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Hormones And Fat Loss

Discussion in 'Scientific Studies' started by Hans, Nov 18, 2018.

  1. Hans

    Hans Member

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    This thread is dedicated to the combination of most hormones that might have the most impact on fat loss and their interactions with each other and which should be kept high and which low. So here goes:

    Insulin
    By now we should know that insulin isn't the cause of fat gain. People might think it is because it increases lipogenesis, inhibits lipolysis and promotes fat storage. There is just one study I'd like to point out here.
    In this study by Hall et al., they compared two groups: one reduced carbs and the other reduced fats, while keeping protein and calorie intake the same (1). The low carb group lost 53g/day of body fat, whereas the high carb diet lost 89g/day of body fat. At the end of the study, insulin decreased significantly in the low carb group and remained the same in the low-fat group. However, this did not prevent fat loss. Based on these findings, we can definitely reject the statement that carbohydrate restriction and insulin reduction is required for fat loss.
    Plus, in a study by Hellerstein et al. they found that daily overfeeding with 150–200 g fat and 750–1000 g carbohydrates led to a de novo synthesis of 5 g fat per day, equivalent to < 3 % of the total fat consumed (2).
    Carbohydrates are needed to support thyroid function, increase thyroid hormone conversion, keep glycogen stores full, stimulate glucose oxidation and speed up the metabolic rate, keep lipolysis under control, keep cortisol and adrenaline low, increase ATP and CO2 production, increase thermogenesis, glutathione synthesis, etc.

    Leptin
    Leptin, a hormone predominantly made by adipose cells, reduces hunger, stimulates energy expenditure (thermogenesis) via SNS, enhances the secretion of TRH, upregulating thyroid function, increases steroidogenesis, etc.
    Although this might seem like a good hormone to keep high, thyroid hormones and leptin are inversely correlated and leptin and TSH are positively correlated. So actually, more leptin, higher TSH, more inflammation, etc. Obese people are also leptin resistant, hence hyperphagia.
    Leptin inhibits hyperphagia by triggering the release of histamine in the hypothalamus, and histamine in turn prevents the downregulation of leptin receptors which mediates leptin resistance.

    Histamine
    People with high histamine, also known as histadelics, are generally slender and struggle to gain weight. Histamine increases lipolysis, leptin receptors and leptin sensitivity in the brain, reduces hunger, increases thermogenesis, etc. Histamine receptor H1 antagonism increases hunger and weight gain.
    In a recent Chinese study, people received supplemental histidine (2 g, twice daily) or matching placebo, for 12 weeks. Insulin sensitivity improved significantly in the histidine-supplemented subjects, and this may have been partially attributable to loss of body fat. Body mass index (BMI), waist circumference and body fat declined in the histidine-supplemented group relative to the placebo group; the average fat loss in the histidine group was a robust 2.71 kg. Markers of systemic inflammation such as serum tumour necrosis factor-alpha (TNF-α) and interleukin (IL)-6, non-esterified fatty acids and oxidative stress also decreased in the histidine group (3). Food intake was slightly less on the histidine group, so it's not conclusive if the histidine increased energy expenditure and therefore fat loss or if the fat loss was a result of eating less calories.
    Histidine competes with other neutral amino acids for transport into the brain, and BCAA levels are elevated in obesity, hence reduced histidine transport into the brain, resulting in fewer leptin receptors and low leptin sensitivity. Histidine supplementation might have restored leptin sensitivity and resulted in fat loss.

    However, excess histamine increases serotonin synthesis, inhibits steroidogenesis (through H1, but actually promotes it through H2), promotes inflammation and is inversely correlated with thyroid hormones. Histamine reduces thyroid hormones, T4 and T3 (4) and thyroid administration reduce histamine levels (5). Anti-thyroid drugs alone decreases the sensitivity to histamine (6).

    Cortisol is catabolic, reduces thyroid function, increases circulating BCAA, which might lead to low histamine levels in the brain and reduced metabolic rate.

    Cortisol
    Cortisol is a catabolic hormone, which inhibits steroidogenesis, increases the aromatase, inhibits thyroid hormone production (cortisol and TSH is correlated), conversion and function, slows the metabolic rate, inhibits thermogenesis, etc.
    Adrenalectomy is associated with improvement of obesity and cold tolerance of models of genetic obesity lacking leptin or leptin signal. Evidence also suggests that glucocorticoids may inhibit the action of leptin. So cortisol lowers histamine in the brain and also promotes leptin resistance, slowing the metabolism.

    Catecholamines (adrenaline & noradrenaline)
    Catecholamines act on adrenoreceptors to exert its action. Alpha 2 adrenoceptor inhibits lipolysis, whereas the beta-adrenoceptors promotes lipolysis.
    In a study by Hellstrom et al. they concluded that rapid weight losers were 10-fold more sensitive to the lipolytic effect of noradrenaline and 10-fold less sensitive to the antilipolytic effect induced by the alpha 2-adrenoceptor agonist clonidine than the slow weight losers (7).

    "The rate of FFA and glycerol response to norepinephrine was increased twofold in the cells of obese subjects; no significant reutilization of FFA during catecholamine-induced lipolysis was observed in any of the groups (glycerol/FFA ratio near 1:3). There were no differences in the lipolytic sensitivity to beta 3- or beta 2-adrenoceptor specific agonists between the two groups. However, beta 3-adrenoceptor sensitivity was approximately 50 times enhanced (P = 0.0001), and the coupling efficiency of these receptors was increased from 37 to 56% (P = 0.01) in obesity. Furthermore, the obese subjects demonstrated a sixfold lower alpha 2-adrenoceptor sensitivity (P = 0.04). beta 3-Adrenoceptor sensitivity, but not alpha 2-, beta 1-, or beta 2-adrenoceptor sensitivity, correlated with norepinephrine-induced lipolysis (r = -0.67, P = 0.0001) and fat cell volume (r = -0.71, P = 0.0001). In conclusion, catecholamine-induced rate of FFA mobilization from omental fat cells is accelerated due to elevated rate of lipolysis in obesity, mainly because of an increased beta 3-adrenoceptor function, but partly also because of a decreased alpha 2-adrenoceptor function. This promotes an increased release of FFA to the portal system, which may contribute to the parallel metabolic disturbances observed in upper-body obesity." (8)

    Obese individuals have elevated catecholamines, lipolysis and circulating free fatty acids, but no increase in the oxidation of the fats, hence metabolic syndrome. Boosting catecholamines and lipolysis even more would be really counterproductive, because the problem is elevated lipolysis. So fasting, intermittent fasting, low carb diets, etc, would make it worse by further promoting catecholamine and lipolysis.
    Although alpha 2-adrenoceptors inhibit lipolysis, it also inhibits thyroid hormone secretion. In addition, TSH-induced thyroid hormone secretion is inhibited by alpha 1-adrenoceptor antagonism. So using alpha adrenoceptor agonists (catecholamines, clonidine) or antagonists (yohimbine), will just suppress thyroid function. Beta-adrenoceptors agonists (yohimbine, bitter orange extract, catecholamines, etc.) will also further promote lipolysis, suppress thyroid function and also glucose oxidation.

    T3 reduces alpha-adrenoceptors, thus promoting normal lipolysis. The alpha 2-adrenergic response is completely inhibited in hypothyroid state, hence the out of control lipolysis (9).

    Noradrenaline increases uncoupling, thyroid hormone conversion and significantly enhances lipolysis in the hyperthyroid state. Beta-adrenergic sensitivity and responsiveness are 10- and 2-fold increased, respectively, in hyperthyroid patients. In hypothyroid patients, beta-adrenoceptor responsiveness is reduced by 50%. The number of beta-adrenergic binding sites are doubled in hyperthyroid (10).
    Noradrenaline actually inhibits lipolysis in the hypothyroid state, by binding mostly to alpha 2 adrenoceptors. So, even when trying to "tap" into the stress hormones for fat loss isn't going to do much when thyroid function is suboptimal.

    Noradrenaline and thyroid hormones work in synergy, but are inversely correlated. High catecholamines mean low thyroid hormones, and vise versa.
    Stimulation of UCP1 by norepinephrine alone, as judged by the denervation of brown adipose tissue (BAT) in hypothyroid rats, is quite modest, 2- to 3-fold, whereas the stimulation is 18- to 20-fold in the presence of thyroid hormones. Likewise, the stimulation of UCP1 by T3 on denervated BAT was also quite modest, barely significant. Both are needed for fat loss.

    Endocannabinoids
    Cannabinoid (CB) receptors and their putative ligands, arachidonylethanolamide (anand-amide) and 2-arachidonylglycerol (2-AG), activates the opioid receptor, that suppresses steroidogenesis, increases prolactin, promote lipolysis, etc. Blocking the CB1 receptor leads to fat loss.

    Thyroid
    TSH is elevated in obesity. Despite the higher plasma TSH levels, TSH receptors are less expressed on adipocytes of obese vs. lean individuals. This reduced TSH receptor expression might induce down-regulation of thyroid hormone receptors and thyroid hormone action, thereby further increasing plasma TSH and FT3 concentrations and constituting a condition of peripheral thyroid hormone resistance. So it might not help to supplement with thyroid, or this would increase thyroid requirements significantly, because of reduced thyroid receptors (11). Cortisol, leptin, histamine, estrogen, serotonin, endotoxins, PUFAs, oxidative damage, etc., all inhibit thyroid function and will result in a rise in the wrong hormones.

    Both UCP1 expression and BAT temperature elevation in response to norepinephrine correlates nicely with TH receptor occupancy by T3 (12). Interestingly, transgenic mice with a disruption of the D2 gene (dio 2), were cold intolerance, in spite of normal plasma T3 concentration. DIO2 seem essential for uncoupling and thermogenesis and not necessarily total T3 levels.
    Elevated T4 levels inhibit uncoupling, whereas T3 promotes it. Slow conversion of T4 to T3 will inhibit uncoupling. Cortisol, inflammation, sluggish liver function, fasting, etc., inhibits DIO2.

    Serotonin (5-HT)
    Inhibition of serotonin signaling or its synthesis in adipose tissue may be an effective treatment for obesity and its comorbidities (13).
    5-HT inhibits thermogenesis through 5-HT3 in BAT and increased lipogenesis through 5-HT2a in WAT.
    Ondansetron (a 5-HT3 antagonist) increased cyclic AMP production and phosphorylation of hormone-sensitive lipase (HSL) and protein kinase A substrate in the presence of the β3AR agonist.
    5-HT1B inhibits dopamine is the frontal cortex, 5-HT2A increases prolactin and is significantly associated with obesity, 2-HT2C increases glucocorticoids, 5-HT4 are associated with estrogen receptors (14).
    Reduced serotonin transporter (SERT) function is associated with obesity, insulin resistance (15). Sodium is a cofactor for SERT, and will directly aid in lowering serotonin.

    Inhibition of 5-HT synthesis leads to inhibition of lipogenesis in epididymal white adipose tissue (WAT), induction of browning in inguinal WAT, activation of adaptive thermogenesis (UCP) in brown adipose tissue (BAT), DIO2, PGC-1a and increased mitochondrial number and size.

    PUFAs (prostaglandins, leukotrienes), NO, cortisol, histamine, estrogen, increase TPH1, the enzyme that synthesizes serotonin.

    Dopamine
    Dopamine promotes energy expenditure and exploration. high dopamine makes you want to be active and use your senses. A common misconception of dopamine is that it's associated with addiction and obesity. However, increased dopamine does not promote the consumption of tasty food. The craving for tasty junk food is because of low dopamine, and the desire to increase it. When dopamine is high, there craving for sugar and other tasty foods fades away. High dopamine is essential for proper fat loss and the ability to stay on a healthy diet. Low dopamine promotes binge eating of easily obtainable, tasty, and most of the time, unhealthy foods.
    Rats with elevated dopamine rats don’t go for easy food, but rather spend more time and energy to obtain more difficult to obtain food even when the reward is the same. A high carb diet promotes dopamine, whereas a low carb diet lowers dopamine.

    Estrogen
    The aromatase is elevated in obesity and hypothyroid and increased by inflammation, estrogen, serotonin, histamine, excess catecholamines, cortisol, etc.
    Estrogen reduces insulin sensitivity, promotes inflammation and fat gain, inhibit thyroid hormone production, promotes lipolysis, inhibits uncoupling, etc.
    Aromatase inhibitors most often promote fat loss and lean mass gains.

    Testosterone and DHT
    Testosterone increases the metabolic rate and lean mass retention and promotes the loss of bodyfat. Testosterone is converted the more potent androgen DHT, which cannot be aromatized. DHT reduced lipogenic enzymes and inhibited incorporation of fatty acid into triglyceride in adipocytes differentiated from preadipocytes from all fat depots. Supraphysiological doses of DHT does not significantly promote fat loss or lean mass gains.
    It's been found that patients sufferings from muscle wasting because of AIDS, lose the most muscle when their DHT is low, even though their testosterone is normal. Patients with the most DHT, lost the least amount of lean mass (16). So DHT is high anti-catabolic and essential to keep high during fat loss.

    Growth hormone
    Growth hormone promotes lipolysis and is thought to aid in the retention of lean mass during fat loss. However, most studies only found a benefit to GH in GH deficient individuals. A GH deficiency seen obesity is a result of obesity and not a cause thereof, so trying to boost it is not the answer, and it might make the problem worse, by promoting lipolysis, insulin resistance and other side effects.

    "Results: GH administered together with hypocaloric diets did not enhance fat loss or preserve lean tissue mass. No studies provided strong evidence for an independent beneficial effect of GH on visceral adiposity. In all but one study, glucose tolerance during GH treatment suffered relative to placebo.

    Conclusion: The bulk of studies indicate little or no beneficial effects of GH treatment of obesity despite the low serum GH concentrations associated with obesity." (17) (this study is a highly recommended read on GH)

    The "benefit" to GH is because of its conversion to IGF-1, yet the response to IGF-1 is blunted in obesity because of a reduction in IGF-1 binding proteins, leading to poor utilization.

    Conclusion
    It would be essential to keep cortisol, serotonin, growth hormone, estrogen as low as possible while optimizing thyroid hormone and androgen production as well as dopamine levels. Proper thyroid function will promote proper lipolysis and not pathological excessive lipolysis. Anything that will negatively affect thyroid function will result in a rise in the wrong hormones and negatively affect muscle retention and fat loss.
    Things to avoid would be high tryptophan foods, PUFAs, endotoxins, nutrient deficiencies, low carb diet, etc.

    Things to look into are excessive lipolysis inhibitors (niacinamide, aspirin), vitamin E, adrenaline antagonists (inosine, niacinamide), cortisol antagonists (glycine, magnesium, emodin, vitamin D, taurine, niacinamide, aspirin, etc), endotoxin antagonist (glycine, saturated fat, activated charcoal, cascara sagrada, etc.), optimize liver function, optimize digestion, DHT promotes (caffeine, glycine, niacinamide, androsterone, etc), etc.

    That is all for now. If I missed anything, please add on if you wish. This thread is not to discuss which macros work best and if starches should be avoided or not, but mainly about which hormones are involved in fat loss.
     
  2. Blossom

    Blossom Moderator

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    Excellent and informative post @Hans.
     
  3. Captain_Coconut

    Captain_Coconut Member

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    Good stuff. How about Melatonin? @Hans
     
  4. cyclops

    cyclops Member

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    Great post. People have been question if these Peat recommended supplements are useful when trying to lose fat. I think the question is, what is excessive?
     
  5. OP
    Hans

    Hans Member

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    Thanks. I hope a few people might benefit from it and even stimulate a constructive discussion.
    Thanks for the suggestion. Melatonin seem to be suppressed in obesity, but is restored with weight loss. It seems similar to GH in that regard. Interestingly metalonin improves fat loss during a calorie restricted diet, mainly by quenching excessive ROS and lipid peroxides, lowering oxidative stress and inflammation. High levels of HNE (a lipid peroxide) are strongly associated with the development of obesity and its complications, leading to pathogenic cellular changes and promoting numerous disease processes. Toxins and PUFAs are released from adipocytes during fat loss which increase oxidative stress and reduce anti-oxidants, such as glutathione, vitamin E, melatonin, etc. So supplementing melatonin prevents the drop in melatonin during such a stressful phase such as with fat loss. Supplementing vit E rather, or even vit C, might also spare melatonin and quench the free radicals, without the side effect of melatonin accumulation and subsequent metabolism suppression.

    Melatonin Supplementation Lowers Oxidative Stress and Regulates Adipokines in Obese Patients on a Calorie-Restricted Diet
    "Herein, exogenous melatonin stabilized the HNE level in the subjects on a low-calorie diet and prevented a decrease in morning endogenous melatonin concentrations."

    "A 30-day calorie-restricted diet combined with melatonin supplementation resulted in a statistically significant weight loss, whereas a low-calorie diet per se yielded only a slight reduction in body weight."

    "Melatonin may increase the energy expenditure by activating brown adipose tissue [20]. It also preserves mitochondrial functions."

    Thanks. Everyone's rate of lipolysis is different so supplementation should be tweaked to that. Some people might need really big doses of niacinamide and/or aspirin to stop excessive lipolysis, whereas other don't have to use it at all. I do think they are great supplements to consider, because they inhibit cortisol, lower serotonin, increase steroidogenesis, increase the NAD:NADH ratio, etc. all which is essential for optimal thyroid function and metabolism.
     
  6. Captain_Coconut

    Captain_Coconut Member

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    Interesting, so are you saying melatonin can help with weight loss, but also can suppress metabolism if levels are too high?
     
  7. Cirion

    Cirion Member

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    I thought GABA was the antagonist to Melatonin and that you want high GABA and low melatonin? That's what Nathan Hatch says in F*** portion control.

    I thought obese people would have too much melatonin not too little? I'm at a pretty unhealthy weight right now (just starting on RP, and still healing) and would almost definitely say my melatonin is way too high. I can easily sleep basically all day no problem, fueled by torpor hormones like melatonin.

    Now old people do tend to have less melatonin (I think RP said this). But they likely also have low GABA, which would explain why they often don't sleep much at all compared to younger people (old people are infamous for waking up early)
     
  8. Captain_Coconut

    Captain_Coconut Member

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    My understanding is that higher melatonin levels at night correlate with lower cortisol at night, and a higher dhea to cortisol ratio during the day. I have not heard of gaba antagonizing melatonin...
     
  9. OP
    Hans

    Hans Member

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    Melatonin is basically increase during stress, but is protective against oxidative stress.
    Serotonin, depression, and aggression - The problem of brain energy.
    "Misconceptions about serotonin and melatonin and tryptophan, which are metabolically interrelated".

    "Serotonin lowers temperature by decreasing the metabolic rate. Tryptophan and melatonin are also hypothermic."

    Melatonin is also anti-thyroid.
    Melatonin benefits fat loss, because it lowering oxidative stress and inflammation, especially lipid peroxides due to PUFAs. That is why vit E would be a much better substitute, while eating a very low PUFA diet.
    Melatonin synthesis is under the control of thyroid, so once optimal thyroid function is obtained, melatonin production should be more optimal.

    From the study I posted above: "Melatonin deficiency has been demonstrated to correlate with obesity."
    Leptin Action on GABAergic Neurons Prevents Obesity and Reduces Inhibitory Tone to POMC Neurons
    "Remarkably, the vast majority of leptin’s anti-obesity effects are mediated by GABAergic neurons"

    So I would rather say GABA and melatonin might be low in obesity, with serotonin being elevated, causing the fatigue.
     
  10. Cirion

    Cirion Member

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    Melatonin is indeed a hormone that keeps cortisol some what at bay during the night. But it's the negative variant of GABA. Here's the way Nathan explains it:

    You are either in an activation mode (energetic) or inhibition (resting/sleep) mode.

    Activation mode while stressed is fueled through cortisol/adrenaline, and melatonin during sleep. But melatonin doesn't result in restful sleep, and instead results in a heavy torpor/hibernation mode.
    Activation / inhibition mode while relaxed is fueled by the pro-metabolic hormones, a healthy amount of T3, GABA etc...
     
  11. Cirion

    Cirion Member

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    So, you're saying in hypothyroid, both GABA and melatonin production are low? I dunno if I'm on board with this idea. It's easy to raise melatonin. Just promote darkness (or winter) / lack of red light etc...
     
  12. Captain_Coconut

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    So if one is low on melatonin production, increasing thyroid hormone should help to increase melatonin as well? Yet melatonin is anti-thyroid?? All I can say is since I have started taking 3mg melatonin before bed I have been waking up to 98+ temps. So for me at least, melatonin is helping to optimize my metabolism.
     
  13. OP
    Hans

    Hans Member

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    Sorry, you're right, I got it the wrong way round.
    The circadian rhythm of melatonin in hypothyroidism and hyperthyroidism. - PubMed - NCBI
    "The melatonin concentrations were positively correlated with TSH levels in hypothyroidism, and negatively correlated with T3 in hyperthyroidism."

    The study I posted above said that melatonin is lower in obesity, yet this study shows:

    Melatonin Level Variations with Different Behavioural Risk Factors in Obese Female Patients
    "Higher melatonin levels in patients with obesity and concomitant behavioural impairments may be due to its protective effect to fight free radicals and to induce vasodilatation."

    I guess melatonin is elevated to cope with the increase in ROS, until the ROS and RLS becomes too much, and melatonin drops and cannot keep up with the demand so to speak.

    I'm glad that it's helping you.
    REVIEW. Melatonin and the thyroid gland. - PubMed - NCBI
    "A large experimental evidence exists suggesting the inhibitory action of melatonin on thyroid growth and function"

    Melatonin is increased during hypothyroid, and it also suppresses thyroid function. Peat surely isn't a fan of it. Melatonin production is inhibited by blue light and depleted by ROS and RLS.
    Have you every tried a good quality vit E before?
     
  14. Captain_Coconut

    Captain_Coconut Member

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    I take E daily but have never noticed much from it, I take it because I trust that it is good to take. I agree melatonin would not be the best thing to take if one is already hypothyroid, however in those with a healthy thyroid it seems to me that melatonin would be particularly useful in preventing aging - much like DHEA is useful to start taking in our later years. I find it hard to believe that melatonin is really anti-thyroid, largely because it prevents PUFA oxidation and is a powerful aromatase inhibitor. I suspect the heirarchy is as follows: hypothyroid begets low dhea begets high melatonin, because if one is low in dhea theoretically one will be higher in melatonin as they normally provide balance to each-other. Melatonin has also been shown to be elevated during fasting, so it is also quite possible that melatonin is released by the body to protect from the LPO havoc brought on by fasting, my guess is this protective action would be the same in times of low thyroid hormone (ketosis).
     
  15. jamies33

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    This is an interesting article. My eyes go to two polarizing substances for RP fatloss: aspirin and niacinamide. Forum members have commented before about staying away from either one for fat loss, but you are suggesting the opposite
     
  16. OP
    Hans

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    In terms of having excessive lipolysis and cortisol, blocking those would be a very good first start. Remember, niacinamide and aspirin inhibits excessive lipolysis, and not baseline levels. Only at very high dose does it start to inhibit baseline lipolysis. Having low cortisol and a high NAD:NADH ratio just sets the stage for a faster metabolism and a greater ability to burn fat.
    Excessive catecholamines, cortisol, ROS, LPO, endotoxins, low NAD:NADH ratio, etc. inhibits the metabolism and speeds up fat loss.
    I don't see how it would be counterproductive.
     
  17. Cirion

    Cirion Member

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    "Fat burner", "carb burner", it's not black and white. I confess I don't know the complexities of it but from what I now understand/believe, when you improve metabolism your ability to metabolize carbs AND fats improve. You're not just a carb burner nor are you just a fat burner, you're both, at all times. And when you have a strong metabolism backed by a healthy intake of saturated fats AND sugars, you're burning both at once. And by the way, better than you ever would being just a "fat burner" with a poor glucose metabolism. I used to think you could only effectively burn one fuel or the other but that's just simply not true. We must be careful around here not to advocate ultra high carb ultra low fat, because that's the wrong end of the opposite side of the spectrum. That's what the keto diet advocates would have you think. But it's not that simple. Unfortunately, a lot of people do have deranged glucose metabolism though. And that's what has brought many people to these forums. Myself included.

    The problem is not fats, the problem is when the fats you burn are PUFA, and not SFA. That's when havoc is wreaked on your system. And the problem is also when all your body knows how to do is burn fats and not how to metabolize glucose, a problem often exasperated by low carb diets.

    My opinion of why weight gain may occur is simply because that person isn't hormonally healed 100% yet. Weight gain isn't necessarily a bad thing. Yeah it's annoying and I've gained a lot of weight, but I can't be surprised by it because I've abused my body for so long.

    I personally believe we need to get away from "what supplements/hormones support fat loss" and more towards "how can we optimize hormones for good health" because good health begets fat loss automatically without having to think about it. I spent way too much of my life caring about fat loss, at the expense of good health, which is what made me end up on these forums.
     
  18. OP
    Hans

    Hans Member

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    True.
    Everyone is different. Some people cannot tolerate fruit juice, or starch, or lots of fats, some need more protein than others and so on. Some do need a very low fat diet, whereas others need a more balanced diet. Some do better on a liquid diet and others don't. Experimentation is key.
    The reason I made this thread is to discuss which hormones are beneficial to the metabolism to promote healthy fat loss. What hormones should be focused on. I do believe focusing on certain hormones is a good idea, else people should quit their thyroid meds, or serotonin antagonists, aromatase inhibitors, etc.
    I for one would not be satisfied with being just 15% body fat. If I don't eat a certain way for a certain goal, I'm not going to reach it fast enough. I'm not so good at just knowing how much to eat to gain the maximum amount of muscle per month with minimal fat, without some calculations. I'm not saying you can't do it without counting calories and so on, I'm just saying that I'm not going to leave it up to chance. And I'm also not just blindly following formulas, I'm listening to my body and adjusting everything accordingly.
    I'm aiming for a certain goal, not just general health. Great health is included of course, that is why I'm focusing on the important hormones.
    I also made this thread to help others know what to focus on and not just blindly doing stuff, because someone on the internet said so, without looking at the evidence first.
     
  19. Zigzag

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    Tried intermittent fasting, lowcarb with caloric deficit for almost one year. I changed protocols after couple of months so it was like this: 16:8 -> 18:6 -> 20:4. To be honest it didn't help me at all. My blood sugar got worse (107 morning, fasting), TSH went up, didn't lose that much weight I hoped for. I have really bad genetic predisposition to store fat mostly in legs and I hoped to lose it from there. Apparently I lost from upper body but not from legs...
    On the other side keto, slight caloric deficit AND Yohimbine HCL helped me a lot. Of course eating fats most of the time is a nightmare but I lost around 10kgs really fast (I guess most of that was actually water).

    I've made a mistake though and didnt check my blood panel after keto, but I think blood glucose/insulin actually got even worse due to physiological insulin resistance that keto promotes.

    As far as I know fat stored in legs has the most alpha 2-adrenoceptors and in my case, I THINK Yohimbine HCL (which is alpha 2-adrenoceptor inhibitor).
    So basically this time I'll try different approach which will be: moderate carbs, no PUFAs, lowish fat, high protein. I'm still thinking of intermittent fasting if it's actually worth it in my case, cortisol effect was bad and my thyroid got worse (3,5 TSH).
     
  20. LCohen

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    Great post. Thank you so much.
     
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