I also would like to see a sample meal plan for a strict day. Particularly how you keep your fats so low. Also, ho many more calories should you consume if you are not using an androgen.
First off, sir, I did not lie and then attempt to cover it up. If you read my post, you would have seen that I said “No, it’s not going to last for the entire 3 days, but it will certainly last for longer than the overfeeding session- and even that is supported by studies where individuals were previously consuming their normal diets.”
One particular study showed a 40% increase in leptin with an acute 12-hr overfeed that lasted well into the next morning. I don't think that the individuals in this study were eating while they were asleep. That is twice the length of the overfeed; would you say that twice the length is significant? I would; and that's exactly what I said. A leptin spike increases:
Thyroid output
BMR
Thermogenesis
Keep in mind that these subjects were previously consuming their normal diets; which could have been either maintenance or surplus calorie levels. Again, it has not been directly studied as to what happens when bodybuilders on severe diets, adhering to a strict exercise program indulge themselves in a surplus of calories- the real world data seems to suggest that the spike may be greater and last longer; thus you get leaner. Also, leptin levels returned to baseline the morning after; baseline levels are much greater than the leptin levels associated with a severe diet. Even at baseline levels, fat burning is not inhibited- thus you can continue to lose fat; something that is not easily done with plumeted hormone levels. It has not been studied as to how long it takes to return back to the hypo conditions associated with a severe diet.
And it doesn't even matter if the spike doesn't last a few days- it bumps you out of the no-fat-burning rut and allows you to tap back into your fat stores over the next few days. Plenty of real world experiences support this.
I do not appreciate you falsely acusing me- please read more carefully next time. Lastly, it's obvious that you have read my personal info at the end of my article (since you made it a point to state that you are older than me and have your doctorate- as if it mattered), so if you have any further comments, I'd appreciate that you email them to me and stop detracting from the purpose of this thread- to help others achieve their goals; not a pissing match or yet another debate.
For everyone else, the information in my last two posts together states where I am coming from. Hopefully you too can see this.
-JM
Once again, I see no reference to the supposed study which reveals that there is an increase of energy expenditure for ANY amount of time after normal caloric intake is resumed. It doesn’t need to be 3 days, just show me that the metabolic rate is elevated beyond that of the simple act of overfeeding. I would just like to see this study. Someone please show me this groundbreaking study!
It depends on the training done that day, but I’ll give you an example day:
Meal 1 (After HIIT session): 20 grams of Whey and 40 grams of Maltodextrin (20P, 40C, 1F)
Meal 2: Myoplex Plus with added fiber (42P, 25C, 2F)
Meal 3: 3 oz of grilled chicken breast- cooked weight, 1.5 cups of green beans (27P, 11C)
Meal 4: 4 oz of 96% lean top sirloin- raw weight (24P, 4F)
Meal 5: 3 oz of grilled chicken- cooked weight, 1.5 cups of green beans (27P)
Meal 6: Myoplex Low Carb, 15 caps of fish oil (50P, 9C, 21F)
Totals: 190P, 96C, 28F- 1400 calories
Hopefully that is what you were looking for,
-JM
J Clin Endocrinol Metab 1996 Nov;81(11):4162-5
Response of leptin to short-term and prolonged overfeeding in humans.
Kolaczynski JW, Ohannesian JP, Considine RV, Marco CC, Caro JF.
Department of Medicine, Jefferson Medical College, USA.
As one of the postulated roles of the ob gene product, leptin, is regulation of energy balance and preservation of normal body composition, we investigated the effect of acute and chronic calorie excess (weight gain) on serum leptin in humans. Two protocols were employed: 1) acute (12-h) massive (120 Cal/kg) voluntary overfeeding of eight healthy individuals; and 2) chronic overfeeding to attain 10% weight gain, with its subsequent maintenance for additional 2 weeks, involving six normal males. In the acute experiments (protocol 1), circulating leptin rose by 40% over baseline (P < 0.01) during the final hours of overfeeding; this increase persisted until the next morning.
This might seem strange, but I think Joel’s article has finally explained what has been happening to me for a long time. Whenever eating to lean up, I would allow myself one day to eat garbage. I would never notice any noticable change in body fat % until after I had went crazy eating everything. The longest I had ever held out eating very well was three and a half weeks, and at the end of that my results weren’t great. I’m going to bump up my cheating sessions to twice a week and see how it goes. Thanx for the article Joel.
Joel, I agree with Moonpie Phil and would like to see the references to the studies that you mentioned in your article. Also, why are you recommending Myoplex products rather than Biotest’s Grow! and Advanced Protein?
You’d have to go with a much more moderate approach without an androgen; you couldn’t follow the given split, etc. and you wouldn’t be able to cheat as much. I’d recommend androgen usage, but we can discuss options for a moderate cut.
J Neuroendocrinol 2001 Oct;13(10):913-21
The role of leptin in the regulation of energy balance and adiposity.
van Dijk G.
Department of Animal Physiology, Division Neuroendocrinology, School of Behavioural and Cognitive Neurosciences, University of Groningen, Haren, The Netherlands.
Since its discovery, leptin (a 167-amino acid product of the OB gene) has quickly moved to the forefront as an important hormone for regulation of energy balance. It closes a feedback loop from adipose tissue to hypothalamic neuropeptide-containing neural circuitry involved in regulation of food intake and neuroendocrine/autonomic outflow. While increased central leptin signalling reduces adiposity via a reduction in food intake, it also has remarkable metabolic effects that promote leanness, independent of food intake. These include: (i) increased energy expenditure, (ii) in-place degradation of fat, and (iii) increased thermogenesis.
Just for the sake of it, I’m posting the abstract of Joel’s cited study as well as two others which don’t support his theory. Every one of these supports exactly what I’ve been saying this entire post session or thread, whatever you call it. Enjoy!
Am J Physiol 1990 Sep;259(3 Pt 2):R461-9
Energy expenditure and subsequent nutrient intakes in overfed young men.
We investigated the mechanisms of body weight regulation in young men of normal body weight leading unrestricted lives. Changes in total and resting energy expenditure, body composition, and subsequent voluntary nutrient intakes in response to overeating by 4,230 +/- 115 (SE) kJ/day (1,011 +/- 27 kcal/day) for 21 days were measured in seven subjects consuming a typical diet. On average, 85-90% of the excess energy intake was deposited (with 87% of this amount in fat and 13% in protein on average). There was no detectable difference between individuals in susceptibility to energy deposition. The resting metabolic rate, averaged for fasting and fed states, increased during overfeeding (mean +/- SE, 628 +/- 197 kJ/day, P less than 0.01), but at least some of this amount was obligatory expenditure associated with nutrient assimilation. No significant increase in energy expenditure for physical activity or thermoregulation resulted from overfeeding. Thus energy expenditure did not substantially adapt to increased energy intake. However, significant decreases in voluntary energy intake (1,991 +/- 824 kJ/day, P less than 0.05) and fat intake (48 +/- 11 g/day, P less than 0.01) followed overeating, indicating that adaptive changes in nutrient intakes can contribute significantly to body weight regulation after overeating.
Int J Obes Relat Metab Disord 2001 May;255):593-600
Changes in energy metabolism in response to 48 h of overfeeding and fasting in Caucasians and Pima Indians.
OBJECTIVE: Differences in the metabolic response to overfeeding and starvation may confer susceptibility or resistance to obesity in humans. To further examine this hypothesis, we assessed the changes in 24 h energy metabolism in response to short-term overfeeding and fasting in Caucasians (C) and Pima Indians (I), a population with a very high propensity for obesity. METHODS: We measured the changes in 24 h energy expenditure (24 -EE) and 24 h respiratory quotient (24-RQ) in response to 48 h of mixed diet overfeeding (100% above energy requirements) and fasting in a whole body respiratory chamber in 14 male subjects (7 C/7 I, age 30+/-6 y, mean+/-s.d.). Results were compared to a 24 h measurement under eucaloric conditions. RESULTS: Mean 24-EE increased in response to overfeeding and decreased in response to fasting (all changes P<0.01), with no differences between C (+9.1% and -9.1%) and I (+8.6% and -9.6%). Similarly, mean 24-RQ increased/decreased in response to overfeeding/fasting, respectively (all changes P<0.01), again with no differences between C (+0.06 and -0.05) and I (+0.05 and -0.05). The changes in 24-EE in response to overfeeding and fasting were positively correlated (r=0.70, P<0.01), whereas those in 24-RQ were not (r=0.40, NS). CONCLUSIONS: Pima Indians do not appear to have an impaired metabolic response to short-term overfeeding and fasting that could explain their propensity for obesity. Individuals with a large increase in energy expenditure in response to overfeeding appear to have a small decrease in energy expenditure in response to starvation (spendthrift phenotype) and vice versa (thrifty phenotype).
Int J Obes Relat Metab Disord 1995 May;195):331-7
Spontaneous overfeeding with a ‘cafeteria diet’ in men: effects on 24-hour energy expenditure and substrate oxidation.
OBJECTIVE: To investigate the relationship between obesity and ad libitum food intake (quantity and composition) and to assess the impact of ad libitum food intake on energy expenditure and macronutrient oxidation. DESIGN: Male volunteers were first fed a weight maintaining diet for at least 4 days before selecting their food for the next 5 days from two computerized vending machines offering a variety of familiar, palatable foods. 24-h energy expenditure (24EE) and substrate oxidation were measured in a respiratory chamber on the last day of each weight maintenance and ad libitum intake periods. SETTING: Ten day admission on a metabolic research ward. SUBJECTS: Thirty-four non-diabetic Pima Indian males covering a wide range of body weight and body composition (30 +/- 8 y, 102.1 +/- 30.2 kg, 34 +/- 9% body fat, mean +/- s.d.). RESULTS: Weight maintenance requirements averaged 2913 +/- 342 kcal/d. Energy intake during the ad libitum period increased to 4550 +/- 921 kcal/d (12 +/- 1% protein, 40 +/- 4% fat, 48 +/- 4% carbohydrate) i.e., a spontaneous overeating by 54 +/- 32% above weight maintenance requirement, resulting in a 0.9 +/- 1.0 kg body weight gain. Neither the composition of the selected diet nor the degree of overeating was associated with physical characteristics, such as body weight and body composition. When compared with baseline, spontaneous overeating on day 5 was associated with a 396 +/- 233 kcal/d increase in 24EE, a 607 +/- 503 kcal/d increase in carbohydrate oxidation, a 214 +/- 392 kcal/d decreased in lipid oxidation (P < 0.01), and no change in protein oxidation. Increased carbohydrate oxidation correlated with the excess carbohydrate intake (r = 0.69, P = 0.0001) accounting for 68 +/- 13% (mean +/- s.e.e.) of the excess, whereas excess fat intake was not oxidized. CONCLUSION: In response to spontaneous overfeeding on a mixed ‘cafeteria diet’, excess carbohydrate intake is oxidized, suggesting a physiological control of carbohydrate stores, whereas excess fat intake is channeled toward fat stores. None of the observed changes were related to indices of obesity.
Great article Joel. I am gonna give it a try as I lose these last few pounds before I ship off.
Hey Joel, I’m attempting this plan with 4-AD-EC. 190lbs, 12.5%. Currently eating about 2000 calories, I know we all have individual differences, but should dieting be more extreme than this to get the full effect? Next question is…why so little fat on this diet? Since there isn’t much suppression on 4-AD-EC, would it still be a good idea at least in my case to eat plenty of fat to maintain my natural test levels? (In essence the 4-AD would become supplemental). I’ll be on this plan for up to 8 weeks, less if I’m lucky. Thanks in advance.
Just a question to Moonpie Phil, do you only live by what you see in studies? I would assume that every study proving that steroids don’t work were law for you until recently? I have eaten like this every time that I have dieted down and it does not slow the loss of fat. What it does is allow a more positive state of mind while dieting along with keeping the metabolism from falling to repressed levels due to a hypo-caloric diet. I could care less about a study as far as this is concerned because I see the results in myself and apparently, so have many others. What exactly is the problem? To prove it, all you have to do is try it.
Phil, if you look at the references that I pasted from Joel’s article, Refs:1,6,11,12,13,14,15,and 16 ALL contain Leptin in the title of the article. I haven’t read any of those articles yet, but I DO think that what you are looking for is in at least one of these articles. True, I did not see many footnotes in the body of the article(personally, I think they clog up a paper), but I could see where you could think that Joel is pulling this out of thin air. Like Joel stated, many of these studies were conducted on non-bodybuilder-athletic type people, so we CAN’T just go by what the study said as concrete evidence. This would be a good time to investigate this phenomenon in healthy, athletic people. Since you are already a PhD, maybe you can help us in this endeavor 
-The Starkdog
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Dirlewanger M, et al. Effects of short-term carbohydrate or fat overfeeding on energy expenditure and plasma leptin concentrations in healthy female subjects. Int J Obes Relat Metab Disord. 2000 Nov;24(11):1413-8.
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Douyon L, Schteingart DE. Effect of obesity and starvation on thyroid hormone, growth hormone, and cortisol secretion. Endocrinol Metab Clin North Am. 2002 Mar;31(1):173-89.
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Dulloo AG, Jacquet J. Adaptive reduction in basal metabolic rate in response to food deprivation in humans: a role for feedback signals from fat stores. Am J Clin Nutr. 1998 Sep;68(3):599-606.
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Friedl, et al. Endocrine markers of semistarvation in healthy lean men in a multistressor environment. J Appl Physiol. 2000 May;88(5):1820-30.
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Garrow JS. Chronic effects of over- and under-nutrition on thermogenesis. Int J Vitam Nutr Res. 1986;56(2):201-4.
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Kolaczynski JW, et al. Response of leptin to short-term and prolonged overfeeding in humans. J Clin Endocrinol Metab 1996 Nov;81(11):4162-5
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Kozusko FP. Body weight setpoint, metabolic adaption and human starvation. Bull Math Biol. 2001 Mar;63(2):393-403.
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Luke A, Schoeller DA. Basal metabolic rate, fat-free mass, and body cell mass during energy restriction. Metabolism. 1992 Apr;41(4):450-6. Review.
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Mansell PI, MacDonald IA. The effect of underfeeding on the physiological response to food ingestion in normal weight women.
Br J Nutr. 1988 Jul;60(1):39-48. -
de Rosa G, et al. Thyroid function in altered nutritional state.
Exp Clin Endocrinol. 1983 Aug;82(2):173-7. -
Weyer C, et al. Changes in energy metabolism in response to 48 h of overfeeding and fasting in Caucasians and Pima Indians. Int J Obes Relat Metab Disord. 2001 May;25(5):593-600.
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Klein S, et al. Leptin production during early starvation in lean and obese women. Am J Physiol Endocrinol Metab. 2000 Feb;278(2):E280-4.
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Ahima RS, Flier JS. Leptin. Annu Rev Physiol. 2000;62:413-37. Review.
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Bowles L, Kopelman P. Leptin: of mice and men? J Clin Pathol 2001 Jan;54(1):1-3
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Ahima RS, et al. Leptin regulation of neuroendocrine systems. Front Neuroendocrinolgy 2000 Jul;21(3):263-307.
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van Dijk G. The role of leptin in regulation of energy balance and adiposity. J Neuroendocrinol 2001 Oct;13(10):913-21.
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Hespel P, et al. Opposite actions of caffeine and creatine on muscle relaxation time in humans. J Appl Physiol. 2002 Feb;92(2):513-8.
Joel…good work on the article - it was as comprehensive a composition as any that have been in TMag. However, I would like to see you justify yourself by identifying the study that best supports your recommendations and conclusions…do it, and satisfy your critics and your supporters. Simple.
Phil
I think hes pointing at this study:
Response of leptin to short-term and prolonged overfeeding in humans.
Kolaczynski JW, Ohannesian JP, Considine RV, Marco CC, Caro JF.
It shows that acute overfeeding in normal males raises circulating leptin levels by 40% which persists until the next morning. Now I only have access to the abstract so I don’t know the answers to the following questions which may be answered in the full article:
- When the overfeeding was (morning or afternoon of the first day) so I cannot tell whether levels are raised 40% above baseline for 8+ hours or 12+ hours
- How quickly circulating leptin comes down from 40% above baseline
- Whether the response in a severely dieting person would be different
The other references in the article cite metabolic changes that happen via increased leptin.
Sorry to butt in but I thought I'd have a crack at this since this thread seems to be going round in circles.
-eXp
Thank you to those individuals who put some time into their posts on the protocols behalf. I posted two references above.
Surfer Girl- A few individuals asked me for an example strict day, so I just copied a page out of my dietary log. I get Myoplex Products for $0.00 dollars, so that's the economical choice for me. I'm not recommending them, just simply wrote them down because that is what I consumed.
King Protein- Yes, it is neccessary to diet severely to get the optimal effect, BUT should you choose a more moderate approach with 4-AD-EC, I think something along the lines of one cheat meal with one CHO refeed, or 2 cheat meals would work well. Also, cut out the cardio after the weight training and only do 3 HIIT sessions. I didn't mean for the article to address any other issue than severe dieting on androgens; however, overfeeding can be beneficial with a more moderate approach.
Bronx Bomber- What kind of approach will you be using?
As far as the low fat recommendations, when only consuming 1500 calories and using carbs post workout, that doesn't leave much room for fat intake. If you are going to consume more calories with a more moderate approach, certainly bump fat up to ~25%. Again, it's hard to make specific recommendations for anything different than what the article describes. Take a look at your past experiences with cheating and make a sensible choice. My recommdendations are either 2 cheat meals, 2 CHO refeeds, or 1 of each. Good luck, and contact me should you need any further guidance- I'm here to help.
Great article Joel. I used this approach during this past summer, and it definitely works. I was able to finally reach sub 10% for the first time ever. This was while adding some LBM. One thing I noticed that increased the results was to refeed after training. It allowed me to really put away the carbs with zero noticable fat gain the day after. Another thing is that as I got leaner, I found I had to increase the number of refeeds to keep fat loss going. I would have been even leaner if I had figured this out sooner rather than later. Oh well, live and learn. Steve
I just wanted to back Joel here. I have done cheat meals/days during extreme dieting and they have worked well for me. I usually do an entire cheat day on sunday and not only does it not hinder progress but I believe it really does have benefits. I’m going to try cheat meals only on wed and sat one week and then CHO feedings the next week and see how it goes.
Leptin…??? Leptin??? Stop, seriously, you’re making me laugh. Excuse me, but you’re touching upon a subject that was long forgotten about. Leptin was big a few years ago until we discovered that it has no significant effect in normal humans, but in mice lacking the gene is sure works great! Oh and yes, it does matter that I have a doctorate in Physiology and Biophysis as this is my life and I don’t merely read the studies, I submit them for publishing! Your lack of knowledge about leptin demonstrates what I found at the end of your article…a major in exercise science…this explains it all. Here’s an abstract that will get you caught up. Come back when you’ve taken at least one graduate level course involving physiology.
Obes Res 2001 Aug;9(8):462-9
The effects of leptin administration in non-obese human subjects.
Mackintosh RM, Hirsch J.
OBJECTIVE: Body fatness is partly under hypothalamic control with effector limbs that include the endocrine system and the autonomic nervous system (ANS). In previous studies of both obese and never-obese subjects, we have shown that weight increase leads to increased sympathetic and decreased parasympathetic activity, whereas weight decrease leads to decreased sympathetic and increased parasympathetic activity. We now report on the effect of leptin, independent of weight change, on the ANS. RESEARCH METHODS AND PROCEDURES: Normal weight males (ages 20-40 years) were fed a solid food diet, measured carefully to maintain body weight, for 3 weeks, as inpatients at the Rockefeller University General Clinical Research Center. In a single-blind, 22-day, placebo/drug/placebo design, six subjects received leptin 0.3 mg/kilogram subcutaneously for 6 days. ANS measures of amount of parasympathetic control and sympathetic control of heart period (interbeat interval) were made by sequential pharmacological blockade with intravenous atropine and esmolol. Norepinephrine, dopamine, and epinephrine levels in 24-hour urine collections were also measured as well as resting metabolic rate. RESULTS: Sufficient food intake maintained constant body weight in all subjects. There was no evidence that leptin administration led to changes in energy metabolism sufficient to require additional food intake or to alter resting metabolic rate. Likewise, leptin administration did not alter autonomic activity. Parasympathetic control and sympathetic control, as well as the urinary catecholamines, were not significantly affected by leptin administration. Glucose and insulin levels were increased by food intake as expected, but leptin had no affect on these levels before or after food intake. DISCUSSION: ANS responses to changes in energy metabolism found when food intake and body weight are altered were not found in these never-obese subjects given leptin for 6 days. Although exogenous leptin administration has profound effects on food intake and energy metabolism in animals genetically deprived of leptin, we found it to have no demonstrable effect on energy metabolism in never-obese humans. The effects of longer periods of administration to obese individuals and to those who have lost weight demand additional investigation.
Horm Res 2002;58(2):88-93
In vitro Effects of Leptin on Human Adipocyte Metabolism.
Elimam A, Kamel A, Marcus C.
Objective: Leptin receptors are expressed in adipocytes, suggesting potential autocrine/paracrine effects. Studies on the direct effects of leptin on adipose tissue metabolism in different species have yielded controversial data. To assess the in vitro effects of leptin on human adipocyte metabolism: lipolysis, the insulin-induced inhibition of lipolysis and lipogenesis were studied in adipocytes obtained from infants and adults. Methods: Lipolysis was studied by incubating adipocytes with increasing concentrations of leptin or isoprenaline. Glycerol in the incubation medium was measured as an indicator of lipolysis. For the lipogenesis and insulin-induced inhibition of lipolysis experiments, the cells were preincubated with 0, 25, or 250 ng/ml of leptin for 2 h. Results: Leptin did not stimulate lipolysis in human adipocytes, either in children or adults. Preincubation with leptin did not affect the insulin-induced inhibition of lipolysis, but decreased the insulin-induced lipogenesis (p < 0.05). Conclusions: This study shows that leptin has no direct lipolytic effect in human adipocytes. The lack of effect on the insulin-induced inhibition of lipolysis and the negative effect on lipogenesis indicates that the effect of leptin is not at the proximal insulin-signalling pathway but further downstream. Copyright 2002 S. Karger AG, Basel