The discussion debates whether testosterone drives hunger problems, with some users linking it to appetite changes while the OP cites pre-existing eating difficulties and demands a specific mechanism. References appear to related threads on GLP-1 use alongside testosterone, plus timelines for hormone stabilization and SSRI impacts on fullness. Personal attacks label the OP as having psychiatric or substance issues and dismiss the thread. No agreement forms on causes, leaving only the mentioned plan to trial tirz and pursue ADHD input as a concrete step forward.
What this discussion establishesWhether testosterone is driving the hunger issues or if they stem from earlier unrelated factors
Still openRoot causes of the hunger problems and any direct mechanism involving testosterone
Nothing here is advice.
I started retatrutide a bit more than three months back and now suspect I might be a hyporesponder. At 8 mg every six days there is no drop in food noise or appetite at all. Gastric emptying does slow noticeably, yet that alone does not reduce intake. From what little data exists on appetite effects, the suppression seems to plateau at moderate doses, so raising the amount may not help further. As a bodybuilder I stick closely to my meal plan, but nothing ever leaves me satisfied. My hunger signals are so disrupted that I never feel full and always want more food. Last night I ate 600 g cauliflower, 250 g broccoli, 200 g chicken, 1.5 kg of 0 % yoghurt, 140 g apple, 20 g whey, and 10 g natu in one sitting.
I am curious to read what others say. The situation here, and one nearly identical, differs from the usual obesity case. Eating is either irregular or processed so that weight stays low. This looks like a separate problem from what the main three peptides target. Something else such as teso or elora might fit better. I hope more experienced users will comment. Glad the thread was started.
The late researcher John McDougall claimed some overeating problems stem from skipping the satiety that comes with a starch-heavy diet. He recommended eating as much rice, corn, potatoes, bread, beans and lentils as desired. Another route is cagri or elora, with elora carrying fewer sides and lower overdose risk. The intro thread mentioned ADHD and dopamine issues; certain psychiatric medicines, especially stimulants, can lower appetite. Substances like marijuana or anabolic steroids tend to raise it.
I am not following the goal. Is weight loss the aim, given the use of a weight-loss drug?
There are diets built almost entirely around carbs, just as keto removes nearly all carbs. The right approach depends on activity level and daily life. The most useful plan is usually the one that can be kept up over time.
I do not follow the goal either. There is no excess weight, yet the wish is to eat less. Why, if weight is not an issue? The mention of struggling with BED is also unclear; that does not sound like a sleep problem. Retatrutide is unlikely to aid sleep, whereas DSIP or Selank would be more relevant. Supplements such as NAC, glycine, taurine, melatonin, L-theanine, magnesium glycinate or saffron taken an hour before bed can also promote sleep.
Some participants in the trials showed no weight loss and probably also lacked hunger reduction. Trying cagri or elora could be worthwhile because they act on a different receptor. Otherwise it may simply be low sensitivity to GLP-1 medicines.
Although low-carb diets are popular, carbohydrates remain the body’s preferred fuel. Some people appear to need them more, which could explain stronger cravings than other bodybuilders experience. Personal trials of keto and whole30 left me feeling worse, while a starch-based plan improved satiety. Adding healthy carbs for a period might be worth testing. Stacking tirz or cagri with the current peptide is another option.
BED here means binge-eating disorder. An amylin agonist such as cagri or elora may help more with portion control. In my experience GLP-1 medicines reduce food noise better, though I have not yet used any amylin agonist.
The issue is indeed different from obesity or overweight, and the hope is that readers will grasp the intended use of a GLP-1.
Many diets have been tried; carb cycling is the preferred structure because it supports training performance best. The plan already includes far more carbs than average, yet some reduction is still needed for the current goal of getting very lean. Meals below 20 g carbs rely on vegetables, with modest increases allowed when more volume is required. Thanks for the thoughts.
I would like to list the other compounds, but I am unsure whether that is permitted.
As long as the source is not named it should be fine.
A GLP-1 agonist was chosen first because it was expected to reduce food noise.
The present aim is simply to experience less constant hunger.
Several reuptake inhibitors have been prescribed; methylphenidate has been used the longest. As a child it removed appetite so completely that it became a problem. As an adult, doses up to 60 mg produced only mild suppression. Consistent use stopped some time ago. A paper on another option is being read with a view to obtaining a prescription, as it may lower impulsive behaviour. Exogenous androgens have also been started in the last twelve weeks, though the hunger issue predates them. The current dose is 250 mg test per week, producing a total testosterone of 2500 ng/dL and calculated free T of 62 ng/dL.
Performance is best on carb cycling, yet hunger remains high on any plan. Even 350 g of protein in a single day produced no change in appetite, so the diet itself does not appear to be the cause.
For food noise, tirz possibly combined with cagri or elora can be considered. HGH, steroids and testosterone are known to raise appetite in some users.
That matches my own expectation, yet little literature on individual sensitivity to GLP-1 medicines could be located.
After six months on retatrutide reaching 8 mg per week there was still no weight loss. The same relentless food noise has been present for most of life despite never being overweight. Prediabetes appeared in the thirties at a BMI near 18, with strong family history of insulin resistance. Training occurs five or six times weekly. Retatrutide actually increased hunger as the dose rose. Adding cagri up to 2 mg produced no appetite benefit and caused fatigue. Both were stopped. After discontinuation, weight dropped, food noise eased, and inflammation seemed to lessen. More than a month later, tirz has just been started; early days show a clear difference in food noise. Other compounds are also in use; testosterone and GH have not increased hunger in this case, though awareness exists that they can for others.
Testosterone is injected at 36 mg daily. Literature review indicates exogenous androgens do not raise appetite as commonly believed; many actually lower it due to liver effects. The current dose sits at the upper end of TRT. Cagrilintide is being considered; any personal experience with it would be useful.
Thanks for replying; it is helpful to hear from someone in the same sport with similar experiences. Would a private message be acceptable to request occasional updates on how tirzepatide affects food noise?
The comment was not suggesting a diet mistake. Metabolic responses, hormones and weight distribution vary widely between individuals; some gain readily from minimal stimulus while others train hard for modest change.
Single sittings can reach 6000 calories while body weight is only 74 kg; the pattern affects both physical and mental state.
That may clarify the picture. After reaching goal weight on a GLP-1, TRT was started. An initial higher dose raised IGF and Z scores and added weight despite continued 15 mg tirz. Once levels were balanced, weight stabilised for six months on the same tirz dose. The added testosterone appears to increase hunger and limit further loss, resulting in maintenance rather than reduction. The current meal plan seems to fight hunger constantly, and the binge-eating issues may reflect the body seeking fuel for IGF. What are the current IGF and Z values?
Cagrilintide was tried but became unpleasant past 1 mg even though appetite was strongly reduced. Tirzepatide remains the preferred option. Eloralintide may be tested later once pricing improves.
Testosterone has not increased appetite; the compound has been used only twelve weeks while the hunger problem existed long before. IGF-1 level is unknown.
Has retatrutide been used, and how does its appetite suppression compare with tirzepatide?
A private message is fine. Journey updates will also be posted publicly. Tesofensine is being considered because the food-seeking behaviour may be dopamine-driven. Eloralintide remains a backup, though enthusiasm has dropped after the cagri experience.
That conclusion is not trusted because biology changes; retatrutide is already in use. Bro-science claims are generally discounted. No study supports recreational steroid use from a health standpoint, especially at this age. The first step for anyone finding GLP-1 medicines ineffective is to stop other substances and peptides.
An influencer documented a tesofensine trial and reported no appetite effect. The problem is viewed as largely dopamine-related, so SSRIs and SNRIs are also being examined for their potential to reduce reward-seeking around food. Profile visibility is currently unavailable, preventing following of the tirzepatide updates; any reason for that?
Mounjaro was used first, then a switch to retatrutide was attempted. Retatrutide produced noticeably weaker hunger control, so the tirzepatide dose was raised again and retatrutide lowered. The present combination of 8 mg tirz plus 6 mg reta weekly, both split, is working well.
Testosterone reliably increases appetite based on decades of observation. Current TRT plus GH use confirms the pattern. To avoid the appetite increase, lowering the dose would be advisable; the present protocol likely places levels well above normal range.
Responses to GLP-1 medicines vary. The goal was loss of 13 stubborn pounds gained during perimenopause. Diet is already tight and calories very low; a doctor noted a catabolic state. Tirzepatide was chosen over semaglutide or retatrutide to avoid certain sides. Appetite suppression was not wanted and has not occurred. Microdosing 1 mg split actually increased hunger, allowing more normal eating without starvation while still losing 10 lb. Three more pounds remain.
The earlier comment mistakenly addressed the wrong user, so the closing remark can be ignored.
The name is unfamiliar but will be looked up. Social media use is minimal. Multiple SSRIs and SNRIs have already been tried without success. Undiagnosed ADHD is suspected, though that suspicion is common. Following via avatar menu should generate updates; notifications arrive when new followers appear.
A bottle of tesofensine was purchased and half a 500 mcg tablet was taken every other day. Concerns included possible sides, contraindications, and inconsistent dosing in pressed tablets, which is why doses were split. Results were not dramatic, so risk versus reward did not seem favourable. The half-life is long, roughly nine days for the parent and fourteen-plus days for metabolites, requiring four to six weeks for full clearance.
The dosing concern is reasonable. The batch was tested by an independent lab, yet half-tablet use is still planned. The long half-life may reduce day-to-day variation. How did tesofensine feel in practice?
No advertised adverse effects appeared, but use was brief. The tablets were hard and difficult to split accurately. No major changes were noticed, so the balance of risk and reward did not justify continuing. The long clearance time means the drug and metabolites remain in the system for four to six weeks after the final dose.
That matches what occurred for me after exceeding my target.
Appreciate the input, I was about to inquire since it seemed off.
BED stands for Binge Eating Disorder. It appears the OP keeps feeling strong hunger no matter the amount consumed.
Certain individuals who lack enough hunger control from reta respond better to tirz. Reta often falls short on appetite effects. I combine both at modest levels once weekly or less often based on hunger signals, which keeps appetite down and supports steady loss.
On the mental side, eating disorders are now often viewed as issues of excessive control even when a binge feels like loss of control. Work by Marsha Linehan on DBT and especially RO-DBT addresses this, along with articles on overcontrol patterns and transdiagnostic approaches.
I have never placed much stock in therapy for my own case and doubt I could talk myself into pursuing it. Still, thanks for the links, I will look them over.
The comments seem to assume a low-testosterone situation, unlike mine. I am at the high end of TRT and slightly above normal range. These hunger issues predated any androgen use.
Most reports favor tirzepatide for appetite effects, so I am likely to lower the reta dose and add tirz.
This matches my experience through the end of next year. At 77 kg while trimming the last kilos, things move forward until something overrides and the urge to eat becomes overwhelming. Only on reta, now in week three after starting at 1 mg then 2 mg, appetite control has been decent with food noise reduced though hunger still hits at meal times. The strongest effect came early and has lessened despite the recent increase.
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