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Ya it does seem like guys on full carnivore can see a slight decrease in testosterone. Dr Anthony Chaffee says that he’s never seen this, but I’ve seen a few guys report this, so it can happen.
When I was getting free T results of 65 pg/ml with Quest equilibrium dialysis (making me think I needed TRT) I was pure carnivore and drinking alot of coffee. I then tested 111 pg/ml after coming off TRT, and I attributed that increase to stopping the caffeine. However, I realized that I was also eating alot of fruit for that second test.

I am planning to test again soon, on the same meat & fruit diet, with coffee added back in. We will find out whether it was lack of carbs or coffee/caffeine that was the culprit for the low free T.
 
When I was getting free T results of 65 pg/ml with Quest equilibrium dialysis (making me think I needed TRT) I was pure carnivore and drinking alot of coffee. I then tested 111 pg/ml after coming off TRT, and I attributed that increase to stopping the caffeine. However, I realized that I was also eating alot of fruit for that second test.

I am planning to test again soon, on the same meat & fruit diet, with coffee added back in. We will find out whether it was lack of carbs or coffee/caffeine that was the culprit for the low free T.
Are u currently not on HRT?

I’ve always heard that being insulin sensitive can increase SHBG, which would obv lower free T. So makes sense that carnivore could potentially lower free T
 
Are u currently not on HRT?

I’ve always heard that being insulin sensitive can increase SHBG, which would obv lower free T. So makes sense that carnivore could potentially lower free T
That's right, no HRT for now. About the free T, I believe it reflects the rate of production and that SHBG is driven down by higher free T, not the other way around. So assuming this correct, you are simply making or taking less testosterone when your free T is lower.

Cataceous has covered this at length before.
 
It stands to reason that if you are on HRT, this would not be a factor. This would apply to those whose natural production could be influenced by carbohydrate reduction. Please correct me if I am wrong, but exogenous testosterone would not seem to be subject to any nutritional factors.
 
It stands to reason that if you are on HRT, this would not be a factor. This would apply to those whose natural production could be influenced by carbohydrate reduction. Please correct me if I am wrong, but exogenous testosterone would not seem to be subject to any nutritional factors.
Yes, your diet, your sleep, stress, alcohol intake, overtraining, no lifestyle factors affect your testosterone anymore once you're on HRT.
 
Not sure tbh. I didn’t know there was a high cortisol issue when eating low carb. U sure that’s a thing? Everyone that I’ve seen do full carnivore has energy right when they wake up, sleeps great, and has even/ stable energy throughout the day. Doesn’t seem like any of them have cortisol issues. But here’s a vid that I think goes over it. Maybe it would be helpful.


Thanks to everyone who replied to this. The issue as I understand it with cortisol is that at least in some people, no matter how many calories you eat, the lack of carbs and the resulting need for the body to make glucose is perceived as a stress and can create elevated cortisol, which can make it hard to lose body fat and create sleep disruptions. My sleep was definitely harmed when I went too low-carb. Perhaps more time would resolve the problem, but the impact of going in and out of ketosis has always been one of the issues with pure keto and the impact on my workouts motivated me to go back to being lowish carb but not pure keto. If I remember correctly, it is chemically easier for the body to convert protein to glucose than to convert fat to glucose, so perhaps that is why carnivore people don't seem to run into this issue as much as the more traditional keto people.
 
Thanks to everyone who replied to this. The issue as I understand it with cortisol is that at least in some people, no matter how many calories you eat, the lack of carbs and the resulting need for the body to make glucose is perceived as a stress and can create elevated cortisol, which can make it hard to lose body fat and create sleep disruptions. My sleep was definitely harmed when I went too low-carb. Perhaps more time would resolve the problem, but the impact of going in and out of ketosis has always been one of the issues with pure keto and the impact on my workouts motivated me to go back to being lowish carb but not pure keto. If I remember correctly, it is chemically easier for the body to convert protein to glucose than to convert fat to glucose, so perhaps that is why carnivore people don't seem to run into this issue as much as the more traditional keto people.
If you saw Funkmeisters reply above, he predicted the Carnivores prevail. If you are lost… read the first post :)

Stress is the factor that is mentioned in every reference you search on the subject. Without going into unnecessary detail, there is good stress and bad stress. Stress that leads to growth (exercise) is a form of good stress. Stress that leads to anxiety and other negative factors is bad stress. An oversimplification yes, but all stress leads to increased cortisol as that is the body’s mechanism of protection.Cortisol is not an enemy, it is an ally that keeps us all protected from the onslaught of things we face as humans. It’s only when it gets elevated from negative factors that it becomes detrimental.

Your input was invaluable, thank you
 
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That's right, no HRT for now. About the free T, I believe it reflects the rate of production and that SHBG is driven down by higher free T, not the other way around. So assuming this correct, you are simply making or taking less testosterone when your free T is lower.

Cataceous has covered this at length before.
Oh interesting! So being insulin sensitive can decrease free T, and that decrease in free T would be what increases SHBG? How would the body keep total T the same, but decrease free T tho? I thought the only way to lower or raise free T is to adjust binding proteins, such as SHBG and Albumin? How would the body keep total T the same, but lower free T first, before SHBG and/ or albumin levels increased? I would think that the only way for total T to be the same, but free T to increase or decrease, would be if SHBG and/ or Albumin increased or decreased first, binding more or less to the total amount of test in the system, and therefore increasing or decreasing unbound test levels
 
Another interesting thing about how the body regulates free T is it’s desire to maintain homeostasis. These two sets of labs that I had done are a good example of it. As u can see, my protocol was basically the same during both labs. The only difference is in the first set of labs, I was on arimidex, and the 2nd set of labs I was on the equivalent dose of exemestane. Exemestane is known to lower SHBG, while arimidex does not. So what I assume happened was, in the 2nd set of labs, the exemestane lowered my SHBG, which would have increased my free and bio T levels. But as u can see, my free and bio T levels were basically identical between the two labs. What im assuming my body did while I was on exemestane, was decrease my total T, to maintain the same free and bio T levels as I had before while on arimidex. I could be wrong on the exact mechanisms by which my free and bio T levels remained the same, but the point is the body has very interesting mechanisms to attempt to maintain homeostasis the best that it can. Again, that’s what I’m assuming it was trying to do.

Also, as a side note, these labs confirm that E2 is in fact the main stimulator of prolactin production, in the male body. These are some of the lowest prolactin levels I’ve ever had, and it’s simply because I basically bottomed out my E2 levels on the dosages of arimidex and exemestane I was taking at the time

and another side note lol. For anyone wondering what the equivalent dose of exemestane and arimidex are, for most guys, it’s basically 1:1. A full 1mg tab of arimidex is basically equivalent to a full 25mg tab of exemestane



8-15-17 labs were while on this protocol:

Test- 90mg split into EOD dosing

HCG - 800IU split into EOD dosing (Pregnyl HCG)

Arimidex - 0.25mg EOD

Total T - 1299 (250-1100 ng/dL)

Free T - 146.6 (46.0-224.0)

Bio T - 307.8 (110.0-575.0 ng/dL)

SHBG 51 (10-50)

E2 Sensitive - 8

E2 NOT Sensitive - 13

E2 Free - 0.28 (0.2-1.5)

Albumin - 4.6 (3.6-5.1)

DHT - 95 (16-79)

Prolactin - 3.1 (2.0-18.0)



12-13-17 labs were while on this protocol:

Test- 90mg split into EOD dosing

HCG- 800iu split into EOD dosing (Pregnyl HCG)

Exemestane - 6.25mg EOD

Total T - 974 (250-1100 ng/dL)

Free T - 142.6 (46.0-224.0)

Bio T - 287.0 (110.0-575.0 ng/dL)

SHBG 36 (10-50)

E2 Sensitive - 9

E2 NOT Sensitive - 13

E2 Free - 0.28 (0.2-1.5)

Albumin - 4.4 (3.6-5.1)

DHT - 65 (16-79)

Prolactin - 4.5 (2.0-18.0)
 
Oh interesting! So being insulin sensitive can decrease free T, and that decrease in free T would be what increases SHBG? How would the body keep total T the same, but decrease free T tho? I thought the only way to lower or raise free T is to adjust binding proteins, such as SHBG and Albumin? How would the body keep total T the same, but lower free T first, before SHBG and/ or albumin levels increased? I would think that the only way for total T to be the same, but free T to increase or decrease, would be if SHBG and/ or Albumin increased or decreased first, binding more or less to the total amount of test in the system, and therefore increasing or decreasing unbound test levels
So there are multiple things that affect SHBG level, and free T is just one of them. Conversely, SHBG is NOT one of the things that regulates the level of free T. This is the big revelation and point of contention with the traditional understanding. Free T is being regulated by the HPTA adjusting output of the testicles up or down (or your dose of exogenous T) and SHBG is just a bystander to that process. The effect of SHBG increasing or decreasing is to increase or decrease the total testosterone value associated with a given free T value.

Being insulin sensitive would tend to increase SHBG. If free T is equal, this would have the effect of increasing total testosterone.

More here:


@Cataceous please chime in if needed to correct or elaborate on these statements.
 
Thanks to everyone who replied to this. The issue as I understand it with cortisol is that at least in some people, no matter how many calories you eat, the lack of carbs and the resulting need for the body to make glucose is perceived as a stress and can create elevated cortisol, which can make it hard to lose body fat and create sleep disruptions. My sleep was definitely harmed when I went too low-carb. Perhaps more time would resolve the problem, but the impact of going in and out of ketosis has always been one of the issues with pure keto and the impact on my workouts motivated me to go back to being lowish carb but not pure keto. If I remember correctly, it is chemically easier for the body to convert protein to glucose than to convert fat to glucose, so perhaps that is why carnivore people don't seem to run into this issue as much as the more traditional keto people.
ya I think once ur fat adapted, the potential cortisol spikes are no longer an issue. The majority of people on long term carnivore don’t have any symptoms of elevated cortisol, from what I’ve seen

I would like to do full carnivore at some point, but idk if I ever will, due to my plans to lift weights until the day I die, and idk if I could ever get used to lifting without carbs in my system. I think I would always think about how much better my workouts would be with them
 
Another interesting thing about how the body regulates free T is it’s desire to maintain homeostasis. These two sets of labs that I had done are a good example of it. As u can see, my protocol was basically the same during both labs. The only difference is in the first set of labs, I was on arimidex, and the 2nd set of labs I was on the equivalent dose of exemestane. Exemestane is known to lower SHBG, while arimidex does not. So what I assume happened was, in the 2nd set of labs, the exemestane lowered my SHBG, which would have increased my free and bio T levels. But as u can see, my free and bio T levels were basically identical between the two labs. What im assuming my body did while I was on exemestane, was decrease my total T, to maintain the same free and bio T levels as I had before while on arimidex. I could be wrong on the exact mechanisms by which my free and bio T levels remained the same, but the point is the body has very interesting mechanisms to attempt to maintain homeostasis the best that it can. Again, that’s what I’m assuming it was trying to do.

Also, as a side note, these labs confirm that E2 is in fact the main stimulator of prolactin production, in the male body. These are some of the lowest prolactin levels I’ve ever had, and it’s simply because I basically bottomed out my E2 levels on the dosages of arimidex and exemestane I was taking at the time

and another side note lol. For anyone wondering what the equivalent dose of exemestane and arimidex are, for most guys, it’s basically 1:1. A full 1mg tab of arimidex is basically equivalent to a full 25mg tab of exemestane



8-15-17 labs were while on this protocol:

Test- 90mg split into EOD dosing

HCG - 800IU split into EOD dosing (Pregnyl HCG)

Arimidex - 0.25mg EOD

Total T - 1299 (250-1100 ng/dL)

Free T - 146.6 (46.0-224.0)

Bio T - 307.8 (110.0-575.0 ng/dL)

SHBG 51 (10-50)

E2 Sensitive - 8

E2 NOT Sensitive - 13

E2 Free - 0.28 (0.2-1.5)

Albumin - 4.6 (3.6-5.1)

DHT - 95 (16-79)

Prolactin - 3.1 (2.0-18.0)



12-13-17 labs were while on this protocol:

Test- 90mg split into EOD dosing

HCG- 800iu split into EOD dosing (Pregnyl HCG)

Exemestane - 6.25mg EOD

Total T - 974 (250-1100 ng/dL)

Free T - 142.6 (46.0-224.0)

Bio T - 287.0 (110.0-575.0 ng/dL)

SHBG 36 (10-50)

E2 Sensitive - 9

E2 NOT Sensitive - 13

E2 Free - 0.28 (0.2-1.5)

Albumin - 4.4 (3.6-5.1)

DHT - 65 (16-79)

Prolactin - 4.5 (2.0-18.0)
So these labs are a good demonstration of the principles we are talking about here. We're saying that free T is reflecting only the rate that testosterone is introduced to your system, either by endogenous production or exogenous administration, and is not influenced by SHBG. Your rate of testosterone production was kept constant and so your free T was kept constant, even as SHBG and total testosterone changed dramatically.

Between this, the fact that free T is what your body is trying to maintain a certain level of for homeostasis, and the fact that free T is the driver of hypogonadal symptoms or the lack of them, you can see why total testosterone is relatively meaningless by comparison. Total T tells you alot about your SHBG level, and not very much about whether you are hypogonadal or eugonadal.
 
So there are multiple things that affect SHBG level, and free T is just one of them. Conversely, SHBG is NOT one of the things that regulates the level of free T. This is the big revelation and point of contention with the traditional understanding. Free T is being regulated by the HPTA adjusting output of the testicles up or down (or your dose of exogenous T) and SHBG is just a bystander to that process. The effect of SHBG increasing or decreasing is to increase or decrease the total testosterone value associated with a given free T value.

Being insulin sensitive would tend to increase SHBG. If free T is equal, this would have the effect of increasing total testosterone.

More here:


@Cataceous please chime in if needed to correct or elaborate on these statements.
Ohhh ok, this makes sense. Think this basically explains what happened in the two sets of labs that I posted. It also explains why people tend to see lower total T levels when using DHT derivatives. DHT derivatives lower SHBG. So if I’m understanding correctly, it would make sense that the decrease in SHBG would decrease total T levels, right?
 
So these labs are a good demonstration of the principles we are talking about here. We're saying that free T is reflecting only the rate that testosterone is introduced to your system, either by endogenous production or exogenous administration, and is not influenced by SHBG. Your rate of testosterone production was kept constant and so your free T was kept constant, even as SHBG and total testosterone changed dramatically.

Between this, the fact that free T is what your body is trying to maintain a certain level of for homeostasis, and the fact that free T is the driver of hypogonadal symptoms or the lack of them, you can see why total testosterone is relatively meaningless by comparison. Total T tells you alot about your SHBG level, and not very much about whether you are hypogonadal or eugonadal.
Ain’t that the truth. When I was hypogonadal I had a total T between 600-700. Had all the symptoms except sexual issues. Free T was either bottom of the barrel, or below the bottom of the reference rage, depending on which set of labs i look back at. Had around 3 sets of labs on nothing, and all of them showed the same thing. Healthy levels of total T, high SHBG, very low free T
 
Ohhh ok, this makes sense. Think this basically explains what happened in the two sets of labs that I posted. It also explains why people tend to see lower total T levels when using DHT derivatives. DHT derivatives lower SHBG. So if I’m understanding correctly, it would make sense that the decrease in SHBG would decrease total T levels, right?
Yes
 
... It also explains why people tend to see lower total T levels when using DHT derivatives. DHT derivatives lower SHBG. So if I’m understanding correctly, it would make sense that the decrease in SHBG would decrease total T levels, right?
That's probably the primary effect. There may also be a secondary effect: Having more SHBG bound to DHT or derivatives is tantamount to having less SHBG, also lowering total testosterone. This effect can be enhanced when the binding affinity for SHBG of DHT/derivative is higher than testosterone's.
For example: Kb(T) < Kb(DHT) < Kb(mesterolone)
 
So I just finished watching this. Dr. Mercola’s views on nutrition surprised me a bit. He apparently thinks it’s very unhealthy and not good for overall metabolic health to consistently eat less than around 150g of carbs per day. Unless the person has cancer. He then thinks it’s correct to limit carbs, but then once the person is in remission, and regains their metabolic health, he feels they should then return to eating at least around 150g of carbs per day. He personally eats around 450-500g of carbs per day! He says he eats around 3-4lbs of watermelon every single morning, sometimes 5lbs. And that’s all flesh, not including any of the rind

Ive never heard someone that’s so passionate about health/ longevity advocate for eating up to 500g or carbs per day before. What do u guys think of his views on nutrition?

 
First of all, I give him great credit for being open to changing his views over time when presented with new information. Most people refuse to listen to anything that doesn't agree with some pre-conceived point-of-view and they just try to fit everything into a conclusion they've already drawn. Where he is now is very close to the the Perfect Health Diet recommendations which I've suggested here many times as a home-base for people to start with, with the exception that PHD recommends "safe starches" such a potatoes and white rice as the primary source of carbs instead of fruit. That said it is important to remember that this type of eating is for healthy people, which excludes probably at least 80% of people in the US and Canada. (Defining healthy is a longer conversation.) Also, I don't think he has thought through all the implications of what he is saying (such as metabolic inflexibility actually being an inability to access fat stores for fuel, and low-carb diets often being much better for cancer patients) so I think he has jumped the gun a little bit with his confidence level and the implications of what he is saying. He is getting a lot of his current info from the Ray Peat camp (which is close to PHD except for the fruit and the amount of carbs) however I think he needs to run some of what he is saying by some of the nutritional big-brains like Chris Masterjohn, Dom D'Agostino and James D'Nicoloantonio. There is a lot of individual variability as well that would argue for erring on the lower side of carb intake (at least for a while) for most people. I generally stay in the 50-200 grams of carbs per day range depending on my activity and food cycle schedule. PHD is very-well researched and aligns with what the longest-lived healthiest people on the planet do, so it is hard to argue against for someone whose genes and circumstances permit it.
 
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First of all, I give him great credit for being open to changing his views over time when presented with new information. Most people refuse to listen to anything that doesn't agree with some pre-conceived point-of-view and they just try to fit everything into a conclusion they've already drawn. Where he is now is very close to the the Perfect Health Diet recommendations which I've suggested here many times as a home-base for people to start with, with the exception that PHD recommends "safe starches" such a potatoes and white rice as the primary source of carbs instead of fruit. That said it is important to remember that this type of eating is for healthy people, which excludes probably at least 80% of people in the US and Canada. (Defining healthy is a longer conversation.) Also, I don't think he has thought through all the implications of what he is saying (such as metabolic inflexibility actually being an inability to access fat stores for fuel, and low-carb diets often being much better for cancer patients) so I think he has jumped the gun a little bit with his confidence level and the implications of what he is saying. He is getting a lot of his current info from the Ray Peat camp (which is close to PHD except for the fruit and the amount of carbs) however I think he needs to run some of what he is saying by some of the nutritional big-brains like Chris Masterjohn, Dom D'Agostino and James D'Nicoloantonio. There is a lot of individual variability as well that would argue for erring on the lower side of carb intake (at least for a while) for most people. I generally stay in the 50-200 grams of carbs per day range depending on my activity and food cycle schedule. PHD is very-well researched and aligns with what the longest-lived healthiest people on the planet do, so it is hard to argue against for someone whose genes and circumstances permit it.
What’s PHD? Any way to give a quick synopsis?
 
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