Anyone Shed Their Belly-hip Fat?

[kayumochi]

Dropping all liquid fats worked for me.

 

[BigBrain]

adrenaline works amazing for fat loss with minimal to non muscle loose (if you keep weight lifting) , also you need to get more protein like beef and milk. I cant understand how ppl say stress hormones re so evil bad . They re defenitly needed for rapid weight loss particularly the stubborn fat. Believe you will never ever loose it with out those stress hormone like adrenaline. Also if you have more thyroid t3 hormones your catecholamine will have much stronger impact. Increased adrenaline will also increase your T,DHT and HGH which is also very nice for fat Loss

 

[schultz]

Pavel and Dan John have a good book called Easy Strength that is focused on frequent low to mid weight strength training with intuitive progression. The emphasis is on habitually doing the work not on exactly how much you lift. Also kettlebell workouts in general are great for fat loss. You want to do explosive compound movements, not long duration and not heavy.

Oh cool, I wasn't aware they did a book together.

find out your maintenance calorie intake. Drop that with 10 or 20%, start walk a bit more. Do some strength training. Eat Peaty foods with focus on low fat

Exactly. I would imagine this advice would work for the majority of people.

@schultz did you accompany this with any specific dietary changes? Or was it just calories in vs calories out?

Yah I tend to be much more controlled when I'm consciously trying to lose fat. Things like getting gelatin everyday (3 or 4 tbsp), whereas normally I wouldn't be so consistent. I drink a lot of latte's throughout the day and it's my main source of calories. I switched from 1% to skim and then I add 1 tsp of MCT oil for every 1.5 cups of milk into the latte with 1 tsbp sugar and 5g of Taster's Choice instant coffee. I drink around 5 of these a day or so and really enjoy them. Since it's winter I make broth (like a mushroom and leafy greens broth) and add gelatin to it. I have this for lunch with orange juice, sometimes with a slice of sourdough. I don't go crazy on starch because I'm prone to overeating it, but a slice of bread a day is no biggie, especially since I make the bread myself and sour it for quite a while (24-36 hours).

Fat tends to be 40g or so per day. Calories are around 2200 per day. A friend of mine loses weight consistently at this amount of calories exactly like me and we have sort of decided it's the perfect amount for fat loss (at least for us). He kept his calories at 2200 last spring and just kept dropping fat until he was quite low with no negative side effects. He walked a lot and weight trained once a week or sometimes once every 2 weeks (nothing crazy). He was insanely lean. We will see if the same thing happens to me.

 

[DuggaDugga]

adrenaline works amazing for fat loss with minimal to non muscle loose (if you keep weight lifting) , also you need to get more protein like beef and milk. I cant understand how ppl say stress hormones re so evil bad . They re defenitly needed for rapid weight loss particularly the stubborn fat. Believe you will never ever loose it with out those stress hormone like adrenaline. Also if you have more thyroid t3 hormones your catecholamine will have much stronger impact. Increased adrenaline will also increase your T,DHT and HGH which is also very nice for fat Loss

The stress hormones are catabolic to muscle tissue, which are used as substrate for gluconeogenesis. Many, many studies on the effects of cortisol and adrenaline on adipose growth and differentiation (especially abdominal) are available on pubmed. So, no, stress hormones are not required for fat loss. Quite the opposite actually. Muscle preferentially burns fat at rest. The best thing you can do is to avoid stress hormones to keep fatty acids from being released into the blood stream where they inhibit glucose uptake. There are countless studies on the effects of stress hormones down-regulating thyroid activation and the production of testosterone. It's important to consider what you're communicating to your body when you induce stress hormones: the need to spare glucose for the brain and RBC (insulin resistance), the decreased importance of immunity and reproduction, and whatever else it takes to survive short-term in the face of a threat. This isn't something beneficial to low-fat, high-muscle, and general well-being.

Interaction of the endocrine system with inflammation: a function of energy and volume regulation

Cortisol was demonstrated to be a muscle-catabolic factor inducing rapid release of amino acids from muscle [43]. Glucocorticoids stimulate overall lipolysis at the whole-body level [44], but glucocorticoids may specifically inhibit abdominal lipolysis because chronic hypercortisolemia secondary to Cushing’s syndrome is characterized by distinct abdominal obesity. Recent data point toward cortisol-induced increase of visceral fat on the basis of visceral 11β-hydroxysteroid dehydrogenase type 1 availability [45]. Thus, cortisol would support lipolysis and re-allocation of lipids to visceral stores and elsewhere.

Cortisol is an important stimulator of glycogenolysis and gluconeogenesis in the liver [46]. Cortisol inhibits bone formation by blocking osteoblasts, decreasing osteocalcin levels, and interfering with several other pathways [37]. Cortisol supports insulin resistance so that energy-rich substrates cannot be taken up into muscle, liver, and fat tissue [47].

Acute response of human muscle protein to catabolic hormones.
Cortisol increases gluconeogenesis in humans: its role in the metabolic syndrome. - PubMed - NCBI

 

[BigBrain]

thats bull ***t in my own experience cortisol is catabolic yes also maybe adrenaline, but i dont say you have to increase it chronically only temporary. Also alot of bodybuilder use ephidrine for fat loss paricularly the stubborn fat.
Also like i said a increased t3 will automatically increase cortisol and adrenaline production it will increase all hormones. And im talkin about super lean the last % of bodyfat only can be lost by adrenaline and alot of t3 androgens.

Yes of course cortisol will lead chornically to more fat and more muscle loose , because the body usees cholesterol then only for chortisol production then the body cant use it for adrogen synthisis because its used for chortisol. As consequence you loose muscle and gain fat. And there is evidence that 10 kg muscle only burn about 100 calories per ****** day thats nothin. So pls dont post bull****. Also adrenaline isnt made from cholesterol so it dont take the precursor for androgens synthisis. Adrenaline highly supports lypolsis and increase DHT significantly. The Study you showed above is for cortisol and like i said cortisol can increase your performance in sports, but im still not a fan of it because it take not only from bodyfat the energy also from muscle issues. BUT THATS NOT THE CASE for adrenaline.

Sorry for beeing little bit aggresive but you guys dont have seem experience in those things. So dont take it personally i dont want to attack some1 thats my experience

 

[DuggaDugga]

thats bull ***t in my own experience cortisol is catabolic yes also maybe adrenaline, but i dont say you have to increase it chronically only temporary. Also alot of bodybuilder use ephidrine for fat loss paricularly the stubborn fat.
Also like i said a increased t3 will automatically increase cortisol and adrenaline production it will increase all hormones. And im talkin about super lean the last % of bodyfat only can be lost by adrenaline and alot of t3 androgens.

Yes of course cortisol will lead chornically to more fat and more muscle loose , because the body usees cholesterol then only for chortisol production then the body cant use it for adrogen synthisis because its used for chortisol. As consequence you loose muscle and gain fat. And there is evidence that 10 kg muscle only burn about 100 calories per ****** day thats nothin. So pls dont post bull****. Also adrenaline isnt made from cholesterol so it dont take the precursor for androgens synthisis. Adrenaline highly supports lypolsis and increase DHT significantly. The Study you showed above is for cortisol and like i said cortisol can increase your performance in sports, but im still not a fan of it because it take not only from bodyfat the energy also from muscle issues. BUT THATS NOT THE CASE for adrenaline.

Sorry for beeing little bit aggresive but you guys dont have seem experience in those things. So dont take it personally i dont want to attack some1 thats my experience

Post research backing any of what you're saying and I'll address it directly.
Start by explaining mechanistically how "temporary" cortisol and adrenaline promote health. Also explain how lypolysis is beneficial to supporting oxidative metabolism, insulin sensitivity, and thyroid function.
Provide references.

 

[mattypolso]

Dropping all liquid fats worked for me.

Do you include coconut oil in this? So I'm assuming you keep fats to dairy fat, butter, tallow?

 

[BigBrain]

here study says high intensity workout (adrenaline)
High-Intensity Intermittent Exercise and Fat Loss

acute and chronic stress
Acute Stress Enhances while Chronic Stress Suppresses Cell-Mediated Immunityin Vivo:A Potential Role for Leukocyte Trafficking - ScienceDirect

resting metabolic rate (muscle)
Evaluation of Specific Metabolic Rates of Major Organs and Tissues: Comparison Between Men and Women

here are some of them there maybe alot more but you can look up if you want

 

[kayumochi]

Do you include coconut oil in this? So I'm assuming you keep fats to dairy fat, butter, tallow?

Nope. I gorged on coconut oil for years and only when I gave up all liquid fats, including coconut oil, butter, lard, etc did that stubborn fat go away. I am not recommending that you or anyone else give up all liquid fats (and consume only fats that meat & dairy contain) but am only pointing out what worked for me.

 

[DuggaDugga]

This is going to have to be a multi-part response, but let's start from the top:

here study says high intensity workout (adrenaline)
High-Intensity Intermittent Exercise and Fat Loss

So first I'll note that you called out 'adrenaline' in parentheses, which aligns with previous statements you've made about the supposed benefits of adrenaline as distinguished from other stress hormones like cortisol. In the paper you provided on high intensity exercise, they explicitly note that all the stress hormones increase during and for some duration after exercise:

Hormones that have been shown to increase during HIIE include catecholamines, cortisol, and growth hormones. Catecholamine response has been shown to be significantly elevated after Wingate sprints for both men and women [17, 18]. Catecholamine response to HIIE protocols that are less intensive than the Wingate protocol have also been shown to be elevated. For example, Christmass et al. [19] measured catecholamine response to long (24 s/36 s recovery) and short (6 s/9 s recovery) bout intermittent treadmill exercise and found that norepinephrine was significantly elevated postexercise. Also Trapp et al. [15] found significantly elevated epinephrine and norepinephrine levels after 20 min of HIIE cycle exercise (8 s/12 s and 12 s/24 s protocols) in trained and untrained young women. Bracken et al. [16] examined the catecholamine response of 12 males who completed ten 6-second cycle ergometer sprints with a 30-second recovery between each sprint. From baseline, plasma epinephrine increased 6.3-fold, whereas norepinephrine increased 14.5-fold at the end of sprinting (Figure 1). The significant catecholamine response to HIIE is in contrast to moderate, steady state aerobic exercise that results in small increases in epinephrine and norepinephrine [20]. The HIIE catecholamine response is an important feature of this type of exercise as catecholamines, especially epinephrine, have been shown to drive lipolysis and are largely responsible for fat release from both subcutaneous and intramuscular fat stores [21]. Significantly, more β-adrenergic receptors have been found in abdominal compared to subcutaneous fat [22] suggesting that HIIE may have the potential to lower abdominal fat stores. Aerobic endurance training increases β-adrenergic receptor sensitivity in adipose tissue [23]. Interestingly, in endurance trained women, β-adrenergic sensitivity was enhanced, whereas the sensitivity of the anti-lipolytic α2 receptors was diminished [24]. However, no data are available concerning HIIE training effects on β or α2 adrenergic receptor sensitivity of human adipocytes.

GH concentration was still ten times higher than baseline levels after 1 hour of recovery. Venous blood cortisol levels have also been shown to significantly increase after repeated 100 m run sprints in trained males [26], after five 15-second Wingate tests [27], and during and after brief, all-out sprint exercise in type 1 diabetic individuals [28].

So, suppose somehow that adrenaline is still an effective way to lower abdominal fat. How then do we address the fact that growth hormone and cortisol are also increased? How then do we address that each of those hormones induce insulin resistance?
Epinephrine-induced Insulin Resistance in Man
Mechanisms of Glucocorticoid-Induced Insulin Resistance: Focus on Adipose Tissue Function and Lipid Metabolism
Growth hormone induces cellular insulin resistance by uncoupling phosphatidylinositol 3-kinase and its downstream signals in 3T3-L1 adipocytes. - PubMed - NCBI

A common mechanism links the secretion of these hormones. even though the adrenal medulla and cortex have different embryologic origins and biochemical properties and very different mechanisms controlling their secretory activities. ie. a cholinergic nervous input stimulates medullary secretion while a hormone. corticotropin (ACTHI. activates secretion from the cortex. This mechanism is made possible by an intra-adrenal portal vascular system. which provides the medulla with uniquely high concentrations of glucocorticoids. These high concentrations are needed to induce the medullary enzyme. phenylethanolamine-N-methyltransferase (PNMT). which controls the synthesis of epinephrine from norepinephrine.

These data were thought to indicate that: (1) adrenal PNMT activity is largely confined to the medulla; and (2) epinephrine synthesis is controlled by the availability of ACTH, but indirectly, via a route that involvesthe secretion of glucocorticoids from the adrenal cortex

http://web.mit.edu/****/www/pdf/986.pdf

Glucocorticoid and epinephrine are important stress hormones secreted from the adrenal gland during critical illness. Adrenal glucocorticoid stimulates phenylethanolamine N-methyltransferase (PNMT) to convert norepinephrine to epinephrine in the adrenal medulla. Glucocorticoid is sometimes used in catecholamine-resistant septic shock in critically ill patients. By suppressing adrenal glucocorticoid production, glucocorticoid therapy might also reduce the secretion of epinephrine during stress. To investigate this, we used a mouse model subjected to glucocorticoid therapy under basal conditions (experiment 1) and during stress (experiment 2). In experiment 1, pellets containing 0% to 8% dexamethasone were implanted subcutaneously in mice for 4 weeks. In experiment 2, animals received 14 days of intraperitoneal injections of normal saline, low- or high-dose dexamethasone, followed by 2 h of restraint. We found that in experiment 1, adrenal corticosterone did not differ with dexamethasone treatment. Phenylethanolamine N-methyltransferase messenger RNA levels and adrenal catecholamines were highest in the 8% dexamethasone group. Compared with experiment 1, restrained control mice in experiment 2 had high adrenal corticosterone, which decreased with dexamethasone. Phenylethanolamine N-methyltransferase messenger RNA content doubled with restraint but decreased with dexamethasone treatment. As in experiment 1, adrenal catecholamine content increased significantly with dexamethasone treatment. We conclude that without stress, when adrenocorticotropic hormone is low, high doses of exogenous dexamethasone stimulate PNMT and catecholamine synthesis, likely independently of adrenal corticosterone concentration. After stress, adrenocorticotropic hormone levels are elevated, and exogenous dexamethasone suppresses endogenous corticosterone and PNMT production. Nonetheless, catecholamines increase, possibly due to direct neural stimulation, which may override the hormonal regulation of epinephrine synthesis during stress.

Glucocorticoid treatment--effect on adrenal medullary catecholamine production. - PubMed - NCBI

So secretion of glucocorticoids and adrenaline are intimately linked. We can't look at adrenaline in isolation.

Now, I did want to address this point previously quoted and bolded, as I believe this is where the idea that adrenaline is good for fat removal:

Significantly, more β-adrenergic receptors have been found in abdominal compared to subcutaneous fat [22] suggesting that HIIE may have the potential to lower abdominal fat stores. Aerobic endurance training increases β-adrenergic receptor sensitivity in adipose tissue [23].

So the author's position is that basically that in order to lose fat, you need to promote its release into the circulation. However. . . .

Obesity-induced insulin resistance is a major risk factor for the development of type 2 diabetes. Basal fat cell lipolysis (i.e., fat cell triacylglycerol breakdown into fatty acids and glycerol in the absence of stimulatory factors) is elevated during obesity and is closely associated with insulin resistance. Inhibition of adipocyte lipolysis may therefore be a promising therapeutic strategy for treating insulin resistance and preventing obesity-associated type 2 diabetes. In this review, we explore the relationship between adipose lipolysis and insulin sensitivity. After providing an overview of the components of fat cell lipolytic machinery, we describe the hypotheses that may support the causality between lipolysis and insulin resistance. Excessive circulating fatty acids may ectopically accumulate in insulin-sensitive tissues and impair insulin action. Increased basal lipolysis may also modify the secretory profile of adipose tissue, influencing whole body insulin sensitivity. Finally, excessive fatty acid release may also worsen adipose tissue inflammation, a well-known parameter contributing to insulin resistance. Partial genetic or pharmacologic inhibition of fat cell lipases in mice as well as short term clinical trials using antilipolytic drugs in humans support the benefit of fat cell lipolysis inhibition on systemic insulin sensitivity and glucose metabolism, which occurs without an increase of fat mass. Modulation of fatty acid fluxes and, putatively, of fat cell secretory pattern may explain the amelioration of insulin sensitivity whereas changes in adipose tissue immune response do not seem involved.

Adipocyte lipolysis and insulin resistance. - PubMed - NCBI

Adrenaline directly increases lactate release and lipolysis and inhibits insulin-stimulated glucose uptake in the perfused human leg. Adrenaline has no direct effects on peripheral amino acid metabolism. Adrenaline-induced lactate release from striated muscle may be an important mechanism underlying hyperlactatemia in the critically ill.

Effects of adrenaline on lactate, glucose, lipid and protein metabolism in the placebo controlled bilaterally perfused human leg. - PubMed - NCBI

Not surprisingly the lipolysis stimulated by adrenaline is involved in effectively stimulating what we typically call type II diabetes, insulin insensitivity. This makes sense, because the fat in your blood inhibits glucose uptake.

Obesity is invariably associated with insulin resistance. In most obese subjects, plasma FFA levels are increased. Physiologic increases in plasma FFA levels cause insulin resistance in both diabetic and nondiabetic subjects by producing several metabolic defects: (1) FFA inhibit insulin-stimulated glucose uptake at the level of glucose transport or phosphorylation (or both); (2) FFA inhibit insulin-stimulated glycogen synthesis; and (3) FFA inhibit insulin-stimulated glucose oxidation. (This last-mentioned defect probably does not contribute to insulin resistance.) FFA probably also cause hepatic insulin resistance, which results in increased rates of endogenous glucose production in relationship to the prevailing degree of hyperinsulinemia. Lastly, FFA support between 30 and 50% of basal insulin secretion and potentiate glucose-stimulated insulin secretion in short-term and long-term settings. The stimulatory action of FFA on b-cells enables obese individuals who do not have a genetic predisposition to develop type 2 diabetes mellitus to compensate for their FFA-potentiated insulin resistance with an increase in FFA-mediated insulin secretion. In contrast, subjects who are genetically predisposed to develop type 2 diabetes may be unable to secrete sufficient amounts of insulin to compensate for their FFA-induced insulin resistance. This situation will lead to an increase in blood glucose concentration and eventually to type 2 diabetes.

Free fatty acids-the link between obesity and insulin resistance. - PubMed - NCBI

So, adrenaline can't be unraveled from other stress hormones, and the free fatty acids released during stress impair efficient metabolism.
And finally, I think you and I agree that T3 and testosterone are both relevant to building muscle and burning fat. So let's consider adrenaline and free fatty acids in relation to that.

Infusion of adrenaline in healthy dogs in a dose simulating spontaneous release of the catecholamine during experimental myocardial infarction produced a significant decrease in the conversion of thyroxine (T4) to triiodothyronine (T3) and a moderate increase in the conversion of T4 to reverse-triiodothyronine (rT3). Similar changes in deiodination of T4 to T3 and to rT3 were also observed when adrenaline was added in vitro to liver and heart homogenates. These results are consistent with a direct effect of adrenaline on T4 deiodination as degradation of exogenous T4, T3 and rT3 was only slightly increased under the experimental condition employed. The present study suggests that increased tissue exposure to adrenaline might contribute to the hormonal changes seen in at least some case of the 'low T3 syndrome'.

In vivo and in vitro effects of adrenaline on conversion of thyroxine to triiodothyronine and to reverse-triiodothyronine in dog liver and heart. - PubMed - NCBI

In an attempt to study thyroid hormone and catecholamine interaction, in vitro effects of epinephrine and chemically related compounds (norepinephrine, asthpul, aldomet, alotec, effortil and ephedrine) on deiodination of thyroxine and triiodothyronine by muscle homogenates or slices of muscle and liver, and on deiodination of monoiodotyrosine and diiodotyrosine by liver slices have been studied in complete darkness. I131-labeled thyroxine and triiodothyronine were deiodinated in the presence of muscle homogenate and of slices of muscle and liver during 2 hours incubation, but not in the absence of muscle homogenate or in the presence of boiled homogenate. Epinephrine, within the wide dose range used, inhibited deiodination of iodothyronines by muscle homogenate, but oxidized material(s) of epinephrine was without effect. Another 4 compounds (norepinephrine, asthpul, aldomet and alotec) with 2 OH groups at 3 and 4 or 3 and 5 of the benzene ring did also inhibit enzymatic deiodination of iodothyronine. However, 2 compounds (effortil and ephedrine) without 2 OH groups failed to affect enzymatic deiodination. In the presence of dilute rat plasma, muscle homogenate failed to deiodinate thyroxine, but it manifested its action when free thyroxine was increased by adding salicylate. Epinephrine inhibited deiodination of thyroxine by muscle homogenate in the presence of dilute rat plasma and salicylate. Epinephrine and another 6 compounds failed to affect deiodination of monoiodotyrosine and diiodotyrosine by liver slices. It is concluded that epinephrine and another 4 chemically related compounds with 2 OH groups at the benzene ring specifically inhibit enzymatic deiodination of thyroxine and triiodothyronine at least in vitro.

Effects of epinephrine and chemically related compounds on enzymatic deiodination of thyroxine, triiodothyronine, monoiodotyrosine and diiodotyrosine in vitro - ScienceDirect

In healthy men, a decrease in plasma testosterone levels was observed in the context of metabolic stress. While physiological mechanisms underlying this response are unclear, there are several lines of evidence suggesting circulating epinephrine's influence on plasma testosterone levels. The purpose of this study was to directly relate stress-induced changes in plasma testosterone and epinephrine. The stressor used was blockade of glucose metabolism with pharmacological doses (40 mg/kg) of 2 deoxyglucose (2DG). Arterial plasma samples from 10 healthy males were assayed at 20 minutes intervals for 60 minutes for the concentrations of testosterone, epinephrine and related biochemicals. Bolus administration of 2DG resulted in progressive decline in testosterone and increases in epinephrine and norepinephrine plasma levels (mean change from baseline: 29, 2530 and 186%, respectively). Inverse correlation was detected between both absolute (r(s)=-0.72; df=8; p=0.017) and baseline-corrected testosterone concentrations at the 60 minute time point and epinephrine area under the curve values. Our results suggest that adrenomedullary activation may be involved in stress-induced testosterone effects. The implications of these data for the understanding of the role of catecholamines in glucoprivic stress response are discussed.

Inverse relationship between plasma epinephrine and testosterone levels during acute glucoprivation in healthy men. - PubMed - NCBI
Note that the stressor they used was blocking glucose metabolism. Recall what free fatty acids do.

The purpose of this study was to discover whether severe dietary carbohydrate (CHO) restriction modifies the relationship between exercise intensity and hormonal responses to exercise. Changes in the plasma adrenaline (A), noradrenaline (NA), growth hormone (hGH), testosterone (T), and blood lactate (LA) during an incremental exercise performed until volitional exhaustion were determined in 8 physically active volunteers after 3 days on low CHO (< 5% of energy content; L-CHO) and isocaloric mixed (M) diets. Following L-CHO diet, the basal plasma A, NA, and hGH concentrations were increased, whilst T and LA levels were decreased. During exercise all the hormones increased exponentially, with thresholds close to that of LA. Neither the magnitude nor the pattern of the hormonal changes were affected by L-CHO diet except the NA threshold, which was lowered. Blood LA response to exercise was diminished and LA threshold was shifted towards higher loads by L-CHO diet. It is concluded that restriction of CHO intake (a) does not affect the pattern of changes in plasma A, hGH, and T concentrations during graded exercise but lowers NA threshold, indicating increased sensitivity of the sympathetic nervous system to exercise stimulus; (b) alters the basal and exercise levels of circulating hormones, which may have an impact on the balance between anabolic and catabolic processes and subsequently influence the effectiveness of training.

The effect of low-carbohydrate diet on the pattern of hormonal changes during incremental, graded exercise in young men. - PubMed - NCBI

The acute effects of a 20 min constant rate intra-arterial infusion of LH and catecholamines on testicular blood flow and plasma testosterone concentrations were examined in sodium pentobarbitone anaesthetized rats. Ovine LH (2.5 microgram/min) elicited a 6-fold increase in testosterone concentration and a significant decrease of testicular vascular resistance. Noradrenaline and adrenaline (0.4 microgram/min) caused significant depressions in the plasma testosterone levels. The catecholamines induced no absolute changes in testicular blood flow but noradrenaline caused an increase in testicular vascular resistance. It was concluded that the catecholamine induced reductions in testosterone concentrations were not due to a vascular effect on the testis.

The effects of LH, adrenaline and noradrenaline on testicular blood flow and plasma testosterone concentrations in anaesthetized rats. - PubMed - NCBI

Acute adrenaline exposure (and stress in general) decrease thryoid function and testosterone production. We can focus on the fact that adrenaline promotes the release of free fatty acids, but I think it's better we consider what else is going on in the organism as that's happening before, during, and after.

 

[BigBrain]

yeah you repling what i said with this studies that adrenaline highy supports lypolisis and fat burn and induce insulin ressistance, BUT LIKE i said we have to do the things temporary not chronically. Im not telling you to walk your whole life with 10 times elevated adrenaline value. Adrenaline and cortisol are both important hormones but only when they re needed. Also is HGH/GH highly desirable because its increase fat loss and is anabol and anti- catabol for muscle. When you want fat loss then you want use your own bodys fat so for this period time its not a problem if you re insulin sensivity is lower. It will rise after those hormones sink.

I know that peat dont like HGH i dunno why. Compared to the both stress hormones Adrenaline/Cortisol HGH supports fat loss and increase lean mass.

Btw i never recommend low carb diet or anything like this . I personally hate low carb and would never ever recommend any1 this quackering. Only maybe in a therapeutic way.

 

[DuggaDugga]

yeah you repling what i said with this studies that adrenaline highy supports lypolisis and fat burn and induce insulin ressistance, BUT LIKE i said we have to do the things temporary not chronically. Im not telling you to walk your whole life with 10 times elevated adrenaline value. Adrenaline and cortisol are both important hormones but only when they re needed. Also is HGH/GH highly desirable because its increase fat loss and is anabol and anti- catabol for muscle. When you want fat loss then you want use your own bodys fat so for this period time its not a problem if you re insulin sensivity is lower. It will rise after those hormones sink.

I know that peat dont like HGH i dunno why. Compared to the both stress hormones Adrenaline/Cortisol HGH supports fat loss and increase lean mass.

Btw i never recommend low carb diet or anything like this . I personally hate low carb and would never ever recommend any1 this quackering. Only maybe in a therapeutic way.

Releasing fat into your boodstream doesn't mean it's "burned". Your body is already burning fat allday long. Releasing a spike of free fatty acids into your blood through stress hormones dysregulates metabolism, lowers thyroid function, and decreases the hormones of health at large, as I've provided evidence on. This is exactly what you don't want to do. If you want to lose fat, lower its consumption, increase muscle mass through non-stressful anabolic stimuli, and remove catabolic stimuli like psychological stress, intense exercise, etc.

Regarding growth hormone, I don't think it's as simple as you make it out to be (as with adrenaline). I suggest you read about IGF-1 to help form a more comprehensive view of what's going on.
Many of GH anabolic effects seem to be mediated by IGF-1.

GH has a net anabolic effect on protein metabolism, as it stimulates protein synthesis while repressing proteolysis96, 114-118. However, data suggest that the effects of GH on protein metabolism may be mediated by IGF-195, 119. It has also been hypothesized that the GH-induced increase in FFA flux from the adipose tissue could, via the provision of substrates for gluconeogenesis (such as ketone bodies, and acetyl CoA); abrogate the need for amino acids, and consequently proteolysis120. This theory has been supported by studies which show that GH increases lipid oxidation in both humans and rodents88, 95-97. A possible mechanism of GH-induced protein synthesis was demonstrated in the H4IIE rat hepatoma cell line; GH activated the mTOR signaling pathway, an established pathway involved in protein synthesis121. However, a caveat of using rat hepatoma cell lines is that, unlike differentiated hepatocytes, these cell lines express IGF-1Rs as well as IGF-1122. Thus, GH exerts a net anabolic effect on protein metabolism either directly or via IGF-1.

Similar to adrenaline, although GH promotes lipolysis, it also promotes adipogenesis.

GH also plays a role in adipocyte differentiation (adipogenesis). Differentiation of small pre-adipocytes into large, mature adipocytes is associated with an increased capacity to store TG and a higher lipolytic ability57. Several in vitro studies in 3T3-L1 adipocytes have shown that GH may directly induce adipogenesis via activation of STAT5 and its subsequent association with PPAR-γ (peroxisome proliferator-associated receptor-γ), an established adipogenic factor. However, Fleenor et. al. showed that GH treatment of 3T3-L1 pre-adipocytes during their differentiation was associated with a concomitant increase in IGF-1 expression; while Kawai et. al. demonstrated that STAT5 activation (nuclear translocation) was GH-independent 24 hours after induction of adipogenesis in the presence of GH. These data suggest that while STAT5 may associate with PPAR-γ during adipogenesis, GH may mediate this effect only during the early phase and that other STAT5 activators may come into play during the later phases of adipogenesis58-60. This hypothesis is supported by the observation that STAT5 is involved in the development of the immune system and the effects of glucocorticoids on body growth and fatty acid metabolism (reviewed in61). Thus, identifying the alternative stimuli for STAT5 activation during adipogenesis may help clarify the role of GH during the process.

And, again, GH promotes insulin resistance

GH represses glucose uptake in the adipose tissue via as yet unclear mechanisms. In vitro studies show that GH preferentially down-regulates the glucose transporter-1 (GLUT-1) in the adipose tissue-derived 3T3-F442A cell line62. Moreover, treatment of rats with an anti-rat GH antibody increased the membrane localization of GLUT-1 and GLUT-4, most-likely by up-regulating GLUT-1 protein content and altering the sub-cellular localization of GLUT-463. bGH-transgenic mice also have increased expression of the p85α regulatory sub-unit of PI3K in the adipose tissue, which has been associated with insulin resistance. Furthermore, the opposite was found in the GH-deficient (GHD) lit/lit mice which harbor a mutation in the GHRH receptor (GHRHR) gene64. Dose-dependent increase in p85α expression was also shown in 3T3-L1 preadipocytes treated with GH65. Thus, GH may inhibit insulin action in the adipose tissue, either at the level of glucose uptake or the PI3K.

Biological Effects of Growth Hormone on Carbohydrate and Lipid Metabolism

If we consider what else is going on, GH doesn't seem like necessarily such a great thing to promote. It does increase lipid oxidation, but it also decreases glucose oxidation, likely to spare it as energy substrate for the brain and RBC during stress, which means insulin resistance, lower pentose phosphate pathway activity, decrease pryuvate dehydrogenase phosphotase activity, etc. This has implications on thyroid and androgens like we've already discussed. It's interesting you should mention low-carb dieting as not recommended (I agree), because adrenaline and GH largely promote a hormone profile similar to a diet devoid of carbs.

 

[BigBrain]

well you take everything to seriously yes what i mean with GH is igf1 which is converted by liver to igf1. What i dont understand most of ppl like you, say fat lypolsis is strictly dangerous like many other ppl include hamster. But how you want loose fat bro with out fat tissue breakdown by lypolisis. Also like i said allready almost 3 times i never said that anything is chronicly good. But there is no way in order to loose bodyfat you need to breakdown bodyfat tissue.

There is now the thing when you have heavy or intense work out like heavy weight lifting or sprinting, this ***t will increase all types of hormones so like t3, HGH, DHT, T cortisol and adrenaline and reduce in estrogen this will release fat molecule from your fat tissue . Now you re right it doenst mean that your body will use those fat molecules as energy resource. But he will use them if you keep train hard he will utelize them. So there is the clue how to loose fast body fat or start loose stubborn fat in general. Just train intensely hard go over your limits try to increase those bodyfat burn hormones and DONT eat high protein or high leucin which stimulates insulin and this ***t will sabotage your effort. Not whole effort but in signigicant way. And now my friend you do this one or two times in a week not every day . Thats the thing.

Do everything in cycles never chronicly. Also that studies re 100 % true but you need to understand that the results are only for limited period of time. If you increase those hormones like a mention above doenst mean that they re now for your whole Life elevated. The body will balance it and return to normal.

The thing with adipogenesis by HGH is really confusing me how it can increase fat lypolsis and same way start adipogenesis , but maybe there is way to counter the adipogenesis. I dont know but maybe you know why.

Everything acts slighlty differently , it depends on the individual.

 

[YourUniverse]

This is going to have to be a multi-part response, but let's start from the top:


So first I'll note that you called out 'adrenaline' in parentheses, which aligns with previous statements you've made about the supposed benefits of adrenaline as distinguished from other stress hormones like cortisol. In the paper you provided on high intensity exercise, they explicitly note that all the stress hormones increase during and for some duration after exercise:


So, suppose somehow that adrenaline is still an effective way to lower abdominal fat. How then do we address the fact that growth hormone and cortisol are also increased? How then do we address that each of those hormones induce insulin resistance?
Epinephrine-induced Insulin Resistance in Man
Mechanisms of Glucocorticoid-Induced Insulin Resistance: Focus on Adipose Tissue Function and Lipid Metabolism
Growth hormone induces cellular insulin resistance by uncoupling phosphatidylinositol 3-kinase and its downstream signals in 3T3-L1 adipocytes. - PubMed - NCBI



http://web.mit.edu/****/www/pdf/986.pdf

Glucocorticoid treatment--effect on adrenal medullary catecholamine production. - PubMed - NCBI

So secretion of glucocorticoids and adrenaline are intimately linked. We can't look at adrenaline in isolation.

Now, I did want to address this point previously quoted and bolded, as I believe this is where the idea that adrenaline is good for fat removal:


So the author's position is that basically that in order to lose fat, you need to promote its release into the circulation. However. . . .

Adipocyte lipolysis and insulin resistance. - PubMed - NCBI

Effects of adrenaline on lactate, glucose, lipid and protein metabolism in the placebo controlled bilaterally perfused human leg. - PubMed - NCBI

Not surprisingly the lipolysis stimulated by adrenaline is involved in effectively stimulating what we typically call type II diabetes, insulin insensitivity. This makes sense, because the fat in your blood inhibits glucose uptake.


Free fatty acids-the link between obesity and insulin resistance. - PubMed - NCBI

So, adrenaline can't be unraveled from other stress hormones, and the free fatty acids released during stress impair efficient metabolism.
And finally, I think you and I agree that T3 and testosterone are both relevant to building muscle and burning fat. So let's consider adrenaline and free fatty acids in relation to that.


In vivo and in vitro effects of adrenaline on conversion of thyroxine to triiodothyronine and to reverse-triiodothyronine in dog liver and heart. - PubMed - NCBI

Effects of epinephrine and chemically related compounds on enzymatic deiodination of thyroxine, triiodothyronine, monoiodotyrosine and diiodotyrosine in vitro - ScienceDirect


Inverse relationship between plasma epinephrine and testosterone levels during acute glucoprivation in healthy men. - PubMed - NCBI
Note that the stressor they used was blocking glucose metabolism. Recall what free fatty acids do.



The effect of low-carbohydrate diet on the pattern of hormonal changes during incremental, graded exercise in young men. - PubMed - NCBI


The effects of LH, adrenaline and noradrenaline on testicular blood flow and plasma testosterone concentrations in anaesthetized rats. - PubMed - NCBI

Acute adrenaline exposure (and stress in general) decrease thryoid function and testosterone production. We can focus on the fact that adrenaline promotes the release of free fatty acids, but I think it's better we consider what else is going on in the organism as that's happening before, during, and after.

Im confused, one of your links says that both T and Lactic acid were decreased on a low carb diet. Isnt low lactic acid a good thing?

 

[BigBrain]

idk if is it good or bad but its an adaptation to high volume training like drop sets in weight lifting and it increase HGH

 

[Deleted member 5487]

What lifestyle and diet changes made the biggest difference?

If anyone has any pics to show the change, that’d be very interesting :)

Sprints. The only way.

40-70 yards 90% max speed.Warm up very well. Breath through nose during the 2 minutes of rest. Plenty of boiled potatos after.

Start with 2 then 4 then 5 then 6 then 8 and stay there.

Study from like 2010 showed weight loss was like 16X more effective then jogging or any sort of steady state. Sprint just 2-3 times a week, is insane for muscle growth and weight loss.

Nobody does them, and everyone struggles with their physique. If only they knew lol. The insulin sensitivity is also incredible. Hitting 100 bpm and flushing hot skin after three salted pressure cooked potatoes.

Granted I am 22 and athletic but if u want results I cannot press this enough. Everyone wants to just go low fat or cut carbs, movement and adaptation are the only way to really get great physiques.

 

[cyclops]

Yea, sprints are the best workout you can do.

 

[Palpatine]

Yes, sprints are great... But at my age, 45, 2-3 times a week would crush my cns and testosterone.

Once a week, max, for us older guys, mixed in with other resistance/weight training.

 

[BigBrain]

Yes, sprints are great... But at my age, 45, 2-3 times a week would crush my cns and testosterone.

Once a week, max, for us older guys, mixed in with other resistance/weight training.

i think it has nothin to do with age. For example last time i did 4 sprints and after that i totally shut down. Got headache nausea and overall bad feeling. I think its very effective in fat burning, and thus leads to a higher toxins burden in blood. I was 21 years old. Almost ripped but those last fat was stubborn fat which is i think most pufas most toxins stored in whole body.

 

[YourUniverse]

Mark Rippetoe, the man behind Starting Strength, writes about the need to tailor the program to the individual especially in regards to their age. Older people definitely need more rest. For example, instead of working out M/W/F/M/W/F over 2 weeks (lifting with ~1 day rest) as is typical, he may have a 70 year old man come in and lift with 2 days rest (M/Thur/Sun/Wed/Sat etc). Now theres something to be said for attitude, which i think is that, we can recover from probably quite a bit more than we think we can; or, said differently, if we think we need a full week of recovery, then we will need a full week of recovery, whether or not physiologically its true