestinal sensory signals from gut peptides to neurotransmitters and things we can call adiposity signals. Only a few though are considered key "controllers" of energy balance. These key controllers reveal themselves when you create an energy deficit. Reduction or elimination of food intake results in a rapid initial decrease in circulating leptin levels and insulin. Leptin levels continue to decrease with continued fat loss.

With a decrease in circulating leptin levels comes a decreased delivery of leptin to the central nervous system (CNS)which alters the balance of several hypothalamic neurotransmitters which brings about an increase in appetite and food consumption.

Conversely leptin and insulin reduce food intake through their interactions with short-term satiation signals such as the intestinally derived gut peptide, cholecystokinin (CCK).

Circulating ghrelin appears to act along with leptin as an adiposity signal in the CNS. Food restriction/elimination increases plasma ghrelin levels which together with the decrease in leptin rapidly stimulates food intake.

It is the trilogy of leptin, ghrelin and cholecystokinin (CCK) that we are most concerned with in the control of food consumption. If you are unable to control the intake of food, insulin levels really won't matter for the reason that you simply will not lose fat.

Like insulin, long-term elevations in leptin, (due to increased adiposity stores) can lead to resistance in leptin signaling and deficits in the ability of these adiposity hormones to neuronally affect body weight regulation. So an overfed state that continues for long periods of time leads to fat accumulation and elevated levels of leptin which brings a decrease in sensitivity to the effects of leptin.

Each macronutrient (fats, carbohydrates and protein) present in the diet can affect these body weight signaling pathways differently. Since macronutrient composition is very important lets look at what happens.

Low Carb Higher Fat/Protein Diet

Carbohydrate-restricted diets with relatively elevated monounsaturated fatty acids and protein, have been found to be effective in reducing body weight, total body adiposity, blood pressure, and waist circumference in overweight people. This type of diet has been found to lead to significant reductions in circulating adiposity signals (leptin and insulin), significantly increased ghrelin concentrations, and significantly increased post meal rise in CCK concentrations (short-term satiation signals) without bringing about an increase in daily food intake.

What happens is that ghrelin increases and leptin decreases and as would be expected subjectively people report feeling less satisfied. However subjective assessments can not be trusted because people lose fat. Yet the rise in ghrelin and lowering of leptin should increase hunger.

The explanation is simply that the satiety signaling through escalating cholecystokinin (CCK)levels is increased day by day. A person eats a meal with higher fats and protein and low carbs and they feel satiated because cholecystokinin (CCK)levels are higher then if they were eating a different macronutrient profile. Over time each meal will result in higher and more prolonged cholecystokinin (CCK)levels which further increases feelings of fullness. This peaks about 2 weeks after staring this type of diet. At that time cholecystokinin (CCK) following a meal remains elevated at least to two (2) hours post-meal. This allows individuals to go without eating for longer periods of time which is very important in bringing about fatloss.

It is chronic exposure of the small intestine to protein and fat that brings about release of CCK from intestinal endocrine I cells. Circulating CCK binds to CCK-1 receptors in the dorsal vagal complex (a region that controls meal size) and satiety ensues.

However increased cholecystokinin (CCK)levels are not sufficient to completely over come hunger induced by elevated Ghrelin and lower Leptin levels. A second explanation is simply that leptin sensitivity in the CNS is increased. The conclusions of these studies is that a carbohydrate-restricted diet together with weight loss normalizes leptin signaling.

It is a narrow rope we walk though because a substantial body of work finds that high fats in the diet can lead to leptin resistance. Lets take a look at what we could say is an opposite type diet and see if we can reconcile this apparent disparity.


Low Fat High Carb/Protein Diet


Fat-restricted diets, produce weight loss by increasing CNS sensitivity to leptin, allowing energy intake, adipose mass, and leptin levels to fall without a compensatory increase in appetite.

These types of studies often find either no or more often some decrease in leptin levels. The failure for leptin fall to bring about increased food intake is attributed to a rise in leptin sensitivity. The conclusion of several studies is simply that dietary fat restriction enhances leptin sensitivity in the CNS and the periphery and that returning people to 35% fat diets rapidly abates the increase in leptin sensitivity.

In addition these diets do not increase Ghrelin levels so Ghrelin will not act to induce hunger. CCK also does not appear to be increased so there is no rise in satiety signally. The sole mechanism to explain the feeling of fullness is an increase in leptin sensitivity.


Reconciling the two macro-nutrient extremes

In my opinion it is the continued presence of both carbohydrates and fats in a diet that results in decreased leptin sensitivity and removal of one in a diet will enhance leptin sensitivity.

Toggling between these two extremes probably has some benefit. The worry is often that circulating fatty acids may bring deposition in organs and muscle and this will lead to insulin resistance in peripheral tissue as well as effect health. It will be important to better match energy utilization with energy input when ingestion of fats is used as an energy substrate. We must also keep an eye on the liberation of fatty acids into circulation.

A diet such as a carbless PWO relies heavily on protein and fats are adjusted to match energy needs. When you break a carbless PWO diet I am conjecturing that 8 hours of carbup will not substantially hinder the build up of cholecystokinin (CCK)levels that we enjoy with just proteins and fats.

If you prolong the Carbless PWO or really any diet w/o carbs for 48 hours + I feel very confident in saying that an 8 hour carb up will not effect the increase in cholecystokinin (CCK)levels and that a quick return to carbless will mean that after several weeks of this toggling eating pattern will result in increased feelings of post-meal satiety and the ability to go w/o a meal for longer periods of time.

This would require that you lift weights every third day. An every other day weight-lifting program would mean less of a percentage of time in the carbless state and I am unsure how that would effect cholecystokinin (CCK)levels. However a true fatloss protocol is primarily focused on muscle preservation and significant fatloss and so an every third day weight-lifting pattern would be exactly what you would want.


How does this fit within a fat loss plan?

The overall goal is to maintain significant periods of time when the body will mobilize the release of fat stores and use them for energy. Energy input, especially of the kind that will result in prolonged periods of storage activity interfere with the overall fatloss goal. Keeping the primary storage hormone insulin quiet is absolutely necessary so that we may spend significant periods of time engaged in lipolysis.

During this period of time we will want to be in an energy deficit. This will not happen if we are unable to control those forces that prompt us to eat. To that end taking steps to increase leptin sensitivity and build up CKK levels serves our purpose.

Using GHRP-6 (which is a ghrelin mimetic) is unwise as it will increase feelings of hunger. Growth hormone as we will discuss is a tool we will use to increase the release of fatty acids from fat cells so we will need to increase its release. We do not want to do this at the expense of violating the satiety we work so hard to build.

GHRP-2 and Ipamorelin are two GHRPs that are capable of increasing the GH we will need without making us hungry.

Creating a proper environment for fat loss from exercise

It has long been known that for practical purposes, the effect of exercise on energy expenditure is essentially confined to the increased energy expenditure during exercise. Exercise and training do not appear to enhance resting metabolic rate (RMR).

However many studies going back 25 years have demonstrated a post-exercise reduction of respiratory quotient (RQ) for several hours (1-6) which is more pronounced and sustained after prolonged glycogen-depleting exercise. This results from a post-exercise increase in free fatty acid (FFA) levels (from the lipolytic response to exercise), during a time of reduced glucose availability as a result of glycogen depletion.

The respiratory quotient is the ratio of the volume of carbon dioxide produced when a substance is oxidized, to the volume of oxygen used. A RQ of 1.0 means that we produce the same volume of carbon dioxide (CO2) as the volume of oxygen (O2) we take in. RQ of 0.7 means that we take in more oxygen and we produce less carbon dioxide. Carbohydrates have an RQ of 1.0 and fats have RQ of about 0.7. Research demonstrates that high carbohydrate diets have higher RQ and low carbohydrate diets have lower RQ. When our RQ is closer to 1.0 we are burning more carbohydrates as fuel and when our RQ gets closer to 0.7 we are burning more fat.

So a post-exercise reduction in respiratory quotient means we move away from using carbohydrates as an energy source in favor of fats.

Without prior glycogen depletion, aerobic exercise of at least 20 minutes duration is required to bring about a response that stimulates lipolysis (7). So the fats that we will use for energy come from lipolysis unless we make the mistake of choosing to ingest carbohydrates PWO which will have the effect of moving the RQ back toward 1.0. In that situation the body will leave more of the fatty acids alone and they will remain and redeposit. If we make the mistake of choosing to ingest fats PWO we add to the supply of fat available for use as energy. As we have less need for energy this will surely mean a deposition of fat.

If we make the correct choice and ingest nothing, then the lower RQ and the available FFAs will mean we burn the fats we liberate for energy.

The effects of aerobic exercise on fat balance come from increased fat oxidation during exercise and a temporary depression of respiratory quotient following exercise. Maximizing these events will maximize fatloss.


Exercise

The rate of fat oxidation is approximately proportional to the FFA levels in the blood. Increasing FFA levels will promote a reduced respiratory quotient (RQ) during exercise (8,9).

Intensity

The intensity and duration of exercise influences the exercise RQ (10). High intensity exercise in excess of 70% VO2 max (i.e. exceeding the "aerobic threshhold') tend to selectively increase the burning of carbohydrate. An increased proportion of fat is burned during moderate intensity exercise.

Duration

In addition, as exercise is prolonged and glycogen stores are gradually depleted, RQ tends to decline as fats must provide a higher proportion of energy needs (11).

Therefore prolonged continuous exercise (at least 35-60 min) of moderate intensity, conducted when serum FFA levels are maximal, should optimize the amount and proportion of fat burned during exercise (10).


Maximizing pre-workout FFA

To create high FFA levels, exercise should be done on an empty stomach away from meals and/or preferably during morning fasting's metabolism, when no food has been consumed for at least 8 hours. Food consumption prior to or during exercise will result in an insulin-mediated suppression of FFAs while increasing blood glucose, and this will favor carbohydrate oxidation.

Boosting FFA

Caffeine

FFA levels can be boosted further by pre-administration of an effective dose of caffeine (12,13), equivalent to one or two cups of strong coffee. For the reason that the impact of oral caffeine on FFAs is delayed, the caffeine should be taken at least 45-60 min prior to the exercise session. Caffeine consumption prior to exercise has been shown to spare glycogen and reduce the respiration quotient in exercising humans (12,14,15). Caffeine's efficacy in this regard will be higher in individuals who are not carbohydrate loaded (16), and who have not developed caffeine resistance stemming from excessive habitual use.

GHRP-2, Ipamorelin, Modified GRF(1-29) and GH Frag (176-191)

I don't need to elaborate much on this as much more detailed information is available throughout this forum. Suffice it to say that use of these items to increase GH or its lipolytic fragment will increase the amount of FFAs in circultaion.

These GH effectors should be dosed prior to exercise. They can be taken with coffee and should add to exercise induced FFA as well as post-exercise FFAs.


Increasing the liver's capacity for lipid oxidation

In short the more carntine you can have delivered to and retained in the mitochondria of muscle cells, the more oxidation of fats will occur. Insulin and it also appears Choline increase the transport and retainment of Carnitine in muscle. L-Carnitine has a slow release rate from tissue and thus will build up over time if taken daily. Oral bioavailability is lower then injection but still of substantial cumulative benefit.

L-Carnitine (in injectable or oral form) should always be ingested when you take exogenous insulin and/or when you are spiking insulin with carbohydrates throughout the week. In addition the following oral regime taken 45 minutes prior to exercise (at coffee time) should provide benefit.

1.3 - 2 grams of Choline and 1 - 1.4 grams of L-Carnitine.

Notes:

1. Bahr R, Ingnes V, Vaage O et al. Effect of duration of exercise on excess postexercise 02 consumption. J Appl Physiol 1987; 485-490.

2. Maehlum S, Grandmontagne M, Newsholme E A, Sejersted O M. Magnitude and duration of excess postexercise oxygen consumption in healthy young subjects. Metabolism 1986; 35: 425-429.

3. Bielinski R, Schutz Y, J6quier E. Energy metabolism during the postexercise recovery in man. Am J Clin Nutr 1985; 42: 69-82.

4. Flatt J P. Dietary fat, carbohydrate balance, and weight maintenance: effects of exercise. Am J Clin Nutr 1987; 45: 296-306.

5. Chad K, Quigley B. The effects of substrate utilization, manipulated by caffeine, on post-exercise oxygen consumption in untrained female subjects. Eur J Appl Physiol 1989; 49: 48-54.

6. Weststrate J A, Weys P, Poortvliet E et al. Lack of a systematic sustained effect of prolonged exercise bouts on resting metabolic rate in fasting subjects. Eur J Clin Nutr 1990; 44: 91-97.

7. Carlson L A, Edelund L G, Oro L. Studies on blood lipids during exercise. J Lab Clin Med 1963; 61: 724--729.

8. Costill D L, Coyle E, Dalsky Get al. Effects of elevated plasma FFA and insulin on muscle glycogen usage during exercise. J Appl Physiol 1977; 43: 695--699.

9. Hickson R C, Rennie M J, Conlee R K et al. Effects of increased plasma fatty acids on glycogen utilisation and endurance. J Appl Physiol 1977; 43: 829-833.

10. Andrews J F. Exercise for slimming. Proc Nutr Soc 1991; 50: 459-471.

11. Flatt J P. Dietary fat, carbohydrate balance, and weight maintenance: effects of exercise. Am J Clin Nutr 1987; 45: 296-306.

12. Chad K, Quigley B. The effects of substrate utilization, manipulated by caffeine, on post-exercise oxygen consumption in untrained female subjects. Eur J Appl Physiol 1989; 49: 48-54.

13. Bellet S, Kershbaum A, Finck E. Response of free fatty acids to coffee and caffeine. Metabolism 1968; 17: 702-707.

14. Costill D L, Dalsky G P, Fink W J. Effects of caffeine ingestion on metabolism and exercise performance. Med Sci Sports 1978; 10: 155-158.

15. Essig D, Costill D L, Van Handel P J. Effects of caffeine ingestion on utilization of muscle glycogen and lipid during leg ergometer cycling. Int J Sports Med 1980; 1: 86-90.

16. Weir J, Noakes T D, Myburgh K, Adams B. A high carbohydrate carbohydrate diet negates the metabolic effects of caffeine during exercise. Med Sci Sports Exerc 1987; 19: 100-105.