Hormonale effecten van extreem crashdieten?

**dynobet** · 19-05-2010, 00:30

Even een stukje copy paste uit het boek ultimate diet 2.0
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So you decide to diet, reducing carbs, calories or both. Vary rapidly, blood glucose and
insulin levels are going to be reduced. This is good as it releases the "block" on fat mobilization.
Additionally, catecholamine release typically goes up (at least initially), further increasing fat
mobilization from fat cells. This causes blood fatty acid levels to increase. This is also good, as it
tends to promote fat burning in tissues such as liver and muscle. This effect is facilitated if you
deplete liver and muscle glycogen, as glycogen depletion tends to increase the use of fatty acids

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for fuel. The increase in blood fatty acid levels also has the short-term effect of causing insulin
resistance. As I mentioned, this is a good thing on a diet since it spares glucose and helps promote

fat oxidation. So far, so good, right?
Unfortunately, along with these good effects, a lot of bad things start to happen. I already
described many of the central adaptations above: changes in leptin, ghrelin, Peptide YY (and
certainly other hormones) "tell" your brain that you're not eating enough. This causes changes in
the various neurochemicals stimulating a number of negative adaptations. I want to note that
the response is not immediate, there is a lag time between the changes in all of these hormones
and the body's response. But that's not all.
There are also many other adaptations which occur when you diet, so let's look at some of
those. First and foremost, the drop in leptin directly affects liver, skeletal muscle and fat cell
metabolism, mostly for the worse.
While the drop in insulin mentioned above causes better fat mobilization, it causes other
problems. One is that testosterone will bind to sex-hormone binding globulin (SHBG) better,
lowering free testosterone levels (this is in addition to the drop in total testosterone). As well,
insulin is anti-catabolic to muscle, inhibiting muscle breakdown. The increase in cortisol that
occurs with dieting enhances protein breakdown as well as stimulating the conversion of protein
to glucose in the liver. Additionally, a fall in energy state of the muscle impairs protein synthesis
(although it increases fatty acid oxidation). The mechanism behind this is more detail than I
want to get into here. But the combined effect of these processes is that protein synthesis is
decreased and breakdown is accelerated; this causes muscle loss.
On top of that, high blood fatty acid levels tend to impair the uptake of T4 (inactive
thyroid) into the liver. There are also changes in liver metabolism that impair the conversion of
T4 to T3 (active thyroid). Both of these processes cause decreased blood levels of T3. There is
some evidence that high blood fatty acid levels causes tissues to become resistant to thyroid
hormone itself (this is part of why just taking extra thyroid on a diet doesn't fix all of the
problems). After the initial increase, there is also a drop in nervous system output (that can
occur in as little as 3-4 days after you start a diet). Along with the drop in thyroid, insulin and
leptin, this explains a majority of the metabolic slowdown that occurs. The change in liver
metabolism (and the reduction in insulin) also impairs the production of IGF-1 from GH.
All of these adaptations serve two main purposes. The first is to slow the rate of fat loss,
as this will ensure your survival as long as possible. Related to that, the body tends to shut down
calorically costly activities. This includes protein synthesis, reproduction and immune function;
there's little point keeping any of these functioning when you're starving to death. The drop in
leptin, and the changes in hormones that occur are a huge part of why men tend to lose their sex
drive (and ability) and women lose their period when they get lean/diet hard.
The second is to prime your body to put fat back on at an accelerated rate when calories
become available again. Decreased metabolic rate and fat burning, along with improved caloric

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storage all conspire to put the fat back on when you start eating again. As I mentioned earlier,
this makes perfect evolutionary sense, even if it presents a huge pain in the ass to us.
I haven't even mentioned the hunger and appetite issue which is a topic worthy of an
entire book. The combination signal sent by leptin, ghrelin, insulin, glucose, and a host of other
hormones (cholecystokinin, glucagon-like peptide 1 and 2, bombesin and many many others) are
all involved in both hunger and appetite. The changes that occur with dieting tend to make both
shoot through the roof: you tend to get and stay hungry, thinking about food nearly constantly.
Bodybuilders and athletes may have unbelievable food control but it still sucks being hungry

constantly when you try to diet.
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To a great degree, most of the adaptations that occur with dieting reverse when you
overeat. Actually, that depends a lot on the situation. As I mentioned above, the body as a whole
tends to defend against underfeeding better than it does against overfeeding which is why it's
generally easier to gain weight than to lose it. Studies where leptin has been increased above
normal (i.e. to try and cause weight loss in overweight individuals) have generally borne this out:
except at massive doses, raising leptin above normal does very little.
There are a couple of theories as to why this might be the case. One theory is that normal
leptin levels send essentially a 100% signal, that is they tell the body that all systems are
normal. It should seem clear that raising leptin above 100% isn't going to do much. Another
possibility is related to something I alluded to above: leptin sensitivity and resistance. It's
thought that people have varying degrees of leptin resistance which means, in essence, that they
don't respond as well to leptin as they should. On top of this, when leptin levels go up, it appears
to stimulate resistance to itself. That is, when leptin gets and stays high, it causes you to
become resistant to its effects.

Both explanations for the failure of high leptin levels to defend against weight gain make
good evolutionary sense. Your body doesn't want to be lean but it doesn't really mind getting fat.
This is because, during our evolution, being fat was never a risk, while being lean was. If
anything, getting fat was a benefit which is why our bodies tend to be so good at it. It's only in
modern times when people can get and, more importantly, stay fat for extended periods, that
being fat is a problem. Ten thousand years from now, perhaps we will evolve defenses against
being fat.

Anyhow, if calories are available all the time, it would make little sense for you to get full
and/or start burning them off. This is what would happen if you were extremely sensitive to
leptin (and does happen in a small percentage of individuals). So high levels of leptin induce

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resistance to itself, keeping you hungry and eating while the food is available. Leptin can induce
resistance to itself in only a few days of overeating.
But we're not really talking about raising leptin above normal here, we're talking about
reversing or preventing the drop that occurs with dieting. In that situation, many of the above
adaptations to dieting will reverse to one degree or another. What degree will depend on how lean
you are, how long you diet, and how long you overeat.
So now you increase your calories and carbs. Let's look at some of what happens when
you do so. First there are all of the central adaptations that occurred during dieting, that will
reverse to some degree while overfeeding. Leptin will go up (noting again that it goes up more
quickly than bodyfat comes on) along with insulin and peptide YY, ghrelin goes down. This signal the hypothalamus that you're eating again signaling that the body can reverse the adaptations
that had occurred in the first place.

In addition, the increase in insulin will reverse the binding of testosterone to SHBG; cortisol
also goes down. With increased carbohydrates, you increase both liver and muscle glycogen.
While this decreases fat oxidation in the muscle, you get improved protein synthesis (the increase in insulin and testosterone and the drop in cortisol have an additional effect).
Of course, with increasing insulin, there is a decrease in blood fatty acid concentrations
which improves insulin sensitivity. Skeletal muscle insulin sensitivity is enhanced even more by
exercise.

The decrease in blood fatty acids, along with changes in liver metabolism will improve both
the uptake and conversion of T4 to T3; along with improvements in nervous system output, this
will help to increase metabolism. You get the idea: with overfeeding, the body reverses the basic

adaptations that occurred to dieting in the first place.
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Kortom veel argumenten voor een cyclisch dieet zoals KETO of UD2.
Overfeeding/underfeeding

Calories: Overfeeding/underfeeding Up/Down

Carbs/fat (energy): Overfeeding/underfeeding Up/Down
Insulin: Overfeeding/underfeeding Up/Down
Total testosterone: Overfeeding/underfeeding Up or no change/Down
Free testosterone: Overfeeding/underfeeding Up/Down
GH Overfeeding/underfeeding Up/Up
IGF-1: Overfeeding/underfeeding Up/Down
Thyroid: Overfeeding/underfeeding Up/Down
Catecholamines: Overfeeding/underfeeding Down/Up
Cortisol: Overfeeding/underfeeding Down/Up
Leptin: Overfeeding/underfeeding Up/Down
Ghrelin: Overfeeding/underfeeding Down/Up
Cellular energy state: Overfeeding/underfeeding Up/Down
Protein synthesis: Overfeeding/underfeeding Up/Down
Bodyfat levels: Overfeeding/underfeeding Up/Down
Muscle mass: Overfeeding/underfeeding Up/Down

Net effect Body: Overfeeding/underfeeding // anabolic Body/catabolic Body
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Eigenlijk kan ik je alleen maar aanraden om het hele boek (ultimate diet 2.0) te lezen. Daar zul je vrijwel alles in vinden wat je nodig hebt.

**Genjuro** · 19-05-2010, 10:36

Bedankt, eigenlijk wist ik deze effecten allemaal al en was ik vooral geinteresseerd in het effect op het lipase-enzyme.

Het leuke is dat al deze effecten makkelijk gecountert kunnen worden, cortisol door halotestin, vermindering van T3 door T3(Captain Obvious strikes again!), leptine moet nog meer onderzocht worden(en zink helpt bij het verhogen), igf-1 var, ghreline meridia.

Enkel het lipase-enzyme moet ik nog meer onderzoeken en dan komt er een mooi kuurontwerp.

**GeneralIx** · 19-05-2010, 10:37

J Strength Cond Res. 2010 Apr;24(4):1074-81.
Anabolic and catabolic hormones and energy balance of the male bodybuilders during the preparation for the competition.
Mäestu J, Eliakim A, Jürimäe J, Valter I, Jürimäe T.

Institute of Sport Pedagogy and Coaching Sciences, Center of Behavioral and Health Sciences, University of Tartu, Tartu, Estonia. [email protected]
Abstract
The purpose of the study was to investigate simultaneous effects of energy balance, caloric intake, and the hormonal anabolic-catabolic balance in bodybuilders prior to competition. Fourteen male bodybuilders took part in an 11-week energy-restricted period to reduce body fat. The subjects were divided into the energy-restricted group (ERG) (n = 7), who were preparing for the competition, or the control group (CG) (n = 7) who continued to train regularly and did not change their dietary or training pattern. Participants were tested at 11 weeks (T1), 5 weeks (T2), and 3 days (T3) before competition for diet, body composition, and fasting hormonal assessment. Body mass and body fat percentage of ERG were significantly (p < 0.05) decreased during the study period. In ERG, insulinlike growth factor-1 (IGF-1) and insulin decreased significantly during the 11-week weight-reduction period (p < 0.05). Testosterone was decreased only from week 11 to week 5 (from 20.3 +/- 6.0 to 18.0 +/- 6.8 nmol/L). Changes in IGF-I concentration were significantly related to changes in insulin (r = 0.741), fat mass (r = 0.705), lean body mass (r = 0.696), and body mass (r = 0.652). Changes in insulin concentrations were significantly related to changes in fat mass (r = 0.630) and lean body mass (r = 0.725). These data indicate that severe energy restriction to extremely low body energy reserves decreases significantly the concentrations of 3 anabolic pathways despite high protein intake. Monitoring of insulin and IGF-1 concentration is suggested to prevent losses in muscle mass in energy-restricted conditions. Other nutritional strategies might be needed to prevent possible catabolic effect during preparation of bodybuilders to competition.

PMID: 20300017 [PubMed - in process]

Van deze is ook het volledige onderzoek vrij te lezen:

J Appl Physiol. 2008 Jul;105(1):58-64. Epub 2008 May 1.
Effects of dietary protein content on IGF-I, testosterone, and body composition during 8 days of severe energy deficit and arduous physical activity.
Alemany JA, Nindl BC, Kellogg MD, Tharion WJ, Young AJ, Montain SJ.

Military Performance Division, US Army Research Institute of Environmental Medicine, Natick, MA 01760, USA.
Abstract
Energy restriction coupled with high energy expenditure from arduous work is associated with an altered insulin-like growth factor-I (IGF-I) system and androgens that are coincident with losses of fat-free mass. The aim of this study was to determine the effects of two levels of dietary protein content and its effects on IGF-I, androgens, and losses of fat-free mass accompanying energy deficit. We hypothesized that higher dietary protein content would attenuate the decline of anabolic hormones and, thus, prevent losses of fat-free mass. Thirty-four men [24 (SD 0.3) yr, 180.1 (SD 1.1) cm, and 83.0 (SD 1.4) kg] participated in an 8-day military exercise characterized by high energy expenditure (16.5 MJ/day), low energy intake (6.5 MJ/day), and sleep deprivation (4 h/24 h) and were randomly divided into two dietary groups: 0.9 and 0.5 g/kg dietary protein intake. IGF-I system analytes, androgens, and body composition were assessed before and on days 4 and 8 of the intervention. Total, free, and nonternary IGF-I and testosterone declined 50%, 64%, 55%, and 45%, respectively, with similar reductions in both groups. There was, however, a diet x time interaction on day 8 for total IGF-I and sex hormone-binding globulin. Decreases in body mass (3.2 kg), fat-free mass (1.2 kg), fat mass (2.0 kg), and percent body fat (1.5%) were similar in both groups (P = 0.01). Dietary protein content of 0.5 and 0.9 g/kg minimally attenuated the decline of IGF-I, the androgenic system, and fat-free mass during 8 days of negative energy balance associated with high energy expenditure and low energy intake.

PMID: 18450989 [PubMed - indexed for MEDLINE]Free Article

**Kevster** · 19-05-2010, 10:43

Originally posted by Genjuro View Post

Bedankt, eigenlijk wist ik deze effecten allemaal al en was ik vooral geinteresseerd in het effect op het lipase-enzyme.

Het leuke is dat al deze effecten makkelijk gecountert kunnen worden, cortisol door halotestin, vermindering van T3 door T3(Captain Obvious strikes again!), leptine moet nog meer onderzocht worden(en zink helpt bij het verhogen), igf-1 var, ghreline meridia.

Enkel het lipase-enzyme moet ik nog meer onderzoeken en dan komt er een mooi kuurontwerp.

Klinkt obvious bro maar dat is niet zo. Door de drop in kcal word T3 niet alleen gedrukt maar worden cellen ook resistent ertegen. Het exogeen opkrikken van T3 is dus niet voldoende.

Denk overigens dat cyclen met kcal veel makkelijker is dan het kunstmatig in "Bulk" houden van je lichaam. Ga UD2 doen!

**GeneralIx** · 19-05-2010, 11:05

@ Sch00m
Kan me niet voorstellen dat in geval van lager T3, je cellen er ongevoeliger voor worden. Doorgaans verschuift de gevoeligheid van cellen in tegengestelde richting als je hormonen (tot een bepaalde grens uiteraard).

**Kevster** · 19-05-2010, 12:00

Originally posted by GeneralIx View Post

@ Sch00m
Kan me niet voorstellen dat in geval van lager T3, je cellen er ongevoeliger voor worden. Doorgaans verschuift de gevoeligheid van cellen in tegengestelde richting als je hormonen (tot een bepaalde grens uiteraard).

Klopt, het word ook niet veroorzaakt door de lage T3 maar door de hoge concentratie FFA in je bloed die weer veroorzaakt word door de verhoogde afgifte van de adreno-hormonen.

**dynobet** · 19-05-2010, 12:42

Originally posted by sch00m View Post

Klinkt obvious bro maar dat is niet zo. Door de drop in kcal word T3 niet alleen gedrukt maar worden cellen ook resistent ertegen. Het exogeen opkrikken van T3 is dus niet voldoende.

Denk overigens dat cyclen met kcal veel makkelijker is dan het kunstmatig in "Bulk" houden van je lichaam. Ga UD2 doen!

ben ik het mee eens. Met ud2 omzeil je vrijwel alle problemen die je normaal gesproken krijgt met crash dieten.
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Twenty-four-hour leptin levels respond to cumulati... [J Clin Endocrinol Metab. 2000] - PubMed result

Abstract

Leptin plays a vital role in the regulation of energy balance in rodent models of obesity. However, less information is available about its homeostatic role in humans. The aim of this study was to determine whether leptin serves as an indicator of short-term energy balance by measuring acute effects of small manipulations in energy intake on leptin levels in normal individuals. The 12-day study was composed of four consecutive dietary-treatment periods of 3 days each. Baseline (BASE) [100% total energy expenditure (TEE)] feeding, followed by random crossover periods of overfeeding (130% TEE) or underfeeding (70% TEE) separated by a eucaloric (100% TEE) washout (WASH) period. The study participants were six healthy, nonobese subjects. Leptin levels serially measured throughout the study period allowed a daily profile for each treatment period to be constructed and a 24-h average to be calculated; ad libitum intake during breakfast "buffet" following each treatment period was also measured. Average changes in mesor leptin levels during WASH, which were sensitive to energy balance effected during the prior period, were observed. After underfeeding, leptin levels during WASH were 88 +/- 16% of those during BASE compared with 135 +/- 22% following overfeeding (P = 0.03). Leptin levels did not return to BASE during WASH when intake returned to 100% TEE, but instead were restored (104 +/- 21% and 106 +/- 16%; not significant) only after subjects crossed-over to complementary dietary treatment that restored cumulative energy balance. Changes in ad libitum intake from BASE correlated with changes in leptin levels (r2 = 0.40; P = 0.01). Leptin levels are acutely responsive to modest changes in energy balance. Because leptin levels returned to BASE only after completion of a complementary feeding period and restoration of cumulative energy balance, leptin levels reflect short-term cumulative energy balance. Leptin seems to maintain cumulative energy balance by modulating energy intake.

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When someone starts a diet, leptin may drop by 30-50% within about a week, obviously they haven’t lost that much of their body fat. After that rapid initial drop, drops in leptin are much slower scaling with body fat loss.
By the same token, with even short-term overfeeding, leptin can come up far more quickly than body fat is gained. This latter fact is part of the basic premise behind refeeding and cyclical dieting. (lyle mc donald).
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Dit geld echter alleen voor overfeeden met koolhydraten:

Effects of short-term carbohydrate or fat overfeed... [Int J Obes Relat Metab Disord. 2000] - PubMed result

Abstract

OBJECTIVE: To determine the effects of excess carbohydrate or fat intake on plasma leptin concentrations and energy expenditure. DESIGN: Ten healthy lean females were studied: (a) during a 3 day isoenergetic diet (ISO); (b) during 3 day carbohydrate overfeeding (CHO OF); and (c) during 3 day fat overfeeding (FAT OF). During each test, basal metabolic rate, the energy expended during mild physical activity and recovery, and 24 h energy expenditure (24 h EE) were measured with indirect calorimetry. The concentrations of glucose and lactate were monitored in subcutaneous interstitial fluid over a 24 h period using microdialysis. Plasma hormone and substrate concentrations were measured in a blood sample collected in the morning of the fourth day. RESULTS: CHO OF increased plasma leptin concentrations by 28%, and 24 h EE by 7%. Basal metabolic rate and the energy expended during physical activity were not affected. FAT OF did not significantly change plasma leptin concentrations or energy expenditure. There was no relationship between changes in leptin concentrations and changes in energy expenditure, suggesting that leptin is not involved in the stimulation of energy metabolism during overfeeding. Interstitial subcutaneous glucose and lactate concentrations were not altered by CHO OF and FAT OF. CONCLUSIONS: CHO OF, but not FAT OF, increases energy expenditure and leptin concentration.

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voor het complete verhaal met alle bronnen:
Bodyweight Regulation: Leptin Part 2 | BodyRecomposition - The Home of Lyle McDonald
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**Genjuro** · 20-05-2010, 10:39

Originally posted by sch00m View Post

Klopt, het word ook niet veroorzaakt door de lage T3 maar door de hoge concentratie FFA in je bloed die weer veroorzaakt word door de verhoogde afgifte van de adreno-hormonen.

Dus gaat het toch gebeuren bij elk low carb dieet...

T3 valt al van de mogelijke middelen-lijst.

UD2.0 eens lezen als ik meer tijd heb, zit in de examenperiode.

Hormonale effecten van extreem crashdieten?