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Some recent blood work - low cholesterol

From the study Dante posted above.

" The reduction in cLDL was accompanied by a dose-dependent
elevation in cHDL in all patients. In the 10% subjects with the best response the effect on cHDL was very striking −64.6% (Table 1). In addition, metabolic syndrome patients presented a highly significant (Pb0.0001) reduction in blood glucose levels (mean value of −18.9% under 500 mg BPF treatment (C1 group) and −22.4% in C2 group). No changes in glucose levels were recorded after 30 days in the placebo group (Fig. 2, Table 2). These data suggest that BPF induces complex effects on metabolic regulation. As reported in Table 1 the maximum effect for all cholesterol parameters was seen in patients taking 1000 mg BPF daily, but differences between 500 mg and 1000 mg dosage were statistically significant only for cHDL. In addition, we evaluated the efficacy of BPF depending on the metabolic disorder, but the differences were not statistically significant (PN0.05) (Table 1). This suggests that BPF consump-tion corrects common mechanisms of cholesterol metabolism similarly deregulated in all 3 groups of patients."

So it seems going from 500mg a day to 1000mg a day there was a significant difference in increases in HDL. So yeah I'm definitely going to start 1000mg.


Sent from my SM-N900V using Tapatalk 2
Was just reading this exact study. I have been doing 1 cap in the morning prebreakfast shake and 1 in the afternoon pre my postworkout meal.

I will get bloods in a couple weeks and see where i am at. My last blood work was on cycle and lipids were jacked up!! HDL was 19, LDL was 181, and total 215, ratio of 11.3 [emoji20]
 
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ok so would it be safe to say anyone who has high ldl, and total cholesterol, yet decent hdl, that 500 mlg might be the most beneficial instead of the 1000 mlg as the hdl might raise to a level that some might not want? it may sound stupid but ive read and been told that u dont want a really high hdl either, as it may or may not cause issues down the road?....

im not looking for a shit storm because of what ive said, im just looking for answers....
 
I would say that seems dangerous to me such a low HDL. But not sure how it comes into play when total cholesterol is so low. How'd you get it so low?

Sent from my SM-N900V using Tapatalk 2

If your total cholesterol is on the low side of the reference range than your HDL will also be on the low side as well. Same deal for LDL. What does matter is you Total/HDL ratio which is good.
 
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Your cholesterol should go down definitely...but your HDL should come up. I will be highly disappointed if this doesn't pan out. ive been taking the 500mg 500mg dose 2x daily to get the 1000mg a day that was shown to be the most effective. I just had bloodwork done and will get the results in about a week. It will be very disappointing if my HDL isn't up at least 20% (im expecting 30-40% raise)..... There was a 42% raise in human subjects if I remember right (read abstract many months ago) at the 1000mg dose

Hypolipemic and hypoglycaemic activity of bergamot polyphenols: from animal models to human studies. - ResearchGate

fulltext is on right side of page


Please update us on your latest bloodwork results.:headbang:
 
You guys really focus too much on HDL. The research doesn't substantiate your focus.

The first thing that makes low HDL virtually useless as a predictor in an androgen using population is upregulated reverse cholesterol transport. If the job of HDL that we we are primarily concerned with is reverse cholesterol transport and androgens upregulate reverse cholesterol transport then how can you argue that a low HDL for an androgen using exercising bodybuilder should be judged on the same scale as a natural sedentary person?

Example - "By lowering high density lipoprotein (HDL) cholesterol, testosterone contributes to the gender difference in HDL cholesterol and has been accused to be pro-atherogenic. The mechanism by which testosterone influences HDL cholesterol is little understood. We therefore investigated the effect of testosterone on the gene expression of apolipoprotein A-I (apoA-I), hepatic lipase (HL), scavenger receptor B1 (SR-BI), and the ATP binding cassette transporter A1 (ABCA1), all of which are important regulators of HDL metabolism. Testosterone led to a dose-dependent up-regulation of SR-BI, which was assessed on both the mRNA and the protein levels. As a functional consequence, we observed an increased HDL(3)-induced cholesterol efflux from macrophages. At supraphysiological dosages, testosterone also increased the expression of HL in HepG2 cells. These data suggest that testosterone, despite lowering HDL cholesterol, intensifies reverse cholesterol transport and thereby exerts an anti-atherogenic rather than a pro-atherogenic effect."

This also tells us what we should be concerned with. It is not HDL but rather cholesterol efflux capacity.

Example - "It is unclear whether high-density lipoprotein (HDL) cholesterol concentration plays a causal role in atherosclerosis. A more important factor may be HDL cholesterol efflux capacity, the ability of HDL to accept cholesterol from macrophages, which is a key step in reverse cholesterol transport. We investigated the epidemiology of cholesterol efflux capacity and its association with incident atherosclerotic cardiovascular disease outcomes in a large, multiethnic population cohort. We measured HDL cholesterol level, HDL particle concentration, and cholesterol efflux capacity at baseline in 2924 adults free from cardiovascular disease who were participants in the Dallas Heart Study. In contrast to HDL cholesterol level, which was associated with multiple traditional risk factors and metabolic variables, cholesterol efflux capacity had minimal association with these factors. Baseline HDL cholesterol level was not associated with cardiovascular events in an adjusted analysis. In a fully adjusted model that included traditional risk factors, HDL cholesterol level, and HDL particle concentration, there was a 67% reduction in cardiovascular risk in the highest quartile of cholesterol efflux capacity versus the lowest quartile. Cholesterol efflux capacity, a new biomarker that characterizes a key step in reverse cholesterol transport, was inversely associated with the incidence of cardiovascular events in a population-based cohort."

That all but proves, on some 3000 people, that HDL does not matter and cholesterol efflux capacity does. These are normal people also not using androgens with upregulated efflux.

One more time for those who find this hard to accept given their constant obsession with their HDL while on androgens. "Cholesterol-efflux capacity, which is a marker of HDL function that measures reverse cholesterol transport, is inversely associated with incident atherosclerotic cardiovascular disease in a large population of patients healthy at baseline. The findings, say researchers, support 'retiring' the HDL cholesterol hypothesis—the idea of simply raising HDL cholesterol to reduce the risk of cardiovascular disease—and instead should shift the focus to measures of HDL functionality."

HDL is low because you don't need as much of it. It's a biofeedback mechanism and not a reliable indicator of anything in an androgen using population and more and more evidence mounts to prove this is true for the general population as well. I think most people don't know this about androgens.

Rex.
 
You guys really focus too much on HDL. The research doesn't substantiate your focus.

The first thing that makes low HDL virtually useless as a predictor in an androgen using population is upregulated reverse cholesterol transport. If the job of HDL that we we are primarily concerned with is reverse cholesterol transport and androgens upregulate reverse cholesterol transport then how can you argue that a low HDL for an androgen using exercising bodybuilder should be judged on the same scale as a natural sedentary person?

Example - "By lowering high density lipoprotein (HDL) cholesterol, testosterone contributes to the gender difference in HDL cholesterol and has been accused to be pro-atherogenic. The mechanism by which testosterone influences HDL cholesterol is little understood. We therefore investigated the effect of testosterone on the gene expression of apolipoprotein A-I (apoA-I), hepatic lipase (HL), scavenger receptor B1 (SR-BI), and the ATP binding cassette transporter A1 (ABCA1), all of which are important regulators of HDL metabolism. Testosterone led to a dose-dependent up-regulation of SR-BI, which was assessed on both the mRNA and the protein levels. As a functional consequence, we observed an increased HDL(3)-induced cholesterol efflux from macrophages. At supraphysiological dosages, testosterone also increased the expression of HL in HepG2 cells. These data suggest that testosterone, despite lowering HDL cholesterol, intensifies reverse cholesterol transport and thereby exerts an anti-atherogenic rather than a pro-atherogenic effect."

This also tells us what we should be concerned with. It is not HDL but rather cholesterol efflux capacity.

Example - "It is unclear whether high-density lipoprotein (HDL) cholesterol concentration plays a causal role in atherosclerosis. A more important factor may be HDL cholesterol efflux capacity, the ability of HDL to accept cholesterol from macrophages, which is a key step in reverse cholesterol transport. We investigated the epidemiology of cholesterol efflux capacity and its association with incident atherosclerotic cardiovascular disease outcomes in a large, multiethnic population cohort. We measured HDL cholesterol level, HDL particle concentration, and cholesterol efflux capacity at baseline in 2924 adults free from cardiovascular disease who were participants in the Dallas Heart Study. In contrast to HDL cholesterol level, which was associated with multiple traditional risk factors and metabolic variables, cholesterol efflux capacity had minimal association with these factors. Baseline HDL cholesterol level was not associated with cardiovascular events in an adjusted analysis. In a fully adjusted model that included traditional risk factors, HDL cholesterol level, and HDL particle concentration, there was a 67% reduction in cardiovascular risk in the highest quartile of cholesterol efflux capacity versus the lowest quartile. Cholesterol efflux capacity, a new biomarker that characterizes a key step in reverse cholesterol transport, was inversely associated with the incidence of cardiovascular events in a population-based cohort."

That all but proves, on some 3000 people, that HDL does not matter and cholesterol efflux capacity does. These are normal people also not using androgens with upregulated efflux.

One more time for those who find this hard to accept given their constant obsession with their HDL while on androgens. "Cholesterol-efflux capacity, which is a marker of HDL function that measures reverse cholesterol transport, is inversely associated with incident atherosclerotic cardiovascular disease in a large population of patients healthy at baseline. The findings, say researchers, support 'retiring' the HDL cholesterol hypothesis—the idea of simply raising HDL cholesterol to reduce the risk of cardiovascular disease—and instead should shift the focus to measures of HDL functionality."

HDL is low because you don't need as much of it. It's a biofeedback mechanism and not a reliable indicator of anything in an androgen using population and more and more evidence mounts to prove this is true for the general population as well. I think most people don't know this about androgens.

Rex.

Thoughts on high LDL associated with Testosterone or other similar compounds?
 
Thoughts on high LDL associated with Testosterone or other similar compounds?


AGREE'!!!!

IF ANYONE has any studies on this, id LOVE to see them, it might explain why my ldl will not go lower than 170.....


Sent from my iPP using Tapatrash
 
Your cholesterol should go down definitely...but your HDL should come up. I will be highly disappointed if this doesn't pan out. ive been taking the 500mg 500mg dose 2x daily to get the 1000mg a day that was shown to be the most effective. I just had bloodwork done and will get the results in about a week. It will be very disappointing if my HDL isn't up at least 20% (im expecting 30-40% raise)..... There was a 42% raise in human subjects if I remember right (read abstract many months ago) at the 1000mg dose

Hypolipemic and hypoglycaemic activity of bergamot polyphenols: from animal models to human studies. - ResearchGate

fulltext is on right side of page

Dante. How did your blood work turn out? Curious how the citrus bergamot did for you.

Sent from my SM-N900V using Tapatalk 2
 
I didnt see it mentioned anywhere, but using t3 will cause total cholesterol levels to plummet severely. So if you're on it and get a test result showing low C, thats why
 
I didnt see it mentioned anywhere, but using t3 will cause total cholesterol levels to plummet severely. So if you're on it and get a test result showing low C, thats why

No I don't take t3.

Sent from my SM-N900V using Tapatalk 2
 
I didnt see it mentioned anywhere, but using t3 will cause total cholesterol levels to plummet severely. So if you're on it and get a test result showing low C, thats why


Oh reaaalllyy? Hmmmm.... How much t3 we talkin here and for how long? If t3 is taken when not really needed then what can that cause sides wise? Id be willing to give that a go considering i got a pretty big bottle of cytomel sitting unused pharm grade up in my cabinet....


Sent from my i-PP using TAPATRASH!
 
CHOLESTEROL, TOTAL87 L100-189 MG/DL

TRIGLYCERIDES 47 0-114 MG/DL

HDL CHOLESTEROL 8 L>39 MG/DL

LDL CHOLESTEROL CALC70 0-119 MG/DL



How low is too low... There are conflicting theories I think from what I've read. But I still wonder if since my total cholesterol is so low, does it matter that my HDL cholesterol is super low.


When I had my check up they said the ratio is what's important. My hdl was 13 and my LDL was Like 109. The ratio then is 8.4 to 1 which is bad becayse the good cholesterol arcs like a vacuum to suck up tge bad. Since the bad still vastly outweigh the good a lot of the bad is available to deposit on the artery walls. My doc suggested increasing fiber(not easy when you have colitis because fiber can trigger a flare up) and also increasing cardio. At the time I was doing none. Added some Cheerios for breakfast and multi grain pasta plus 20 min cardio pwo and good rose to 19 and bad dropped to 97.
 
Oh reaaalllyy? Hmmmm.... How much t3 we talkin here and for how long? If t3 is taken when not really needed then what can that cause sides wise? Id be willing to give that a go considering i got a pretty big bottle of cytomel sitting unused pharm grade up in my cabinet....Sent from my i-PP using TAPATRASH!
You seem surprised?

I know I've mentioned to you about asking your primary care provider to pull a complete thyroid panel, related to your lipid profile.

So you're aware, the correlation exists between overt hypothyroidism and clinically significant hypercholesterolemia. Yet, not everyone responds to a lipid lowering effect from thyroid replacement. I would assume this may be related to nonresponsive thyriod expression/activity on HMG-CoA reductase via hepatic transcription and instability of the mRNA.

Or it may be that you have over activity of PCSK9 protein, in which, I don't believe is responsive to thyroid hormone replacement.

Or you may be a carrier of ApoE4 allele, which has been suggestive of those with elevated cholesterol. .

It should be noted also, hyperthyroidism can lower ones HDL. So be before you decide to self treat with T3, I would recommend staying in a physiological range on FT3. By doing so would require you to pull a thyroid panel every 3-6 months.

Rex is much more experienced in this area than I. Maybe he could expand on this of what he has seen in clinical practice, assuming he has patients with hypothyroidism and hypercholesterolemia?
 
Last edited:
You seem surprised?



I know I've mentioned to you about asking your primary care provider to pull a complete thyroid panel, related to your lipid profile.



So you're aware, the correlation exists between overt hypothyroidism and clinically significant hypercholesterolemia. Yet, not everyone responds to a lipid lowering effect from thyroid replacement. I would assume this may be related to nonresponsive thyriod expression/activity on HMG-CoA reductase via hepatic transcription and instability of the mRNA.



Or it may be that you have over activity of PCSK9 protein, in which, I don't believe is responsive to thyroid hormone replacement.



Or you may be a carrier of ApoE4 allele, which has been suggestive of those with elevated cholesterol. .



It should be noted also, hyperthyroidism can lower ones HDL. So be before you decide to self treat with T3, I would recommend staying in a physiological range on FT3. By doing so would require you to pull a thyroid panel every 3-6 months.



Rex is much more experienced in this area than I. Maybe he could expand on this of what he has seen in clinical practice, assuming he has patients with hypothyroidism and hypercholesterolemia?


Yea u are correct, ive yet to finally find a doc who will abide by my wishes and actually order any of the above mentioned panels....

If they are not to expensive i might have to see if directlabs or pml has those specific blood labs and see how much out of pocket will cost me.....


Sent from my i-PP using TAPATRASH!
 

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