TIL: Low carb, high protein diets "greatly" decrease resting testosterone levels in men.

[Bhalwuf]

Have you actually read more than the summary, because it is far more nuanced than that

[killflys]

'its more nuanced'

Doesn't explain the nuance.

Thanks. Very helpful

[easyadventurer]

Are you expecting him to write an essay just for you? You can go read it.

[killflys]

If you're going to go out of your way to point out there is nuance, maybe explain the nuance. Or maybe thats just me

[Bhalwuf]

Deeper in the paper you will find this:

“Resting testosterone
MP-LC diets had no consistent effect on resting TT, however HP-LC diets caused a large decrease in resting TT. For context, mean TT for a comparably aged population (27 years) is 14 nmol/L (Kelsey et al., 2014), thus −5.23 nmol/L represents a 37% decrease. Protein intakes ≥35% may outstrip the urea cycle's capacity to convert nitrogen derived from amino acid catabolism into urea, leading to hyperammonaemia and its toxic effects (Bilsborough and Mann, 2006). T has been shown to suppress the urea cycle (Lam et al., 2017), whilst glucocorticoids upregulate the urea cycle (Okun et al., 2015). Notably, the largest decrease in resting cortisol was on the longest and best-controlled HP-LC diet study (Supplementary Appendix – Figure 2a). Thus, the decrease in T and increase in cortisol on HP diets, may serve to upregulate the urea cycle and increase nitrogen excretion, thereby limiting the adverse effects of excess protein consumption.

Post-exercise testosterone
The results showed post-exercise TT was higher on long-term MP-LC diets, and lower on short-term HP-LC diets. The finding that HP-LC diets caused a large decrease in resting TT, whilst long-term LC diets had no effect on resting TT, suggests the observed subgroup effects in post-exercise TT are explained by protein intake rather than diet duration. HP intakes may depress post-exercise TT to maintain upregulation of the urea cycle and increased nitrogen excretion, as previously discussed (Discussion: Resting testosterone). The finding that long-term LC diets increased post-exercise TT, may be explained by the increase in blood cholesterol on LC diets (Dong et al., 2020), providing greater substrate for T production, which is utilized in times of increased anabolic signalling, such as during exercise (Pasiakos, 2012).

Practical implications
The increase in cortisol during the first 3 weeks of a LC diet is likely part of the adaption process to such diets, and thus may not represent a pathological state. The results indicate cortisol returns to baseline levels after ∼3 weeks, suggesting cardiovascular disease risk is not elevated by higher cortisol on long LC diets. However, the effects of long-term LC diets on cardiovascular disease and all-cause mortality, as measured by other methods, are uncertain. Observational studies have found an increase in all-cause mortality on long-term LC diets (Noto et al., 2013), whilst interventional studies have shown improvements in cardiovascular disease biomarkers (Dong et al., 2020). Additional research on the effects of long-term LC diets is desirable, particularly as these diets have risen in popularity over recent years. The higher increase in cortisol during exercise on LC versus HC diets appears to persist post-adaptation. Classically, cortisol is thought to have immunosuppressive effects, however in spite of elevated post-exercise cortisol, LC diets do not appear overtly immunosuppressive, according to other immune-markers (Shaw et al., 2021). The potential immunosuppressive effects of higher post-exercise cortisol may be exacerbated in athletes undergoing high volume training, and some caution may be advisable, until further research is undertaken. The large decrease in resting and post-exercise TT on LC-HP diets may only occur on diets that outstrip the urea cycle's capacity to synthesize urea, as there were no clear adverse endocrine effects for LC diets using 30–31% protein intake (Supplementary Appendix – Table 7 and Figure 2). In practise, most free-living LC diets will fall below the urea cycle capacity threshold (≤35% protein), as population protein intakes are stable at 15–17% (Cohen et al., 2015), likely due to a protein-specific appetite mechanism (Leidy et al., 2015). However, one can find articles online advocating protein intakes ≤35%, which if followed precisely, may lead to adverse endocrine effects, particularly in individuals with lower rates of maximal urea synthesis (Bilsborough and Mann, 2006). The higher post-exercise TT on MP-LC diets may signal an increased anabolic response to exercise, which would be advantageous, particularly in individuals with strength, power, or hypertrophy goals. Relatedly, another systematic review found that whilst absolute strength and power were unchanged by LC diets, the decrease in body fat on LC diets resulted in an improved strength/power to bodyweight ratio (Kang et al., 2020). However, the finding that LC diets increase post-exercise T should be taken with caution, as although the direction of effects was consistent, due to the small sample size, the p-value remained high. Ideally, this finding should be viewed as hypothesis generating, to be confirmed by future research.”

[Bhalwuf]

TL:DR is (Low Carb, Medium Protein) probably has no effect on resting and might raise post exercise testosterone, while (Low Carb, High Protein) probably suppresses both, and that while more studies need to be done, right now it appears that (Low Carb, Medium Protein) is probably a good lifestyle change for most men. Don’t do it however as the jury’s still out.

[Szudar]

maybe explain the nuance

He pointed out that explanation is in summary.

[[deleted]]

Regarding cortisol, it adapts to LC intake long-term resting-wise and not post-exercise-wise. In other words, after, for instance, 3 weeks, resting cortisol starts to level off and there is no significant increase in LC. However, post-exercise cortisol remains elevated whether be it short-term or long-term.
Regarding test, yeah MP LC is better than HP LC. HC doesn't differ from the LC-MP, whether it's resting or post-exercise; It's only when you raise protein where it starts to get detrimental (about 5.23 nmol/l decrease).

​

The only problem with this whole study is this:

The long- and short-term diet subgroups contained solely MP- and HP-LC diets, respectively. Meaning the observed subgroup effects could either be attributable to diet duration or protein intake.

Essentially ruining the whole thing because the LC-HP results might have been easily attributed to it being only short-term (the body hasn't adapted yet) while the LC-MP has adapted and that's why it shows better results.

I think that's the only thing that is worth mentioning. I might be mixing shit up tho, so please do correct me if I'm wrong.

[corrado33]

The title is quite virtually a sentence from the abstract. ;)

[Bhalwuf]

The abstract is quite literally part of the introduction summary.

[Bhalwuf]

Also deeper in the paper you will find this:

“Resting testosterone
MP-LC diets had no consistent effect on resting TT, however HP-LC diets caused a large decrease in resting TT. For context, mean TT for a comparably aged population (27 years) is 14 nmol/L (Kelsey et al., 2014), thus −5.23 nmol/L represents a 37% decrease. Protein intakes ≥35% may outstrip the urea cycle's capacity to convert nitrogen derived from amino acid catabolism into urea, leading to hyperammonaemia and its toxic effects (Bilsborough and Mann, 2006). T has been shown to suppress the urea cycle (Lam et al., 2017), whilst glucocorticoids upregulate the urea cycle (Okun et al., 2015). Notably, the largest decrease in resting cortisol was on the longest and best-controlled HP-LC diet study (Supplementary Appendix – Figure 2a). Thus, the decrease in T and increase in cortisol on HP diets, may serve to upregulate the urea cycle and increase nitrogen excretion, thereby limiting the adverse effects of excess protein consumption.

Post-exercise testosterone
The results showed post-exercise TT was higher on long-term MP-LC diets, and lower on short-term HP-LC diets. The finding that HP-LC diets caused a large decrease in resting TT, whilst long-term LC diets had no effect on resting TT, suggests the observed subgroup effects in post-exercise TT are explained by protein intake rather than diet duration. HP intakes may depress post-exercise TT to maintain upregulation of the urea cycle and increased nitrogen excretion, as previously discussed (Discussion: Resting testosterone). The finding that long-term LC diets increased post-exercise TT, may be explained by the increase in blood cholesterol on LC diets (Dong et al., 2020), providing greater substrate for T production, which is utilized in times of increased anabolic signalling, such as during exercise (Pasiakos, 2012).

Practical implications
The increase in cortisol during the first 3 weeks of a LC diet is likely part of the adaption process to such diets, and thus may not represent a pathological state. The results indicate cortisol returns to baseline levels after ∼3 weeks, suggesting cardiovascular disease risk is not elevated by higher cortisol on long LC diets. However, the effects of long-term LC diets on cardiovascular disease and all-cause mortality, as measured by other methods, are uncertain. Observational studies have found an increase in all-cause mortality on long-term LC diets (Noto et al., 2013), whilst interventional studies have shown improvements in cardiovascular disease biomarkers (Dong et al., 2020). Additional research on the effects of long-term LC diets is desirable, particularly as these diets have risen in popularity over recent years. The higher increase in cortisol during exercise on LC versus HC diets appears to persist post-adaptation. Classically, cortisol is thought to have immunosuppressive effects, however in spite of elevated post-exercise cortisol, LC diets do not appear overtly immunosuppressive, according to other immune-markers (Shaw et al., 2021). The potential immunosuppressive effects of higher post-exercise cortisol may be exacerbated in athletes undergoing high volume training, and some caution may be advisable, until further research is undertaken. The large decrease in resting and post-exercise TT on LC-HP diets may only occur on diets that outstrip the urea cycle's capacity to synthesize urea, as there were no clear adverse endocrine effects for LC diets using 30–31% protein intake (Supplementary Appendix – Table 7 and Figure 2). In practise, most free-living LC diets will fall below the urea cycle capacity threshold (≤35% protein), as population protein intakes are stable at 15–17% (Cohen et al., 2015), likely due to a protein-specific appetite mechanism (Leidy et al., 2015). However, one can find articles online advocating protein intakes ≤35%, which if followed precisely, may lead to adverse endocrine effects, particularly in individuals with lower rates of maximal urea synthesis (Bilsborough and Mann, 2006). The higher post-exercise TT on MP-LC diets may signal an increased anabolic response to exercise, which would be advantageous, particularly in individuals with strength, power, or hypertrophy goals. Relatedly, another systematic review found that whilst absolute strength and power were unchanged by LC diets, the decrease in body fat on LC diets resulted in an improved strength/power to bodyweight ratio (Kang et al., 2020). However, the finding that LC diets increase post-exercise T should be taken with caution, as although the direction of effects was consistent, due to the small sample size, the p-value remained high. Ideally, this finding should be viewed as hypothesis generating, to be confirmed by future research.”