Fat loss diet optimization ++

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I made my own. i have instructions somewhere. yes - some people say this is crazy lol.
defy/empower has IM/subq version, 500mg/1ml. various sites sell up to 600mg/1ml IM versions.
I bought some from Chase Irons' site on a recommendation from an associate. Haven't used it yet though. I'll report back when I try it.
 
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Interesting. 'Cooking' is exciting.
I'm sitting in the EU. Gonna look a bit further...
not difficult. grok AI gives you good instructions lol. need benzyl alc, regular carnitine (not any of the l- etc versions), distilled water - or just buy bac water, i know pharmacies in poland for ex. sell it. they key is to get good quality carnitine. you can buy all stuff in EU 100%
 
The following I consider the first "+". The second "+" the compounds I listed above. Just to make this thread a bit more complete.
Supported by current evidence, we propose a possible combination leveraging all mechanisms of action that could pave the way for future studies investigating the weight loss effect and safety profile of such product.

To inhibit the absorption of nutrients, we suggest using phaseolus vulgaris extract (PVE) at a dosage of 3000 mg (1000 mg per meal) daily, and green tea derived epigallocatechin (EGCG) at a dosage of 500 mg daily. In order to reduce appetite and possibly increase energy expenditure, we propose the use of coffee derived caffeine (300 mg/daily) and chrologenic acid (200 mg/daily). Chili pepper derived capsaicinoids or capsinoids may also be considered, at a dosage of 10 mg and 3 mg, respectively, together with L-C at a dosage of 2 g daily, that can also increase fat mobilization. Similarly enhancing beta oxidation and inhibiting lipogenesis, resveratrol and CLA may be considered, given their proven efficacy and absence of reported adverse events, at a dosage of 200 mg and 4 g daily, respectively. Finally, carbohydrate metabolism may be improved with glucose lowering lipoic acid at a dosage of 600 mg daily, with its long-standing history in the treatment of T2D. Most of the cited dietary supplements were also proven to exert anti-inflammatory and antioxidant effects, possibly aiding the resolution of low-grade chronic inflammation typical of weight excess and metabolic derangements (Figure 1).
 

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I feel that adding berberine to my meal reduced the fatigue after a meal.
IMHO berberine is beneficial if your diet is shit and you are pre-diabetic. TBH if you got fatigue after a meal you are eating garbage. i don't care if its organic oats or the best sounding shit out there, fatigue is absolutely not normal if you eat the proper foods. there might be some individual variances, as each person reacts different to foods, but since i switched to a mainly red meat/fruit diet, i get absolutely 0 fatigue. add some potatoes/flour - yes i tank. it is not the carbs either, as i can consume 3oz honey and feel amazing. also berg is a fraud....sorry it is what it is, the amount of BS this guy is spitting out is awful
 
We have good data on decrease in visceral fat:
Growth hormone (GH) has a significant impact on visceral fat, which is the fat stored within the abdominal cavity and is associated with various health risks. Here's a detailed look at how GH affects visceral fat:

## Effects of Growth Hormone on Visceral Fat

1. **Reduction in Visceral Fat**: Growth hormone therapy has been shown to reduce visceral adipose tissue (VAT). This reduction is achieved through the hormone's ability to enhance lipolysis, which is the breakdown of fats, leading to a decrease in fat mass, particularly in the visceral region[1][3][9].

2. **Mechanism of Action**: GH promotes lipolysis by increasing hormone-sensitive lipase activity, which breaks down stored triglycerides into free fatty acids and glycerol. This process is particularly effective in visceral fat depots, making GH a potential treatment for reducing visceral adiposity[8].

3. **Impact on Metabolic Health**: By reducing visceral fat, GH therapy can improve metabolic profiles. This includes ameliorating dyslipidemia (abnormal lipid levels), reducing systemic inflammation, and decreasing cardiovascular risk markers[1][2][4].

4. **GH Deficiency and Visceral Fat**: Individuals with GH deficiency often exhibit increased visceral fat accumulation. GH replacement therapy in these individuals has been shown to decrease visceral adiposity, improve muscle mass, and enhance overall body composition[9][10].

5. **Clinical Studies**: Several studies have demonstrated the efficacy of GH in reducing visceral fat. For example, a study involving HIV-infected individuals showed significant reductions in visceral fat following treatment with recombinant human growth hormone (rHGH)[5]. Another study in middle-aged men with visceral obesity reported an 8.8% reduction in visceral adiposity after six months of GH therapy[10].

6. **Long-term Efficacy and Safety**: While GH therapy shows promise in reducing visceral fat, the long-term efficacy and safety of such treatment require further investigation. Concerns include the potential for insulin resistance and other side effects associated with GH therapy[5][10].

In summary, growth hormone plays a crucial role in regulating visceral fat by promoting lipolysis and improving metabolic health. However, while GH therapy can effectively reduce visceral adiposity, its use must be carefully managed to avoid adverse effects. Further research is needed to fully understand the long-term implications and optimal dosing strategies for GH therapy in reducing visceral fat.

Citations:
[1] Effects of Growth Hormone Releasing Hormone on Visceral Fat, Metabolic and Cardiovascular Indices in Human Studies
[2] Effects of growth hormone-releasing hormone on visceral fat, metabolic, and cardiovascular indices in human studies - PubMed
[3] Effects of growth hormone treatment on visceral adipose tissue
[4] https://onlinelibrary.wiley.com/doi/full/10.1038/oby.2003.27
[5] Recombinant human growth hormone reduces visceral fat in two randomised studies
[6] The Truth About HGH for Weight Loss
[7] https://journals.sagepub.com/doi/10.1177/1178626417703995
[8] The effects of growth hormone on adipose tissue: old observations, new mechanisms
[9] Growth Hormone Decreases Visceral Fat and Improves Cardiovascular Risk Markers in Women with Hypopituitarism: A Randomized, Placebo-Controlled Study
[10] Effect of Growth Hormone on Body Composition and Visceral Adiposity in Middle-Aged Men with Visceral Obesity
 
IMHO berberine is beneficial if your diet is shit and you are pre-diabetic. TBH if you got fatigue after a meal you are eating garbage. i don't care if its organic oats or the best sounding shit out there, fatigue is absolutely not normal if you eat the proper foods. there might be some individual variances, as each person reacts different to foods, but since i switched to a mainly red meat/fruit diet, i get absolutely 0 fatigue. add some potatoes/flour - yes i tank. it is not the carbs either, as i can consume 3oz honey and feel amazing. also berg is a fraud....sorry it is what it is, the amount of BS this guy is spitting out is awful
It's possible that I'm pre-diabetic. Only three months on proper TRT (before too low T on androgel), less fatigue after meals then before and hopefully it will improve further. And yes, after eating potato salad with my steaks (and beer and wine) I got really fatigued. It was my weekend 'cheat'/carb cycle meal day.

I found the content of this Berg video and the video before about loose skin interesting. Cortisol, insulin, HGH... I believe HGH is common denominator for 'healthy' skin.
 

Interesting how berberine works, basically it increases insulin secretion only when needed.
 

Interesting how berberine works, basically it increases insulin secretion only when needed.
yep, so that is a good tool to have if you lifestyle/diet doesn't match, or you plan on overeating, going out etc. on a day to day basis if everything is tuned in it seems a waste of money
 

Considering that the precise mechanisms of dietary betaine protecting against obesity have not been elucidated yet, the possible mechanisms are summarized from in vitro and animal studies as follows (Figure 6). (1) Betaine supplementation could improve lipid lipolysis and reduce lipogenesis. Betaine intervention up-regulated expression of peroxisome proliferator-activated receptor α (PPARα) and downstream fatty acid oxidation-related genes, such as acyl-CoA oxidase 1/2 (ACOX 1/2) [11]. Studies also indicated that betaine increased fatty acid β-oxidation by enhancing muscle carnitine accretion, thus increasing carnitine palmitoyl transferase I-mediated free fatty acid translocation into mitochondria [12,40]. Betaine can also reduce the capacity for fatty acid and triglyceride synthesis by decreasing the activity of sterol regulatory element-binding protein-1c (SREBP-1c), acetyl-CoA carboxylase (ACC), malic enzyme (ME) and fatty acid synthase (FAS) in adipose tissue [12,32] and muscle [11]. (2) Betaine decreases uptake of triglycerides from circulating lipoproteins in adipocytes by reducing the expression of lipoprotein lipase (LPL) [32]. (3) Betaine might increase mitochondrial content and activity in hepatocytes [41] and adipocytes [11], and promote browning of white adipose tissue (WAT) [11]. (4) Betaine supplementation could decrease the levels of homocysteine (Hcy) via transmethylation of Hcy to methionine (Met), which was reported to suppress lipolysis in adipocytes [42]. (5) Betaine promotes protein synthesis. Betaine supplementation stimulates growth hormone (GH) and insulin-like growth factor 1 (IGF-1) secretion and subsequently improves the insulin IRS/Akt-mTOR protein synthetic pathway [31,43]. Betaine may also increase muscle mass by reducing homocysteine thiolactone (HTL), which is a toxic metabolite of excess homocysteine. HTL can inhibit protein synthesis via suppressing insulin/IGF-1 pathway [44].
 
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Considering that the precise mechanisms of dietary betaine protecting against obesity have not been elucidated yet, the possible mechanisms are summarized from in vitro and animal studies as follows (Figure 6). (1) Betaine supplementation could improve lipid lipolysis and reduce lipogenesis. Betaine intervention up-regulated expression of peroxisome proliferator-activated receptor α (PPARα) and downstream fatty acid oxidation-related genes, such as acyl-CoA oxidase 1/2 (ACOX 1/2) [11]. Studies also indicated that betaine increased fatty acid β-oxidation by enhancing muscle carnitine accretion, thus increasing carnitine palmitoyl transferase I-mediated free fatty acid translocation into mitochondria [12,40]. Betaine can also reduce the capacity for fatty acid and triglyceride synthesis by decreasing the activity of sterol regulatory element-binding protein-1c (SREBP-1c), acetyl-CoA carboxylase (ACC), malic enzyme (ME) and fatty acid synthase (FAS) in adipose tissue [12,32] and muscle [11]. (2) Betaine decreases uptake of triglycerides from circulating lipoproteins in adipocytes by reducing the expression of lipoprotein lipase (LPL) [32]. (3) Betaine might increase mitochondrial content and activity in hepatocytes [41] and adipocytes [11], and promote browning of white adipose tissue (WAT) [11]. (4) Betaine supplementation could decrease the levels of homocysteine (Hcy) via transmethylation of Hcy to methionine (Met), which was reported to suppress lipolysis in adipocytes [42]. (5) Betaine promotes protein synthesis. Betaine supplementation stimulates growth hormone (GH) and insulin-like growth factor 1 (IGF-1) secretion and subsequently improves the insulin IRS/Akt-mTOR protein synthetic pathway [31,43]. Betaine may also increase muscle mass by reducing homocysteine thiolactone (HTL), which is a toxic metabolite of excess homocysteine. HTL can inhibit protein synthesis via suppressing insulin/IGF-1 pathway [44].
Note that Betaine and TMG are the same thing AFAIK. It is a methyl donor which may be a benefit to some people, especially those who take niacin in high doses. It is one of my low-risk, low-cost go-to's for leanness.
 
Note that Betaine and TMG are the same thing AFAIK. It is a methyl donor which may be a benefit to some people, especially those who take niacin in high doses. It is one of my low-risk, low-cost go-to's for leanness.
You mentioned it, thanks for the advice .I overlooked it in the past, the studies were inconclusive.
 
I have more mental drive and 'happiness when I'm consuming carbs.
My bad fat rebound was probably also due to metabolic syndrome from antidepressiva and sleep meds. Unfortunately my T deficiency wasn't diagnosed until my joints started to hurt. TRT helped a lot but I still need a bit of antidepressiva and sleep med. I tried everything to avoid it completely but that's life, it's often a trade off. Getting good sleep and mental health has top priority for me.
Now I want to reduce visceral and subcutaneous fat in order to improve my T/E ratio or at least check what impact it really has on the E2 level. Also I really felt super bloated due to lot of visceral fat accumulation .
Just curious, how was it determined that the sleep medications are responsible for your metabolic syndrome?
 
Just curious, how was it determined that the sleep medications are responsible for your metabolic syndrome?
If you expected a lab test then I have to disappoint you. I noticed myself that I gained fat weight although I didn't change my physical activity and nutrition (however I did not track calories). I wondered what's going on and realized that it correlated with the time I started taking the sleep med. I then searched the Internet and found a website where people share their experiences with medications, bingo. I recently asked a psychiatrists about it, and it was confirmed. From observations it seems that antidepressiva in general cause weight (various hypotheses why this might be). To my knowledge there are no RCT with antidepressiva ( healthy vs depressive) to assess long term effects. Just a thought experiment: Imagine someone gains midly fat, only one pound within half a year. Scaling it up to 5 years would result in 10 pounds. I don't think it's a linear relationship (rather sigmoid) but there is certainly an accumulative effect.
 
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If you expected a lab test then I have to disappoint you. I noticed myself that I gained fat weight although I didn't change my physical activity and nutrition (however I did not track calories). I wondered what's going on and realized that it correlated with the time I started taking the sleep med. I then searched the Internet and found a website where people share their experiences with medications, bingo. I recently asked a psychiatrists about it, and it was confirmed. From observations it seems that antidepressiva in general cause weight (various hypotheses why this might be). To my knowledge there are no RCT with antidepressiva ( healthy vs depressive) to assess long term effects. Just a thought experiment: Imagine someone gains midly fat, only one pound within half a year. Scaling it up to 5 years would result in 10 pounds. I don't think it's a linear relationship (rather sigmoid) but there is certainly an accumulative effect.
Okay, the possibility of gaining weight is not metabolic syndrome, or maybe we use differnt defintions.
Metabolic syndrome, also known as insulin resistance syndrome, is a group of conditions that increase the rick of developing dibetes, heart disease, and stroke.


 
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Okay, the possibility of gaining weight is not metabolic syndrome, or maybe we use differnt defintions.
Metabolic syndrome, also known as insulin resistance syndrome, is a group of conditions that increase the rick of developing dibetes, heart disease, and stroke.
I think it's not that closely defined. It's a syndrome. I think it starts with obesity.

The key sign of metabolic syndrome is central obesity, also known as visceral, male-pattern or apple-shaped adiposity. It is characterized by adipose tissue accumulation predominantly around the waist and trunk. Other signs of metabolic syndrome include high blood pressure, decreased fasting serum HDL cholesterol, elevated fasting serum triglyceride level, impaired fasting glucose, insulin resistance, or prediabetes. Associated conditions include hyperuricemia; fatty liver (especially in concurrent obesity) progressing to nonalcoholic fatty liver disease; polycystic ovarian syndrome in women and erectile dysfunction in men; and acanthosis nigricans.
 
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