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Exactly how toxic are methyl PHs

RawStrength

Member
I know everyone talks about how bad for your liver things like superdrol and other methyls are but is there any published data on how toxic they are?

Like in comparison, how toxic is a 5 week superdrol cycle to the liver compared to 5 years of college frat party drinking?

We all demonize methyls but is there any actual data on them? How much worse are methyl prohormones to your liver than alcohol is?

Looking for actual answers not broscience fellas.

Thanks
 
there is actual data on how hepatotoxic superdrol is. I know henry v has some studies he's shared with me.

I dont have them anymore, but im sure he still does.

think of it like this.

it takes your body about an hour to metabolize alcohol.

it takes your body 16hours to metabolize superdrol.

if you are dosing it twice per day, it takes your body over 24hrs to metabolize a days dosage.

if you were to drink and stay drunk on a steady basis, it may compare to methylated steroids, but unfortunately most people dont.

but there are studies on superdrol i know, and im sure on others, like methyl trenbolone, anadrol, anavar, etc.
 
Thanks jbry and HTS!

Didn't think about metabolizing point you made.

So to compare a 4 week cycle if superdrol would be the equivalent to being constantly hammered for 4 weeks?

Doesn't the liver have the ability to regenerate and heal itself? A couple months after a cycle, my liver should be back to how it was pre-cycle?

Thanks guys
 
yea, as long as you dont mess it up beyond repair. you can cause your liver to degenerate so much, it will not repair itself. as has been shown with actual methyl trenbolone, not the bunk shiit so many buy off the black market.

a 4 week cycle of superdrol is still a bit more damaging.

but if you were to keep alcohol in your blood for 4 weeks, over a 24/7 period, it may be similar, it may be worse. I dont think you'll ever see that experiment done, as it is too dangerous.

alcohol is posion to the body, and effects more than just the liver. if people stayed on it like with methylated steroids, im sure they would die, from alcohol poisioning.
 
I don't know how you can compare the long term effects of steroids and hepatotoxicity to frat drinking, but I know the side effects do exist.


The presence of the alkyl group affects the metabolic course of the steroid by preventing the excretion of the steroid as 17-keto steroid. "The presence of the alkyl group also is responsible for undesirable side effects including tissue damage. 17a-alkyl substituted steroids were reported to cause reversible, intraheptic obstructive jaundice due to cholestasis."

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"The disturbing effects of anabolic steroids on the liver function were tested by sulfobromophthalein retention, serum bilirubin, serum lactic dehydrogenase, and total creatinine chromogen assays."

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Moar

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But these are primarily in the elderly, with other potential health issues. Short of reaching death of liver cells, the liver can repair itself.

Drug-induced cholestasis can rarely persist for a considerable time period even after withdrawal of the drug. We report the case of a 55-year-old man with progressive jaundice after oral therapy with 17-alpha-methyltestosterone. Under empiric therapy with ursodeoxycholic acid the condition resolved completely. According to this observation, we suggest a therapeutic trial with ursodeoxycholic acid in cases of prolonged androgen-induced cholestasis.
 
To me, it's not the hepatoxicity to worry about as that can be countered with the appropriate support supplementation, but they beat the living hell out of lipids, which takes longer to correct and the heart is not as resilient of an organ as the liver.
 
this is true, and short of that treatment of blasting the plaque out of the artery walls, (in laymans terms) there is no other means to get rid of the plaque build up caused from high levels of ldl's & vdl's

I've wondered about taking niacin on cycle to help with cholesterol levels. I keep forgetting to buy a bottle though.
 
makes me not want to take ph's

its all mg dependthat too right? I mean 5-10mg of SD for 4 weeks is not going to be as bad as 20 mg or 30 mg for 4 weeks.
 
To me, it's not the hepatoxicity to worry about as that can be countered with the appropriate support supplementation, but they beat the living hell out of lipids, which takes longer to correct and the heart is not as resilient of an organ as the liver.

I think they are of equal importance. We should not neglect the importance of the liver, even if it can recover on its own. Hepatotoxic side effects of steroids have been documented for years while the association between anabolic steroids and heart disease/heart attacks are still not fully understood. Consider the fact that an individual with trashed lipids can walk around and even workout if they wanted to, while a person with liver failure sits in an Emergency Room. Long term is of course important, but short term is just as important. You make a good point, of course.

makes me not want to take ph's

its all mg dependthat too right? I mean 5-10mg of SD for 4 weeks is not going to be as bad as 20 mg or 30 mg for 4 weeks.

Realize that the majority of cases of steroid-induced jaundice occur with prolonged steroid administration (aka therapy). We use these oral methyl steroids at most 4-6 weeks (most of us hopefully).
 
I think they are of equal importance. We should not neglect the importance of the liver, even if it can recover on its own. Hepatotoxic side effects of steroids have been documented for years while the association between anabolic steroids and heart disease/heart attacks are still not fully understood. Consider the fact that an individual with trashed lipids can walk around and even workout if they wanted to, while a person with liver failure sits in an Emergency Room. Long term is of course important, but short term is just as important. You make a good point, of course.



Realize that the majority of cases of steroid-induced jaundice occur with prolonged steroid administration (aka therapy). We use these oral methyl steroids at most 4-6 weeks (most of us hopefully).

what are your thoughts on superdrol @ 5mg for 6 weeks?
 
Well only being able to be on it for max of 6 weeks says it all. If you can only be on it for 5-6 weeks and you can't take a short break and jump right back on, what does that tell you? Oral steroids are definitively pretty toxic.
 
That's why just stick to 5months of 1000mg test/wk :) nice stuff
 
Well only being able to be on it for max of 6 weeks says it all. If you can only be on it for 5-6 weeks and you can't take a short break and jump right back on, what does that tell you? Oral steroids are definitively pretty toxic.

who says that but bros on the boards? Any medical evidence for that?

The anabolic androgenic steroid oxandrolone in the treatment of wasting and catabolic disorders: review of efficacy and safety.

Orr R, Fiatarone Singh M.


Source

School of Exercise and Sport Science, Faculty of Health Sciences, The University of Sydney, Sydney, Australia. [email protected]


Abstract

There has been increasing interest in the development of effective agents that can be safely used to promote anabolism in the clinical setting for patients with chronic wasting conditions as well as in the prevention and treatment of frailty associated with loss of muscle tissue in aging (sarcopenia). One such agent is the anabolic androgenic steroid (AAS) oxandrolone, which has been used in such clinical situations as HIV-related muscle wasting, severe burn injury, trauma following major surgery, neuromuscular disorders and alcoholic hepatitis for over 30 years. In the US, oxandrolone is the only AAS that is US FDA-approved for restitution of weight loss after severe trauma, major surgery or infections, malnutrition due to alcoholic cirrhosis, and Duchenne's or Becker's muscular dystrophy. Our review of the use of oxandrolone in the treatment of catabolic disorders, HIV and AIDS-related wasting, neuromuscular and other disorders provides strong evidence of its clinical efficacy. Improvements in body composition, muscle strength and function, status of underlying disease or recovery from acute catabolic injury and nutritional status are significant in the vast majority of well designed trials. However, oxandrolone has not yet been studied in sarcopenia.Unlike other orally administered C17alpha-alkylated AASs, the novel chemical configuration of oxandrolone confers a resistance to liver metabolism as well as marked anabolic activity. In addition, oxandrolone appears not to exhibit the serious hepatotoxic effects (jaundice, cholestatic hepatitis, peliosis hepatis, hyperplasias and neoplasms) attributed to the C17alpha-alkylated AASs. Oxandrolone is reported to be generally well tolerated and the most commonly documented adverse effects are transient elevations in transaminase levels and reductions in high density lipoprotein cholesterol level.However, optimal risk:benefit ratios for oxandrolone and other agents in its class will need to be refined before widespread clinical acceptance of AASs as a therapeutic option in sarcopenia and other chronic wasting conditions.
 
you shouldn't take a short break from any steroid and jump back on. methylated or not.

if you are on for 3-4 months, and it takes you 2 months to recover, you shouldn't even look at another cycle until 6 months after pct.

same for methyls, if you are on for 1-2 months, and takes 1-2 months to recover, then you shouldn't look at another cycle for another 3-4 months.

but we all dont do that. i know i try, but mess it up sometimes. like now, i tell myself, this 10+ week cycle is going to be my last cycle of the year, but who knows what will happen nov/dec.
 
who says that but bros on the boards? Any medical evidence for that?

you know, I really wish the medical community would study turinabol. I believe it would be safer than anavar.

i know anavar is safe, but i believe tbol to be more user friendly.
 
you know, I really wish the medical community would study turinabol. I believe it would be safer than anavar.

i know anavar is safe, but i believe tbol to be more user friendly.

Based on?
I have run low dosed OT, and have not run Anavar (currently sitting on 5g of var that will be incorporated into my next cycle). From my findings (as I am starting to read alot more on var), very very few have reported sides from Var, and I am talking competitors running it at 100mg, some claiming (keyword: claiming, it is the internet), even post-cycle bloodwork showed non-extravagant liver values, and only slightly altered hdl/ldl. Turinabol, run at a smaller dose (typically) and I have seen reports of highly elevated blood pressure, and others mentioning decent liver stress, as with any oral we can assume hdl/ldl was effected as well...


Then again, it is different for everyone. My 10 week cycle included a total of 8 (split by two weeks) of orals, Oral Turinabol and Epi, and my AST/ALT came back fine, and my bili was slightly out of range. hdl/ldl were similar to precycle. Then again, I used Liver Juice and UDCA.
 
Udca is good stuff.
 
I have ran low dose SD ~5-10mgs over 4 weeks with similar numbers i.e. single digit HDL and high LFT's...same with M1T FWIW
 
I have ran low dose SD ~5-10mgs over 4 weeks with similar numbers i.e. single digit HDL and high LFT's...same with M1T FWIW
So it really isnt mg depeandant?
 
It is imo, but after 4 weeks with some of these methyls it doesn't matter, more of the hormone the quicker, but in the end the same result...for me at least. Also, something else I have noticed with my blood work, is that the more I have used the quicker and easier it is to experience lipid/liver sides
 
princeshock said:
competitive bodybuilders take short breaks, or if any breaks at all. Do you really believe even one guy that competes at the pro level or guys on the road to a pro card are doing cycles with months and months of breaks? Or how about fitness modeling. And especially ectomorphes just to name a few, flex wheeler and frank zane. To look eye catching great like those guys....Yeah you pretty much rely on hormones. Just the truth.

Even if that was true, which it isn't, how does that relate? This conversation is about orals.
 
I base it on my own experience, and it's aa ratio.

the data isn't there for turinabol, but it is there for anavar, because that is the steroid that is used.

but turinabol seems to have a very low androgenic effect as well as not binding strongly to the androgen receptor, this seems to be a connection in side effects, and how strongly an androgen binds to the receptor.

with androgens that bind more strongly to the receptor having more negative side effects.
 
there is actual data on how hepatotoxic superdrol is. I know henry v has some studies he's shared with me.

I dont have them anymore, but im sure he still does.

think of it like this.

it takes your body about an hour to metabolize alcohol.

it takes your body 16hours to metabolize superdrol.

if you are dosing it twice per day, it takes your body over 24hrs to metabolize a days dosage.

if you were to drink and stay drunk on a steady basis, it may compare to methylated steroids, but unfortunately most people dont.

but there are studies on superdrol i know, and im sure on others, like methyl trenbolone, anadrol, anavar, etc.

I see what you are saying here and I agree with your point but alcohol is actually zero order kinetics so saying it takes 1 hour to metabolize alcohol is a bit deceiving. This means no matter how much or little you drink you can't metabolize any faster in normal circumstances (unless you are a chronic alcoholic in which things change at this point).

The type of damage is also different although the exact mechanisms behind steroid-induced hepatotoxicity are not known extremely well. We do understand the cholestatic effects but there are some other things occurring such as oxidation that are being looked into as well. There isn't much money in this sort of research which is why not much has been done on it in the technological era (post 1980's).

Bottom line, don't abuse ANYTHING, use on a short term basis and the lowest effective dosage.
 
To me, it's not the hepatoxicity to worry about as that can be countered with the appropriate support supplementation, but they beat the living hell out of lipids, which takes longer to correct and the heart is not as resilient of an organ as the liver.

You all overlooked this very important point.

First, is altered lipids due to the the hormone it self, or due to the hormones effects on the liver.

Second, we know that high (resting) blood pressure and poor lipid profile is a recipe for CV disease. Basically, the high BP damages the walls of the vessels, cholesterol moves in, an array of inflammation occurs, and the result is a plaque build up and decrease in vessel side. In addition, the high BP causes vessels to loose their elasticity (called loss of vascular compliance..or increase in vascular resistance). This in turn means the heart has to work harder at rest - and as far as we know, this is irreversible.

Next, the issues with high cholesterol do not manifest for many years later. Its not the closing of a vessel that is the problem (usually), but rather the rupture of the plaque. And keep in mind, once the vessel has become damaged and begins building plaque, it is far more likely to continue. How does plaque rupture? Well, plaque stability is one issue - a quite complex issue. The next is blood pressure. During times of high blood pressure (ie. exercise) the force of the blood on the vessel walls and can rupture the plaque. The embolism (piece of plaque) is then carried down stream where it will eventually get lodged into a smaller arteriole - usually one supplying the heart (heart attack) or brain (stroke).

The problem with causation is that its hard to do any type of controlled longitudinal study with steroid use and cardiac events. How do we get subjects (surveys, probably), how do we quantify use, and how do we follow up? That's one of the reasons its hard to draw causation...but it is there. N=1 could be Arnold Schwarzenegger.

Nothing scare me more than atherosclerosis. Except maybe spiders.

Br

Oh...and: high blood pressure and athersclerosis are a common partial cause in erectile dysfunction too.
 
I base it on my own experience, and it's aa ratio.

the data isn't there for turinabol, but it is there for anavar, because that is the steroid that is used.

but turinabol seems to have a very low androgenic effect as well as not binding strongly to the androgen receptor, this seems to be a connection in side effects, and how strongly an androgen binds to the receptor.

with androgens that bind more strongly to the receptor having more negative side effects.

You mean androgenic side effects - not comprehensive side effects.

Br
 
Very interesting ZRED
 
You mean androgenic side effects - not comprehensive side effects.

Br

no, i mean more side effects in general, not just androgenic sides, but all the side effects.

this is just speculation it seems, but looking at androgens, it all starts with how strongly it binds to/interacts with the receptor.

the stronger the androgen, the more side effects the user is likely to experience.

yea, i guess you could call cardiovascular problems and the side effects that are created because of that, and liver hepatotoxicity problems androgenic side effects since it all started with the androgen.
 
Perhaps, but drugs with low AR affinity also seem to pose the same risks. I may be wrong, but don't all lipid hormone PED's bind to the AR?

In fact, other drugs such as methandrostenolone bind the glutamate receptors in the brain and signal neural apoptosis (death). Although, it appears that AR binding can also impact neurotoxicity.
21290409
 
so bascially what I am gathering from all this educational banter is to pin test.
 
Yupp that all I do. I ran a little Winnie and sd just to check something out but in general id much rather stick to test unless ur competing dieting IMO there's no need for anything else. Test gives real solid results if done correctly with minimal sides if your very carefull
 
And i have tried ALOT of stuff most of it was similar to photoshop I looked good on it but once ur off results go off. For example winstrol+masteron ur lean ripped machine but once ur off it all comes back (water fat etc) so why damage bodybfor temporary cosmetic results???? I asked that myself after my extremely heavy cycle last yr. Test is king. Another example is a friend of mine took trend and test and something else 10wks cut man he looked unbeliavble but I kept saying just wait one u drop these cosmetic drugs and what happened booomb all that glory gone. So unless ur competing or photo/movie shoot just 4months test Is perfect
 
I used SD when it first came out. It was supposed to be safe according to the mfg. After six weeks of usage I developed a slight case of jaundice and had blood tests ran. I thought my doctor was going to through me in the hospital. My liver and lipid values were ridiculously high. I had to level with him about my PH usage. Never again. Health before vanity is my motto these days.
 
You all overlooked this very important point.

First, is altered lipids due to the the hormone it self, or due to the hormones effects on the liver.

This is something I've been trying to look into. Oral steroids trash lipids harder than injectables, as a general rule. They also are very hard on the liver. Many (most?) patients with a form of cholestasis show poor blood lipids, usually very high ldl. Often, hdl is high in them as well. There are other cholestasis patients who show high ldl, and low hld. This effect on their blood lipids is due to bile being slowed or blocked. So it seems to me that controlling liver damage is the best way to protect the heart while using orals. High dose NAC combined with selenium is shown to quickly reverse alcohol or tylenol-induced liver damage, and TUDCA and UDCA are shown to alleviate cholestasis. Looking at what is used in studies, most people could use much more NAC in their cycle support, as well as a little supplemental selenium (of course, you have to worry about getting too much selenium).
 
only way for me to get test is in pill form, or transdermally, at least, not until im old enough for trt.

i'll have to stick with 4-androstenediol and 4-dhea. isnt' too bad though.
 
Pretty much everything has been said. But I was cruising medline and ran across this (which there are many more like it):

Send to:






































Psychosomatics. 2010 Jul;51(4):340-4.

Acute hepatitis and personality change in a 31-year-old man taking prohormone supplement SUS500.

Wingert N, Tavakoli H, Yoder E.


Source

Dept. of Psychiatry, Naval Medical Center, Portsmouth, 620 John Paul Jones Circle, Portsmouth, VA 23708, USA.


Abstract

BACKGROUND:

For decades, anabolic-androgenic steroids have been abused to enhance muscle growth. The harm inflicted by these compounds is well documented.

OBJECTIVE:

The authors investigated and report on a case in which a male patient self-prescribed some newer dietary supplements, about which less is known.

METHOD:

The authors report on a case of hepatitis and aggressive personality changes in a 31-year-old man taking purported prohormone agent SUS500 and other, newer supplements.

RESULTS:

Diagnosis was based on history, mental status exam, and laboratory findings. With discontinuation of all supplements and supportive care, the patient's personality changes resolved, and normal liver function returned.

CONCLUSION:

The authors conclude that newer anabolic supplements may cause some of the same side effects as traditional steroid hormones.


PMID: 20587764 [PubMed - indexed for MEDLINE] Free full text
 
I personally don't worry about lipids and believe that the whole cholesterol causes heart disease stuff is complete bunk. Sure, blockages consist of cholesterol - but cholesterol's function in the body (among many things) is to patch up inflammation. They've got cause and effect all bass-ackwards. Sure ... a guy who sits on his ass and smokes all day and has high cholesterol is probably at risk for heart disease - but I think a guy who sits and smokes all day with low cholesterol is just as much at risk.

The problem is ... Science is not "exact". Like this crap where you're supposed to have five servings of veggies per day. Well, they did a detailed study in Europe on the efficacy of that and found no appreciable difference in health between the folks who ate those five servings per day and the ones who didn't.

Now ... how do you think the "scientific" community responded to that study?

Why ... they RAISED the recommended servings of veggies from five per day to EIGHT! LOL - good luck with ingesting that much rabbit food!

As far as cholesterol ... I can remember when anything under "200" was good. Now that's been revised ... and you're limited now to "99" for the "bad" cholesterol - which, there is no such thing as "good" and "bad" cholesterol - it's all the same. LDL and HDL are not cholesterols ... they're lipo-proteins that carry cholesterol.

Back when I worried about my cholesterol - mine was 245.

Now that I don't - it's like 185 but the bastards still tell me it's high because the "bad" stuff is "122" and it can't be any higher than 99. It's a moving target ... LOL

**** them!
 
I know everyone talks about how bad for your liver things like superdrol and other methyls are but is there any published data on how toxic they are?

Like in comparison, how toxic is a 5 week superdrol cycle to the liver compared to 5 years of college frat party drinking?

We all demonize methyls but is there any actual data on them? How much worse are methyl prohormones to your liver than alcohol is?

Looking for actual answers not broscience fellas.

Thanks


I say just take UDCA alongside and not ever worry about this question again. :)
 
You're pretty much on target. Read the book "The Cholesterol Myth". It tells the whole story about how drug companies manipulated the Framingham study to sell their drugs. There is actually research available that shows the people who have higher cholesterol levels are healthier and live longer. By the way my cholesterol has been over 300 for 30 years. I refuse to take satins. I recently completed a stress test and everything is fine. I have 87 and 93 year old uncles whose cholesterol typically runs over 350 and 400, respectively. They don't worry about it at all. In fact high cholesterol is a joke at family reunions.
 
You're pretty much on target. Read the book "The Cholesterol Myth". It tells the whole story about how drug companies manipulated the Framingham study to sell their drugs. There is actually research available that shows the people who have higher cholesterol levels are healthier and live longer. By the way my cholesterol has been over 300 for 30 years. I refuse to take satins. I recently completed a stress test and everything is fine. I have 87 and 93 year old uncles whose cholesterol typically runs over 350 and 400, respectively. They don't worry about it at all. In fact high cholesterol is a joke at family reunions.

Yeah I'm pretty sure doctors are leaning towards the ratios of LDL, HDL and Tri's rather than total cholesterol levels. However, my father at age 60, had recently been checked out and had decent cholesterol count and ratios and passed the stress test fine but had been having chest pains nonetheless. He got a heart cath done and lo and behold 3 important a rather larger arteries were clogged anywhere from 60% to 99%. Two days later he had a triple bypass surgery. We never saw it coming really.

Point being, the greatest risk factor for cardiovascular problems lies in the genetic makeup - the stuff is inherited more or less. If your family has a history of bad heart problems then its just a matter of time when you do too. Keeping cholesterol at healthy ratios and use your heart and you might push the heart trouble back 10-15 years but nothing is for certain.
 
in the end what they've found is that on average, reducing cholesterol levels doesn't impact mortality rate or total lifespan, you just die of something else in around the same time span.
 
I see what you are saying here and I agree with your point but alcohol is actually zero order kinetics so saying it takes 1 hour to metabolize alcohol is a bit deceiving. This means no matter how much or little you drink you can't metabolize any faster in normal circumstances (unless you are a chronic alcoholic in which things change at this point).

The type of damage is also different although the exact mechanisms behind steroid-induced hepatotoxicity are not known extremely well. We do understand the cholestatic effects but there are some other things occurring such as oxidation that are being looked into as well. There isn't much money in this sort of research which is why not much has been done on it in the technological era (post 1980's).

Bottom line, don't abuse ANYTHING, use on a short term basis and the lowest effective dosage.

yeah don't abuse anything. Just do what we're supposed to do with them - kickstart. Otherwise stay away from methyls/orals if your trying to get permenant swoleness from orals alone. Just a bad idea altogether. There is a reason why the really big guys that stay big for decades use the injection steroids rather than orals exclusively. Plus, there are so many other options for the less intense lifters like peptides and SARMS...no need in running 3+ oral methyl cycles a year anymore IMO.
 
Yeah I'm pretty sure doctors are leaning towards the ratios of LDL, HDL and Tri's rather than total cholesterol levels. However, my father at age 60, had recently been checked out and had decent cholesterol count and ratios and passed the stress test fine but had been having chest pains nonetheless. He got a heart cath done and lo and behold 3 important a rather larger arteries were clogged anywhere from 60% to 99%. Two days later he had a triple bypass surgery. We never saw it coming really.

Point being, the greatest risk factor for cardiovascular problems lies in the genetic makeup - the stuff is inherited more or less. If your family has a history of bad heart problems then its just a matter of time when you do too. Keeping cholesterol at healthy ratios and use your heart and you might push the heart trouble back 10-15 years but nothing is for certain.

yeah, its crazy. i smoke cigars and my hdl/ldl came back 67/63. i didnt even know it was possible to have a higher hdl than ldl! needless to say i was pretty happy
 
I personally don't worry about lipids and believe that the whole cholesterol causes heart disease stuff is complete bunk. Sure, blockages consist of cholesterol - but cholesterol's function in the body (among many things) is to patch up inflammation. They've got cause and effect all bass-ackwards. Sure ... a guy who sits on his ass and smokes all day and has high cholesterol is probably at risk for heart disease - but I think a guy who sits and smokes all day with low cholesterol is just as much at risk.

High density lipoprotein (HDL) is anti-inflammatory. LDL, however, is pro-inflammatory to both endothelial cells (the lining of blood vessels) and the smooth muscle controlling vasoconstriction/relaxation.

Morgantini, C., Natali, A., Boldrini, B., Imaizumi, S., Navab, M., Fogelman, A. M., et al. (2011). Anti-Inflammatory and Antioxidant Properties of HDLs Are Impaired in Type 2 Diabetes. Diabetes. doi: 10.2337/db11-0378.

Gora, S., Maouche, S., Atout, R., Wanherdrick, K., Lambeau, G., Cambien, F., et al. (2010). Phospholipolyzed LDL induces an inflammatory response in endothelial cells through endoplasmic reticulum stress signaling. The FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 24(9), 3284-97. doi: 10.1096/fj.09-146852.

Calvayrac, O., Rodríguez-Calvo, R., Alonso, J., Orbe, J., Martín-Ventura, J. L., Guadall, A., et al. (2011). CCL20 Is Increased in Hypercholesterolemic Subjects and Is Upregulated By LDL in Vascular Smooth Muscle Cells: Role of NF-{kappa}B. Arteriosclerosis, thrombosis, and vascular biology. doi: 10.1161/ATVBAHA.111.235721.

The problem is ... Science is not "exact". Like this crap where you're supposed to have five servings of veggies per day. Well, they did a detailed study in Europe on the efficacy of that and found no appreciable difference in health between the folks who ate those five servings per day and the ones who didn't.

Now ... how do you think the "scientific" community responded to that study?

Why ... they RAISED the recommended servings of veggies from five per day to EIGHT! LOL - good luck with ingesting that much rabbit food!

I dislike what is considered a serving of vegetable and what is not...but we know several things.

1. Vegetables contain a high amount of anti-oxidants and phytonutrients.
2. The western diet is highly acidic and inflammatory, and consuming vegetables is one way to increase alkaline consumption and anti-inflammatory phytonutrients.
3. The bodybuilding community spends countless dollars on useless NO products that for the most part do not increase nitric oxide production or values. Vegetable consumption increases both.

Of course, these things are not seen after acute consumption, but chronically. I'd be interested to see that study.

As far as cholesterol ... I can remember when anything under "200" was good. Now that's been revised ... and you're limited now to "99" for the "bad" cholesterol - which, there is no such thing as "good" and "bad" cholesterol - it's all the same. LDL and HDL are not cholesterols ... they're lipo-proteins that carry cholesterol.

Or, it could be because the scientific community is looking at longitudinal studies and starting to see correlations between values and heart disease incidents. There is a HUGE difference between the functions of LDL and HDL. It all comes down to the oxidation of LDL and its effects on the blood vessel...and endothelial sheer stress (caused by high bp).

Steinberg, D. (2009). The LDL modification hypothesis of atherogenesis: an update. Journal of lipid research, 50 Suppl, S376-81. doi: 10.1194/jlr.R800087-JLR200.

Tada, T., Nawata, J., Wang, H., Onoue, N., Zhulanqiqige, D., Ito, K., et al. (2008). Enhanced pulsatile pressure accelerates vascular smooth muscle migration: implications for atherogenesis of hypertension. Cardiovascular research, 80(3), 346-53. doi: 10.1093/cvr/cvn211.

Back when I worried about my cholesterol - mine was 245.

Now that I don't - it's like 185 but the bastards still tell me it's high because the "bad" stuff is "122" and it can't be any higher than 99. It's a moving target ... LOL

**** them!

Probably because most of the bastards haven't the slightest idea about cholesterol or lipid metabolism, and they go off a BS study from the 1950's.

What's perhaps more important that absolute numbers if the ratio of LDL to HDL, and HDL to total cholesterol.

Lemieux, I., Lamarche, B., Couillard, C., Pascot, A., Cantin, B., Bergeron, J., et al. (n.d.). Total cholesterol/HDL cholesterol ratio vs LDL cholesterol/HDL cholesterol ratio as indices of ischemic heart disease risk in men: the Quebec Cardiovascular Study. Archives of internal medicine, 161(22), 2685-92. Retrieved August 24, 2011, from Invalid Link Removed.

Fernandez, M. L., & Webb, D. (2008). The LDL to HDL cholesterol ratio as a valuable tool to evaluate coronary heart disease risk. Journal of the American College of Nutrition, 27(1), 1-5. Retrieved August 24, 2011, from Invalid Link Removed.


Br
 
Yeah I'm pretty sure doctors are leaning towards the ratios of LDL, HDL and Tri's rather than total cholesterol levels. However, my father at age 60, had recently been checked out and had decent cholesterol count and ratios and passed the stress test fine but had been having chest pains nonetheless. He got a heart cath done and lo and behold 3 important a rather larger arteries were clogged anywhere from 60% to 99%. Two days later he had a triple bypass surgery. We never saw it coming really.

Point being, the greatest risk factor for cardiovascular problems lies in the genetic makeup - the stuff is inherited more or less. If your family has a history of bad heart problems then its just a matter of time when you do too. Keeping cholesterol at healthy ratios and use your heart and you might push the heart trouble back 10-15 years but nothing is for certain.

It also has a lot to do with the stability of the plaques that form in your arteries. Plaques with thin shells are far more apt to rupture than plaques with thick, highly fibrous/calcified shells.

Br
 
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