Since our body’s are designed to store fat in times of famine and stress. Wouldn’t it make since that cortisol is not only catabolic but can be anti lipogenic and pro fat storing to protect itself? Therfore since carbs are needed to reduce cortisol wouldn’t being on a low carb, low calorie diet all the time keep cortisol levels elevated and potential thwart fat loss especially around those last inches of protective fat? I am not just talking about post exercise induced cortisol, I am also talking about cortisols natural rise in the morning, how would it ever lower if you stay low carb all day like fat fast, keto diet or allesi’s recommendations to keep carbs low & use low carb grow and glutamine postworkout?Any thoughts here guys? I think I have been experiencing this because I have been busting my ass with meltdown training and intervals, again very CORTISOl ELEVATING, & using low carb grow and glutamine PWO , also keeping carbs to 30 g of veggies daily and getting in flax, and fish oil, My body is not burning fat from the area’s I desire like abdomen, I think actually my little rolls look more prevailant despite my strict eating and hardcore training. This protocol I think actually just stresses your nervous system out more causing even more rise in cortisol, not increases in fat loss. Any experts please reply.
Cortisol definately causes lipolysis(fat mobilization) and has recently been shown to do so. Am J Physiol Endocrinol Metab 2002 Jul;283(1):E172-7. Effects of cortisol on lipolysis and regional interstitial glycerol levels in humans.
Djurhuus CB, Gravholt CH, Nielsen S, Mengel A, Christiansen JS, Schmitz OE, Moller N.
Department of Endocrinology and Diabetes, University Hospital of Aarhus, Aarhus Kommunehospital, Denmark. cbd@dadlnet.dk
Cortisol’s effects on lipid metabolism are controversial and may involve stimulation of both lipolysis and lipogenesis. This study was undertaken to define the role of physiological hypercortisolemia on systemic and regional lipolysis in humans. We investigated seven healthy young male volunteers after an overnight fast on two occasions by means of microdialysis and palmitate turnover in a placebo-controlled manner with a pancreatic pituitary clamp involving inhibition with somatostatin and substitution of growth hormone, glucagon, and insulin at basal levels. Hydrocortisone infusion increased circulating concentrations of cortisol (888 +/- 12 vs. 245 +/- 7 nmol/l). Interstitial glycerol concentrations rose in parallel in abdominal (327 +/- 35 vs. 156 +/- 30 micromol/l; P = 0.05) and femoral (178 +/- 28 vs. 91 +/- 22 micromol/l; P = 0.02) adipose tissue. Systemic [(3)H]palmitate turnover increased (165 +/- 17 vs. 92 +/- 24 micromol/min; P = 0.01). Levels of insulin, glucagon, and growth hormone were comparable. In conclusion, the present study unmistakably shows that cortisol in physiological concentrations is a potent stimulus of lipolysis and that this effect prevails equally in both femoral and abdominal adipose tissue.
Publication Types:
Clinical Trial
PMID: 12067858 [PubMed - indexed for MEDLINE]
This study shows that cortisol causes lipolysis equally in abdominal and femoral tissue. However we know that people in with Cushing’s disease high super high cortisol but also accumulate fat around their wasteline(central obesity). So there lies a paradoxical situation. Cortisol causes lipolysis in abdominal tissue but people with high cortisol accumulate fat around the abdomen. My explanation is that cortisol initially causes lipolysis but it also induces hormones that cause lipogenesis, especially in the abdominal region. Glucocorticoids, including cortisol, stimulate lipoprotein lipase in abdominal tissue more than other tissues which with time would lead to central obesity. Glucocorticoids also stimulate angiotensin mRNA expression in the abdomen especially. Angiotensin and especially angiotensin 2 raise blood pressure but they also stimulate lipogeneis big time. So my theory is that cortisol causes central fat accumulation primarily by raising abdominal LPL and angiotensin 2.
Bill? Cy? Berardi? What do you think?
bump
Whether ketosis increases cortisol I wasn’t sure until I came across this study that shows it does (at least in diabetics). Diabetes Care 1982 May-Jun;5 Suppl 1:38-47.Hormone and metabolic profiles in children and adolescents with type I diabetes mellitus.
MacGillivray MH, Voorhess ML, Putnam TI, Li PK, Schaefer PA, Bruck E.
Diurnal concentrations of glucose, the major regulatory hormones, and selected biochemistries were measured serially throughout a 25-h period in 38 healthy type I diabetic patients, 25 patients with acute ketoacidosis, and 20 normal subjects. Poor glucose control, meal intolerance, and hypercortisolemia were the dominant abnormalities in the healthy diabetic subjects. Ketonemia due to elevated plasma beta-hydroxybutyrate concentrations without ketonuria (nitroprusside reaction) was a frequent finding in a group of poorly controlled diabetic subjects. In the patients with acute ketoacidosis, the dominant abnormalities were overproduction of epinephrine and cortisol. High glucagon and growth hormone concentrations were documented in about one-half of these patients. We conclude that (1) the hyperglycemia, meal intolerance, and abnormal ketone body metabolism seen in these patients are caused by inadequacies in their insulin regimens; (2) ketone body underutilization contributes to diabetic ketosis; (3) epinephrine and cortisol overproduction are important components of acute ketoacidosis; and (4) the complex hormone-metabolic interactions in type I diabetes can best be explained by a multihormonal hypothesis with the primary defect being loss of beta-cell function.
PMID: 6821306 [PubMed - indexed for MEDLINE]
Now if this also occurs in normal people on ketogenic diets (which it probably does) then being on on keto diet would make it harder to lose those last few inches around the abdomen. However, I known a lot of bodybuilders who achieved fairly ripped abdomens following a pre-contest keto-diet. My theory is that a keto-diet would speed fat loss; however, the abdominal fat would probably be the last to go. So if you are going for the ripped six pack I would recommend some carbs at least after your workout. Like JMB has pointed out recent research has demonstrated that fat burning is not inhibited in the post-workout period with carb consumption.
I think Ken is failing to differentiate subcutaneous adipose tissue from visceral adipose tissue. Cortisol in normal humans plays an integral part in stimulating lipolysis in subcutaneous adipose tissue,whereas in visceral adipose (noted in central abdominal obesity) it increases LPL and causes a gain or accumulation of visceral fat.
There’s no need for ingestion of carbs and then raising insulin which is lipogenic during a phase meant for ketosis and fat loss.
Thanks for the input Moonpiephil. I was oversimplifing the situation in my mind. Of course I know there is a difference between subcutaneous and visceral fat stores. Cortisol causes an increase in visceral fat stores and not subcutaneous. I am certain that the researchers mentioned above were comparing the lipolysis in femoral versus visceral(abdominal) fat even though they did not specify in the abstract. It would be ridiculous for them to study the effects of cortisol on subcutaneous fat stores because it is well known that central obesity is caused primarily by an increase in visceral fat stores. Therefore, a keto diet would still make it harder to lose visceral fat than subcutaneous fat. And like I already said recent research demonstrates taking carbs after a workout does not affect fat burning. It may knock you out of ketosis for a little while but you will still burn fat. Research still has not shown keto diets to be superior for fat loss anyway (J Okla State Med Assoc 2002 May;95(5):329-31). Fat loss is much more complicated than just taking into account insulin and blood sugar levels.
Yes, but you’re still failing to realize that visceral fat plays no role in how we look so it’s not something to be concerned with in terms of aesthetics. If you’re looking to have a “lean” appearance then subcutaneous fat is what you should be concerned with, and if you’re wanting to stay “healthy” then worry more about visceral fat.
These studies need to be taken a look at. I think cortisol is the reason some may not lose weight on a keto diet.
Moonpiephil, you are right that for looks subcutaneous fat is more important. However, I am also interested in being healthy. Now that I have my abstracts handy let me point some things out. Cortisol increases aromatase activity which will lead the higher estrogen levels (J Steroid Biochem 1988 Apr;29(4):393-399). Estrogens lead to subcutaneous fat deposition (Am J Physiol 1999 Feb;276(2 Pt 1):E317-25). This is one way cortisol may increase subcutaneous fat. More importantly, cortisol has been shown to decrease subcutaneous lipolysis while increasing whole body lipolysis ( J Clin Endocrinol Metab 1998 Feb;83(2):626-31). This is probably one reason why the researchers in the first study I mentioned noted a increase in lipolysis in femoral and abdominal tissue while other observations have noted that cortisol can increases total abdominal fat (s.c. and visceral) in the long run. Therefore by increasing cortisol it could make it more difficult to lose fat not only in visceral but subcutaneous fat as well. In my opinion a ketogenic diet may raise cortisol and make fat loss more difficult than if some carbohydrates are included in the diet at least in the post-workout period. This is especially true since fat oxidation is not suppressed post-exercise even in the presence of a huge amount of carbohydrates(400 grams)(Br J Nutr 2001 Jun;85(6):671-80).
Ken, Great posts. As you know by my threads I am sure, I have a strong interest in endocrinology as well in relation to bb’ing so I have a few questions for the table here.
One, in the studies you mentioned, was calorie balance controlled? I think the ULTIMATE player in fat loss is calorie balance, and I think all too often this is overlooked.
Two, the studies bring up an intriguing point that relates back to the caffeine discussion on this board a while back. With this post in mind, caffeine could really impede the lower ab fat loss by two mechanisms: reduced insulin sensitivity and the facilitation of increased cortisol output. Now i have done keto diets many times, and do rip up on them, but the one area that I fail to ultimately deplete is the lower abdominal surface sponge fat. Now let me say this…this summer I have been dieting since last April with intermittent increases in caloric intake (thus, periods of off dieting)…what i have found is that while a strict keto at the beginning ripped up the majority of me, I had to raise calories and carbs over the summer with a mild calorice deficit (approx -500/day) to actually slowly rip the hell out of this area…I still have a tincy bit of spongey fat left, but let me say that I am the most ripped i have ever been…so interestingly enough, this whole cortisol debate may have some merit.
ANy personal experience out there?
Out,
Vain
Vain-was your calorie increase with carbs? Currently, I am doing a CKD with meltdown/interval stairs and have felt a strength/muscle loss and increased fat gain(calipers) just in the abdominal area. I had thoughts that it may be cortisol as well, so I have increased fat calories to produce a greater fat to protein ratio- to about 500cals below maintenence. Also planning on switching to a MWF or trad CKD training. Ken might be on to a better way with TKD, and I plan to change to that if the above does not work in the next two weeks. This is my first time with the CKD. How do you train when ripping up?
Ken, no offense but you really shouldn’t try to draw conclusions simply based on a few abstracts and then think that you have a sound theory. For every abstract you can find, I can find one disputing it.
I also found an abstract that demonstrates the ingestion of carbs or glucose actually amplifies levels of cortisol.
J Clin Endocrinol Metab 2002 Mar;87(3):1327-36 Related Articles, OMIM, Books, LinkOut
Glucocorticoid regulation of p450 aromatase activity in human adipose tissue: gender and site differences.
McTernan PG, Anderson LA, Anwar AJ, Eggo MC, Crocker J, Barnett AH, Stewart PM, Kumar S.
Division of Medical Sciences, University of Birmingham, Birmingham B15 2TH. p.g.mcternan.20@bham.ac.uk
The distinct gender-specific patterns of fat distribution in men and women (android and gynoid) suggest a role for sex steroids. In keeping with these observations, it has been suggested that estrogens can promote preadipocyte cell proliferation and/or differentiation. The enzyme aromatase P450 is responsible for the conversion of androgen precursor steroids to estrogens and may, therefore, have a role in regulating adipose tissue mass and its distribution. We have investigated the glucocorticoid regulation of aromatase expression in human adipose tissue, specifically to define any site- and gender-specific differences. Abdominal subcutaneous (Sc) and omental (Om) adipose tissue was obtained from male and female patients undergoing elective surgery. After collagenase digestion, preadipocytes were cultured in serum-free medium, for 6-10 d, until confluent with either cortisol (10(-6) M, 10(-7) M) or insulin (500 nM) or a combination of both treatments. Adipocytes were studied in suspension cultures. Aromatase activity was assessed using tritiated [1 beta-(3)H]-androstenedione as substrate. In Sc preadipocytes, basal aromatase activity increased in females from 11.5 +/- 1.4 (mean plus minus SEM) to 28.0 +/- 1.8 pmol/mg x h (n = 17, P < 0.05) with 10(-6) M cortisol. By contrast, in males, aromatase activity was inhibited by 10(-6) M cortisol (19.4 +/- 2.4 pmol/mg x h vs. 7.5 +/- 1.3, n = 9, P < 0.01; men vs. women, P < 0.005). These data were endorsed through Western blot analysis using an in-house antihuman aromatase antibody, which recognized a specific 55-kDa species. Aromatase activity was less at Om sites in preadipocytes, increasing in females from 1.1 +/- 0.2 to 3.2 +/- 0.7 pmol/mg x h with 10(-6) M cortisol (P < 0.05) and in males from 2.6 +/- 0.1 pmol/mg x h to 7.8 +/- 0.3 pmol/mg x h after cortisol (men vs. women, P < 0.001). Cortisol-induced aromatase activity in Om adipocytes from postmenopausal females was higher than that in premenopausal females (P < 0.001). Insulin had no independent effect on aromatase expression, but coincubation of preadipocytes with cortisol and insulin eliminated both gender- and site-specific differences. In conclusion, in women, but not men, cortisol increased aromatase activity at Sc sites, and this may facilitate predilection for Sc adiposity in females. The observed site-, gender-, and menopausal-specific differences in the glucocorticoid regulation of this enzyme may contribute to the gender- and menopausal-specific patterns of fat distribution.
Am J Physiol 1996 Dec;271(6 Pt 1):E996-1002 Related Articles, Books, LinkOut
Effects of morning rise in cortisol concentration on regulation of lipolysis in subcutaneous adipose tissue.
Samra JS, Clark ML, Humphreys SM, Macdonald IA, Matthews DR, Frayn KN.
Nuffield Department of Clinical Medicine, Radcliffe Infirmary, Oxford, United Kingdom.
Cortisol has a well-defined circadian rhythm. The aim of the study was to examine the effect of the morning rise in cortisol concentration on lipolysis in adipose tissue. Ten healthy subjects were studied on two occasions, and six of these were studied on three occasions. During the first two occasions, either a control or cortisol suppression study was performed by using metyrapone, and on the third occasion exogenous cortisol replacement was given in addition to metyrapone. Lipolysis in the subcutaneous adipose tissue of the anterior abdominal wall was studied by measurement of arteriovenous differences. Reduction in the early morning rise in cortisol led to significantly decreased venoarterialized differences for nonesterified fatty acids (P < 0.05) and glycerol (P < 0.01), attributable in part to decreased hormone-sensitive lipase (EC 3.1.1.3) action (P < 0.05) in adipose tissue. At the same time the arterialized plasma triacylglycerol concentration increased (P < 0.005) with a significant reduction in the adipose lipoprotein lipase (EC 3.1.1.34) rate of action (P < 0.05). In the replacement study, values were identical to those of the control study, showing that metyrapone had no nonspecific effects on lipolysis. We conclude that the morning rise in plasma cortisol concentration plays an important role in the regulation of lipolysis in adipose tissue in normal healthy adults.
Horm Behav 2002 May;41(3):328-33 Related Articles, Books, LinkOut
Glucose but not protein or fat load amplifies the cortisol response to psychosocial stress.
Gonzalez-Bono E, Rohleder N, Hellhammer DH, Salvador A, Kirschbaum C.
Department of Psychology, University of Valencia, Spain.
We previously reported that glucose intake amplifies cortisol response to psychosocial stress and smoking in healthy young men, while low blood glucose levels prevented the stress-induced activation of the hypothalamus pituitary adrenal (HPA) axis. However, it remains unknown whether this modulation is specific for glucose load or a more common effect of energy availability. To elucidate this question, 37 healthy men, who fasted for at least 8 h before the experiment, were randomly assigned to four experimental groups, who received glucose (n = 8), protein (n = 10), fat (n = 10), and water (n = 9), one h before their exposure to the Trier Social Stress Test (TSST). Blood glucose levels were measured at baseline and following stress, while salivary cortisol was assessed repeatedly measured before after the TSST. The results show that both absolute cortisol levels and net cortisol increase were greater in the glucose group in comparison to the other groups (F(3,33) = 3.00, P < 0.05 and F(3,33) = 3.08, P < 0.05, respectively. No group differences were observed with respect to perceived stress and mood. Furthermore, the cortisol response was positively correlated with blood glucose changes (r = 0.49, P < 0.002). In conclusion, the results suggest a central mechanism responsible for regulation of energy balance and HPA axis activation, rather than peripheral mechanisms. We thus recommend controlling for blood glucose levels when studying HPA axis responsiveness. (c) 2002 Elsevier Science (USA).
Vain68, the studies I mentioned were acute in nature so it would be difficult to estimate how total calories fit into the mix. I believe the measures were taken after an overnight fast. Moonpiephil, those were some interesting abstracts you came up with and they do have some merit. However, I use research to attempt to explain real world observations. For example, people with hypercortisolemia (Cushings)have increased abdominal fat in mainly visceral but also subcutaneous fat. High stress activity is also linked to central obesity. Most of the studies we provided are only acute in nature and do not tell the whole story. From real world observations it is obvious that high cortisol leads to central obesity, research aside. I know that when I am stressed I see an increase in abdominal fat (s.c. and visceral) and apparently many others do. I can maintain 5-6% body fat through just diet and training but if I add a thermogenic, which can increase cortisol, I find I hard to go any lower and it becomes especially hard to lose my s.c. abdominal fat. Cortisol definately causes acute lipolysis as I have already mentioned I am just using research to try and figure out why this is not the case in the long term. I used estrogen as an example of why cortisol may increase s.c. fat not as a proven fact. That study was in vitro anyways so it may not apply totally in a real human it just gives us an idea. Other in vitro studies show that cortisol increases pre-adipocyte differentiation which is definately not disireable. As far as glucose stimulating cortisol secretion I never said that high blood glucose levels are desireable anyway, except perhaps in the the post-workout period, but like I said high glucose does not affect fat oxidation in this period. A nice stable blood glucose level from eating low glycemic carbs is better for fat burning. The body requires oxaloacetate from carbohydrate metabolism to burn fat most efficiently anyway. Cortisol may be increased from high blood glucose levels but it is also definatley increased during ketogenesis. I am just suggesting that lower blood glucose may be beneficial but not low enough to go keto-genic. If cortisol is incresed by high glucose then perhaps this is why so many americans who eat a high sugar diet along with high stress jobs accumulate abdominal obesity. You see I just use the research to explain real world results. I think the biggest reason cortisol may make it harder to lose abdominal fat is because it increases angiotensinogen mRNA as I have already mentioned. Angiotensinogen and especially angiotensin 2 increase lipogensis especially in the abdominal region and they are increased by glucocorticoids. Now instead of using research to disprove real world observations why don’t you use research to help understand them.
Ken…I give up as it’s hard to debate with someone who doesn’t understand research nor have much of a good background and don’t tell me “I have a BSc in Biology” either as that’s a joke.
Anyhow, using research to explain real world results!!!
Do you know how many factors contribute to real world results? Ok, so for instance, you’re saying that a high level of cortisol is what causes one to reach a point where they can’t lose fat in the “real world” as you say, ok so I suppose insulin isn’t something to be considered in terms of fat gain? I think not. If you had a clue, you’d know that there isn’t ONE cut and dry mechanism for many things in the human body, including fat loss.
Cortisol does NOT conserve subcutaneous fat and oh yeah, ingesting carbs does reduce fatty acid oxidation…get a clue!
Last but not least, I’m sorry but normal humans, EVEN when in a ketogenic state aren’t suffering from hypercortisolemia so your comparison is invalid.
Oh and stop changing your story every other minute. First you say that “Therefore by increasing cortisol it could make it more difficult to lose fat not only in visceral but subcutaneous fat as well. In my opinion a ketogenic diet may raise cortisol and make fat loss more difficult than if some carbohydrates are included in the diet at least in the post-workout period.”
Ok so you’re WHOLE point is that a ketogenic diet doesn’t allow for fat loss or slows it simply because it causes a rise in cortisol and therefore, carbs should be included which cause a rise in blood glucose levels. Ok so then I provide evidence that increasing glucose levels causes a rise in cortisol and then you say some more retarded things that make little sense and it goes on and on. Sad.
A ketogenic diet hasn’t been shown to be superior??!! UM ok, try searching medline a little more junior!
You keep going on and even admitted that visceral fat is the tissue that is increased by cortisol and yet you keep going on about how it doesn’t allow for a six pack.
Last, you sit there and say that you notice that both visceral fat and subQ fat increases in times of stress? Hmmm…exactly how do you measure visceral fat with the naked eye? I’d like to hear this one!
I appreciate the intense science that both of you guys are submitting. But, so it can help us from a practical viewpoint: what is the summary bottomline? IOW, if we keep our systemic insulin levels low, except post-work-out, do regular sprint cardio and lift regularly, that’s how we keep the fat off, correct? I know its KISS…
I used to be pro ketogenic diet 100%, even considering the fact that I never lost much fat on them. I was concious of controlling calories, got enough protein, worked out, etc., but I never lost even giving the diet several weeks at a time on MANY occasions over the last 3 yrs. As Lyle McDonald points out, no diet is truly superior to any other. Keto diets are just a tool and work for some, but dont work well for others. It took me a long time to realize this, but its true. Yes, lower carbohydrate diets do allow for overall better fat loss with more muscle retention, generally speaking. But a true ketogenic diet, despite all the adaptions the human body makes to utilize its main fuel via fats, isn’t really superior to a moderate to low carb diet that isn’t ketogenic, or one that allows deep ketosis (say 30g carbs or less) Again, its individual. One thing that should be realized is the rise in cortisol is short lived when switching to a ketogenic diet and doesn’t remain elevated over a balanced diet at a given calorie defecit.
Well said flex69, I’ll certainly concur with that. 
Just want to point out to Ken Stark that the second study you presented is about humans who suffer from Ketoacidosis (“In the patients with acute ketoacidosis, the dominant abnormalities were overproduction of epinephrine and cortisol.”)and thus you can’t say that this also happens in normal people who don’t suffer from this condition.