BronzeWolf
Banned
good old government wants to have it's taco and eat it
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Weight Loss Before/After Thread! (with pics)
- Thread starter lsslave
- Start date
hockeypuck
Member
You can use all the "causal" terms you want, but when you don't have the double-blinded randomized clinical trials to back it up, then it's an empty statement. There are plenty of trials looking at lowering LDL and then comparing outcomes, enough to create a very statistically strong metanalysis combining 90,000+ patients:BronzeWolf said:
Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins.
I've looked for VLDL/HDL ratio trials; I found zero. Hence my original question. What clinical studies, using real people and measuring disease endpoints like any good clinical trial, are you basing your claim that following VLDL/HDL ratios are better than LDL levels? I've given my evidence; I have yet to see anything significant from you.
Every time you recapitulate the basic science of lipid metabolism without producing any significant clinical evidence tells me that you do not understand the concept of translational or clinical research, much less epidemiology.
If you concede that VLDL measurements are not as reliable, then why were you using it to tell Domino Theory that his mother's cholesterol levels were good? VLDL is not even routinely measured in standard lipid panels. It's only estimated as a percentage of total triglycerides. If anything Domino Theory's mom either got ripped off or someone saw something concerning enough to add it on to the standard panel.BronzeWolf said:
Your last link states in its conclusion that lowering LDL through a statin remains the first line treatment for dyslipidemia, and that targeting HDL/LDL ratios remains a secondary goal for further risk modification. It doesn't even mention VLDL/HDL ratios. I'm not sure why you gave that link, if you were using it as evidence against my claims.
hockeypuck said:
While I don't know anything about VLDL in ratios, you should read some of the links I posted earlier. It talks about the size and shape of LDL and it's tendency to oxidize.
The study you're posting isn't controlled to the point that you can say "lowering cholesterol reduces the risk of heart disease" because statins do way more than just lower cholesterol. So while it's a double blinded randomized study, you've got potential confounding variables to account for. You also should take a look at what I posted because it talks about how low cholesterol is correlated with increased mortality just as much as high cholesterol.
I'm not sure why you see the causation as trivial. If the science is correct, then we could develop more effective therapies, prevention, while reducing side effects.
Some more on it:
http://www.cholesterol-and-health.com/Does-Cholesterol-Cause-Heart-Disease-Myth.html#oxidized
Edit: Just read this one link if you'd like. It's probably the most thorough history of research summarized that I've seen. It's got plenty of references.
hockeypuck
Member
First of all, why the heck should I believe your JAMA study any more than my metanalysis study?teh_pwn said:
1. You claim my metanalysis "isn't controlled to the point..." Your JAMA study isn't even controlled at all, period! Why? Because...
2. Your JAMA study is a retrospective case control study using 230 patients. You do realize the major drawbacks of a retrospective case control study are, right?
3. Your JAMA study is not randomized. You do realize the major drawbacks of non-randomization, right?
4. My metanalysis has 90,000 patients. You do realize what power (1-beta) and Type II statistical error (beta) are, right?
To use figurative terms, your evidence is akin to bringing a pocketknife to a gunfight.
Moreover, you have absolutely NO clinical evidence that the secondary effects of statins are so profound as to "confound" the HMG-CoA reductase mechanism in reducing LDL levels. You are not even using the term "confounding" in its proper epidemiological sense. To extrapolate your claim, we should disregard every medical treatment ever because we can't account for secondary effects (but trust me, we do, and that's what Results tables are for). Using your logic, we should take aspirin off the market because it works in so many ways that we can't show via RCT that it helps treat a heart attack.
My use of "causation" is obviously different from yours. As applicable to real-world practices, the scientific community reserves its use mainly after randomized trials have been done and consensus reached.teh_pwn said:
BronzeWolf
Banned
hockeypuck said:
You can look at the clinical studies, skim through the paper, see LDL and conclude that LDL does not include VLDL and find that that's proof that HDL:LDL ratios have nothing to do with HDL:VLDL ratios. Or you could actually measure VLDL through 175,000 people
With a recent update that suggest a less stronger prediction of CHD with apoB/apoA to LDL.
This is an observational study, which I know does not prove anything, but it does show there might be a link there.
hockeypuck
Member
Um, do you realize that this was an observational study without controlling for treatment, right?BronzeWolf said:
You DO realize that observational studies are on the complete opposite end compared to randomized controlled trials on the spectrum of well-validated studies, right? Observational studies help generate hypotheses, not change clinical practices.
And finally, hopefully you realize that you still haven't answered my question that there has yet to be a single, not even one, prospective trial that shows that treating the VLDL/HDL ratio is at least just as useful as treating the LDL (of which I presented 14 trials). You still haven't found it.
Edit:
And yet you believe it more than a metanalysis of 14 prospective trials, which by study design is out to prove. Outstanding.BronzeWolf said:
BronzeWolf
Banned
Well, thank you for having a decent scientific profile. I will present another good observational study that took 52 countries into account just because I found it very well designed. I also finished revising your meta-analysis and was a little bit confused I admit. I revised the 14 trials analyzed and 1 question popped out:
How are you sure that LDL compared to HDL:VLDL ratio is better if the meta-analysis doesn't compare the metrics?
I found it funny that the same studies meta-analyzed in your study actually were in my controlled trial evidence for apoB/apoA supperiority in fact starting with:
1. Lipoprotein Changes and Reduction in the Incidence of Major Coronary Heart Disease Events in the Scandinavian Simvastatin Survival Study (4S) found the stronger apoB/apoA relationship in the placebo group.
I seem to have seen this one too:
2. Relation between baseline and on-treatment lipid parameters and first acute major coronary events in the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS)
which quotes:
Wait, here is one more! the LIPID one:
3. Relationship Between Lipid Levels and Clinical Outcomes in the Long-Term Intervention With Pravastatin in Ischemic Disease (LIPID) Trial They didn't do the complete math here. You can do it, and find that apoB/apoA is actually stronger than TC/HDL. At the very least, it is equal
4. A much weaker trial, still shows the relationships
5. CARE doesn't measure apoB/apoA ratios so it really is not evidence AGAINST it.
6. Also, statins do lower LDL, but does that mean that they lower apoB? It might seem so, but do they?
You seem to infer that apob/apoa ratios or HDL/VLDL are not succesful predictors of heart diseases. Yet they are shown to be at least equal to HDL/LDL ratios and there is evidence that they might be superior. You already said it, observational studies are made for challenging hypothesis, and TC/HDL hypothesis is being challenged, whereas apoB/apoA ratios have not been taken into account in clinical trials until very recently, which is why probably there isn't any clinical trial that directly assesses VLDL:HDL ratio treatment.
If there was, we probably wouldn't be having this conversation. But there IS evidence that what I am saying is right, and that the consensus still has not gotten deep enough. I haven't even finished reading the other trials yet.
I really expect your answer :3
How are you sure that LDL compared to HDL:VLDL ratio is better if the meta-analysis doesn't compare the metrics?
I found it funny that the same studies meta-analyzed in your study actually were in my controlled trial evidence for apoB/apoA supperiority in fact starting with:
1. Lipoprotein Changes and Reduction in the Incidence of Major Coronary Heart Disease Events in the Scandinavian Simvastatin Survival Study (4S) found the stronger apoB/apoA relationship in the placebo group.
I seem to have seen this one too:
2. Relation between baseline and on-treatment lipid parameters and first acute major coronary events in the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS)
which quotes:
Wait, here is one more! the LIPID one:
3. Relationship Between Lipid Levels and Clinical Outcomes in the Long-Term Intervention With Pravastatin in Ischemic Disease (LIPID) Trial They didn't do the complete math here. You can do it, and find that apoB/apoA is actually stronger than TC/HDL. At the very least, it is equal
4. A much weaker trial, still shows the relationships
5. CARE doesn't measure apoB/apoA ratios so it really is not evidence AGAINST it.
6. Also, statins do lower LDL, but does that mean that they lower apoB? It might seem so, but do they?
You seem to infer that apob/apoa ratios or HDL/VLDL are not succesful predictors of heart diseases. Yet they are shown to be at least equal to HDL/LDL ratios and there is evidence that they might be superior. You already said it, observational studies are made for challenging hypothesis, and TC/HDL hypothesis is being challenged, whereas apoB/apoA ratios have not been taken into account in clinical trials until very recently, which is why probably there isn't any clinical trial that directly assesses VLDL:HDL ratio treatment.
If there was, we probably wouldn't be having this conversation. But there IS evidence that what I am saying is right, and that the consensus still has not gotten deep enough. I haven't even finished reading the other trials yet.
I really expect your answer :3
hockeypuck, by not controlled I meant you had multiple variables. Your study may control statins, but it doesn't control "lowering cholesterol". I'll dig more stuff up sometime over the next few days (I'm only awake due to storm hitting Austin), but it has to do with statins reducing inflammation which makes oxidized LDL occur less. Statins may also reduce heart disease because they lower both the good and bad LDL. But if there's subtypes that oxidize and cause issues as much of the science has been discussing in the past 25 years, then why shouldn't we understand how that works? The side effects of statins do exist, and low choleseterol increases total mortality in general (but maybe not with statin induced low cholesterol, I'd have to check). But if a hammer is hitting the patient on the head, wouldn't removing the hammer be better than taking aspirin?
And this is why I can't have chocolate in my house. I took the recommendation of some here to get some good dark chocolate without all the BS and attempted to eat it in moderation. It lasted about 3 hours before I finished all 3 bars. So, I had about 1300/1400 calories plus sugars, etc. Granted, I haven't had a cheat day in about a week, so I guess I can consider this my cheat day and all, but chocolate is definitely my weakness. I guess next time I get a craving for it I'll just buy one dark chocolate bar since I know it won't survive the day in my house.
On the bright side, I'm still losing weight and all, but I definitely felt sick to my stomach after this and like a total scum bag for giving in.
On the bright side, I'm still losing weight and all, but I definitely felt sick to my stomach after this and like a total scum bag for giving in.
Cosmic Bus
pristine morning snow
1stStrike said:
That's exactly what happens every time I think I can have anything sweet on hand. A couple weeks will go by before I'll convince myself "this time will be different!" and I grab some cookies or candy at the store with the intent of going through them in moderation, only to have the whole package gone within a day or so.
I've settled on some sugar-free Jello for when the cravings hit, but it just isn't the same. :\
jts
...hate me...
92.1kg today. Still trucking my way to the 90kg/200lb mark 
It can't come soon enough.
Now, I want to post some of my findings. Anecdotal, of course.
I've found that if you're on a weight loss momentum, you can easily lose the weight you accidentally gained on a day-off from your diet, and then some.
Here's what I mean: a week and a day ago, on January 23rd I hit the 93.5kg mark. It was very nice, but as I reported I kept that weight almost intact for, like, 4-5 days. I know, I was probably turning some fat into muscle as you guys said, but still I'm too overweight to stop dropping at least a few pounds every other day - I can't keep building muscle up to 93.5kg on dieting alone.
So on Friday 28th, while I still had the same weight, I proceeded to have a cheat day. Had a McD's for lunch, bread on the dinner, and then went out with my friends, lots of beer and by the end of the night, I had a greasy burger. I got to bed around 4-5AM.
Then, by 11AM, I woke up and did my weight-in. I jumped from the 93.somethings to 95.2kg! Shocking setback! Around 1.5kg gained, or around 3.3lbs. I now think that that weight-in was probably taken too soon after eating, especially eating junk, thus not giving it enough time to get out of my system.
Still, I had a fasting day that saturday. Worried about 5 days of intact weight followed by a fast weight gain, I just went for a perfect fasting day, in which I had really nothing but water.
By Sunday morning I was already back to 93.7ish. Crisis averted, hooray! But I kept focused and that Sunday I had nothing but grilled chicken breast. Just pure chicken breast with a pinch of salt and garlic. By Monday morning I was on the 93.0!! New fasting day, had half a glass of skin milk though. Tuesday morning (today) I weighted 92.1kg.
So, after that cheat day, soon enough I lost not only the weight I gained because of it, but also quickly overcame the plateau of sorts I was in.
What do you guys think, can a very occasional cheat day induce some sort of shock on the system, making the body accelerate all those weight loss processes and stuff? (if you return to your diet, of course).
Also, on ADF, I've found out that it's much easier to fast on your eating day and eat on your fasting day :lol
But you can't do anything about it. You're hungry on the fasting day because you ate on the previous day, and you're not that that hungry on your eating day because you starved on the previous day. Stupid body!
Sorry for any bad english.
It can't come soon enough.
Now, I want to post some of my findings. Anecdotal, of course.
I've found that if you're on a weight loss momentum, you can easily lose the weight you accidentally gained on a day-off from your diet, and then some.
Here's what I mean: a week and a day ago, on January 23rd I hit the 93.5kg mark. It was very nice, but as I reported I kept that weight almost intact for, like, 4-5 days. I know, I was probably turning some fat into muscle as you guys said, but still I'm too overweight to stop dropping at least a few pounds every other day - I can't keep building muscle up to 93.5kg on dieting alone.
So on Friday 28th, while I still had the same weight, I proceeded to have a cheat day. Had a McD's for lunch, bread on the dinner, and then went out with my friends, lots of beer and by the end of the night, I had a greasy burger. I got to bed around 4-5AM.
Then, by 11AM, I woke up and did my weight-in. I jumped from the 93.somethings to 95.2kg! Shocking setback! Around 1.5kg gained, or around 3.3lbs. I now think that that weight-in was probably taken too soon after eating, especially eating junk, thus not giving it enough time to get out of my system.
Still, I had a fasting day that saturday. Worried about 5 days of intact weight followed by a fast weight gain, I just went for a perfect fasting day, in which I had really nothing but water.
By Sunday morning I was already back to 93.7ish. Crisis averted, hooray! But I kept focused and that Sunday I had nothing but grilled chicken breast. Just pure chicken breast with a pinch of salt and garlic. By Monday morning I was on the 93.0!! New fasting day, had half a glass of skin milk though. Tuesday morning (today) I weighted 92.1kg.
So, after that cheat day, soon enough I lost not only the weight I gained because of it, but also quickly overcame the plateau of sorts I was in.
What do you guys think, can a very occasional cheat day induce some sort of shock on the system, making the body accelerate all those weight loss processes and stuff? (if you return to your diet, of course).
Also, on ADF, I've found out that it's much easier to fast on your eating day and eat on your fasting day :lol
But you can't do anything about it. You're hungry on the fasting day because you ate on the previous day, and you're not that that hungry on your eating day because you starved on the previous day. Stupid body!
Sorry for any bad english.
I've found that the best way for me to stop from indulging is to keep everything in my kitchen healthy. If I really want to cheat, I'll do it when I'm going out with somebody or something. But sitting at home watching TV or whatever? Not a good time to have treats.1stStrike said:
D
Deleted member 17706
Unconfirmed Member
Today marks the first week since I started the "slow carb" diet from the 4 Hour Body book. On Tuesday morning last week I weighed 216.8 lbs. This morning when I weighed myself (before even pooing), I was down to 209.6 lbs.
I'm pretty impressed so far.
The only hard part about this diet for me has been totally cutting out beer except on "cheat days". I'm dealing with it, though.
Anyway, I completely eliminated any "white carbs"--anything starchy or processed. No grain products, no rice. I only get my carbohydrates from beans (I tend to stick to black beans and lentil beans). I never consumed much sugar before, but I have made sure to fully eliminate that as well. I also do not consume any milk or dairy products.
Pretty much this leaves me with vegetables, fish, meat, beans, eggs, and seasoning.
When I wake up in the morning I drink a 500ml bottle of chilled water on an empty stomach. I do this pretty much immediately after waking up.
For breakfast, which I eat within 30-40 minutes of waking, I have been eating one or two organic eggs mixed with organic egg whites, a couple of turkey sausages, some ground chicken sausage, lots of spinach and lettuce, and some beans (generally served with some combination of salsa, hot sauce and guacamole). I try to eat a lot at breakfast, since apparently this helps the metabolism for the entire day. I sometimes mix it up, but my breakfast always contains some combination of greens, meat, eggs, and beans.
Lunch is usually a trip to Chipotle for a Salad Bowl (no dressing, no rice, no corn, no sour cream, no cheese, extra beans and veggies, chicken or beef, added tomato salsa and guacamole), or I go to a salad bar and get a combination of greens, meats and beans, and sometimes fish.
For dinner I generally pan fry some seasoned meat (usually chicken) and serve it with veggies and beans.
About 30 minutes to an hour before sleeping I take a cold shower. I start it with lukewarm water, which I wash myself in, then gradually work the water down to its coldest setting and stand in it for at least five to ten minutes. I mostly stand with my back to the water so it hits the lower neck/upper back area. This should eventually induce shivering, but it's very relaxing at the same time and you'll feel awesome after stepping out of it.
For exercise, I don't do much cardio. I'm sure it would help, and I try to get some in at least once a week, though. All I do is sets of 30 "air squats" and "wall presses" at least three times a day (generally a bit after a meal). I also do at least 50 sit ups a day. For the first couple of days my legs were jelly since I'd never done many squats in my whole life.
That's it! A few minor lifestyle changes and some very mild exercise and I've dropped a bit over 7 lbs. in one week! My goal is to get back down to 160 or so.
I'm pretty impressed so far.
The only hard part about this diet for me has been totally cutting out beer except on "cheat days". I'm dealing with it, though.
Anyway, I completely eliminated any "white carbs"--anything starchy or processed. No grain products, no rice. I only get my carbohydrates from beans (I tend to stick to black beans and lentil beans). I never consumed much sugar before, but I have made sure to fully eliminate that as well. I also do not consume any milk or dairy products.
Pretty much this leaves me with vegetables, fish, meat, beans, eggs, and seasoning.
When I wake up in the morning I drink a 500ml bottle of chilled water on an empty stomach. I do this pretty much immediately after waking up.
For breakfast, which I eat within 30-40 minutes of waking, I have been eating one or two organic eggs mixed with organic egg whites, a couple of turkey sausages, some ground chicken sausage, lots of spinach and lettuce, and some beans (generally served with some combination of salsa, hot sauce and guacamole). I try to eat a lot at breakfast, since apparently this helps the metabolism for the entire day. I sometimes mix it up, but my breakfast always contains some combination of greens, meat, eggs, and beans.
Lunch is usually a trip to Chipotle for a Salad Bowl (no dressing, no rice, no corn, no sour cream, no cheese, extra beans and veggies, chicken or beef, added tomato salsa and guacamole), or I go to a salad bar and get a combination of greens, meats and beans, and sometimes fish.
For dinner I generally pan fry some seasoned meat (usually chicken) and serve it with veggies and beans.
About 30 minutes to an hour before sleeping I take a cold shower. I start it with lukewarm water, which I wash myself in, then gradually work the water down to its coldest setting and stand in it for at least five to ten minutes. I mostly stand with my back to the water so it hits the lower neck/upper back area. This should eventually induce shivering, but it's very relaxing at the same time and you'll feel awesome after stepping out of it.
For exercise, I don't do much cardio. I'm sure it would help, and I try to get some in at least once a week, though. All I do is sets of 30 "air squats" and "wall presses" at least three times a day (generally a bit after a meal). I also do at least 50 sit ups a day. For the first couple of days my legs were jelly since I'd never done many squats in my whole life.
That's it! A few minor lifestyle changes and some very mild exercise and I've dropped a bit over 7 lbs. in one week! My goal is to get back down to 160 or so.
D
Deleted member 17706
Unconfirmed Member
ch0mp said:
I hear that about the immune system. It's definitely built up my endurance for cold temperatures. I started noticing this the day after my first cold shower. I've always been weak against the cold, but the day after taking a cold shower, I didn't feel uncomfortable at all walking a bit outside in nearly freezing temperatures with just a long sleeved shirt on.
I need time to study oxidized LDL a bit more, but I just wanted to post real quick about statins efficacy. I'm not seeing this picture of consensus. I'm finding lots of controlled, double blind placebo trials finding either no effect on heart disease or an improvement in heart disease but no change in total mortality. I also ran across a couple of odd studies that were halted (JUPITER).
Carotid Atorvastatin Study in Hyperlipidemic Post-MEnopausal Women: a Randomised Evaluation of Atorvastatin Versus Placebo (CASHMERE)
Rosuvastatin in Older Patients with Systolic Heart Failure
Simvastatin with or without Ezetimibe in Familial Hypercholesterolemia
Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(08)61240-4/abstract
We should also look at total mortality when evaluating the benefits (or cons) of statins.
Higher Total Serum Cholesterol Levels Are Associated With Less Severe Strokes and Lower All-Cause Mortality: Ten-Year Follow-Up of Ischemic Strokes in the Copenhagen Stroke Study
http://stroke.ahajournals.org/cgi/reprint/38/10/2646
I think more relevant to this topic is that eating saturated fats, or (supposedly) increasing cholesterol organically doesn't affect mortality. We know this from real world evidence of entire cultures eating over 50% of their energy as saturated fat and having unusually low heart disease:
http://www.ajcn.org/content/34/8/1552.long
http://www.ajcn.org/content/early/2010/01/13/ajcn.2009.27725.abstract
http://www.nejm.org/doi/pdf/10.1056/NEJM197104012841304
http://ije.oxfordjournals.org/content/26/6/1182.full.pdf
I'll look for other effects of statins outside of LDL synthesis and absorption, but as far as the Keys lipid hypothesis, I'm not finding a shred of evidence for it. Statins may be improving some risk factors, but I doubt it has anything to do with total cholesterol levels or total LDL levels.
Carotid Atorvastatin Study in Hyperlipidemic Post-MEnopausal Women: a Randomised Evaluation of Atorvastatin Versus Placebo (CASHMERE)
http://bmartinmd.com/Cashmere_Study_Pfizer.pdf
Rosuvastatin in Older Patients with Systolic Heart Failure
http://www.nejm.org/doi/full/10.1056/NEJMoa0706201
Simvastatin with or without Ezetimibe in Familial Hypercholesterolemia
http://www.nejm.org/doi/full/10.1056/NEJMoa0800742
Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(08)61240-4/abstract
We should also look at total mortality when evaluating the benefits (or cons) of statins.
Higher Total Serum Cholesterol Levels Are Associated With Less Severe Strokes and Lower All-Cause Mortality: Ten-Year Follow-Up of Ischemic Strokes in the Copenhagen Stroke Study
http://stroke.ahajournals.org/cgi/reprint/38/10/2646
I think more relevant to this topic is that eating saturated fats, or (supposedly) increasing cholesterol organically doesn't affect mortality. We know this from real world evidence of entire cultures eating over 50% of their energy as saturated fat and having unusually low heart disease:
http://www.ajcn.org/content/34/8/1552.long
http://www.ajcn.org/content/early/2010/01/13/ajcn.2009.27725.abstract
http://www.nejm.org/doi/pdf/10.1056/NEJM197104012841304
http://ije.oxfordjournals.org/content/26/6/1182.full.pdf
I'll look for other effects of statins outside of LDL synthesis and absorption, but as far as the Keys lipid hypothesis, I'm not finding a shred of evidence for it. Statins may be improving some risk factors, but I doubt it has anything to do with total cholesterol levels or total LDL levels.
betweenthewheels
Member
Zefah said:
Nice. I've been reading the 4 Hour Body as well.
Though, i'm omitting beans/lentils to get into Ketosis. I keep forgetting the ice water after waking though, heh.
I wish I could take a cold shower but it's the worst feeling in the world. I've been putting ice packs on my back every night.
For exercise i'm doing the kettlebell swing, it's pretty awesome...considering I have no space in my apartment.
Anyway, great book overall, lots of cool things in there.
Congrats on the loss btw, you gotta be feeling good about that
D
Deleted member 17706
Unconfirmed Member
betweenthewheels said:
I've read a lot about the kettlebell swing. I'll have to look into it.
It definitely feels great to lose weight this quickly while still enjoying my diet and not exercising a ton. Dropping around a pound a day definitely helps keep motivation up.
I've been considering trying to omit beans as well to speed up the process (although I'm not sure my weight loss can get much faster than it is right now). I'm just worried that I won't be able to keep myself full.
So reading some of the scientific literature on the lipid hypothesis still doesn't show a consensus, but the oxidized lipid hypothesis seems to have some solid causal data to support it. Lots of research on it in the past 10 years.
In this study they compare the accuracy of predicting coronary artery disease between Global Risk Factor Assessment Score (GRAS - traditional lipid hypothesis) vs oxidized LDL.
http://atvb.ahajournals.org/cgi/content/full/21/5/844
They found that GRAS was 49% while oxLDL was 82%.
http://atvb.ahajournals.org/cgi/content-nw/full/21/5/844/T3
Another study finds that oxLDL is a good indicator in otherwise apparently healthy men:
This study attempts to explain why the oxidized LDL is bad. Apparently macrophages gobble it up and become inflammatory.
http://www.jlr.org/content/38/1/101.full.pdf
This study demonstrates how a powerful antioxidant is antiatherogenic.
http://www.ncbi.nlm.nih.gov/pubmed/1466646
This may explain why these statin studies aren't consistent. If statins indiscriminately reduce all LDL, but the problem is small, dense LDL with a tendency to oxidize, then sometimes statins would help and other times harm. But it doesn't have to be this way if a drug is developed that targets the cause of oxLDL, or if people eat fats that aren't rancid.
What causes oxidized LDL isn't as clear. There is some evidence that it is n-6 fatty acids, or too much n-6 AND n-3. I'm beginning to see why Dr Harris recommends elimination of n-6 as opposed to balancing a ratio by adding more n-3. So DominoTheory take note. As an amateur scientist (and not an MD), the more I understand biology and nutrition, the more this list makes sense - I think you should consider applying it to your mother:
http://www.paleonu.com/get-started/
I'm not sure if VLDL is the same thing as the stuff that typically becomes oxLDL.
Some evidence on PUFA increasing oxLDL.
Here EPA was found to mitigate oxidized LDL:
http://www.ncbi.nlm.nih.gov/pubmed/18252023
Looks like this stuff is making it into schools:
http://cmbi.bjmu.edu.cn/www-learn/labmeeting/labmeeting_014.pdf
More research is needed, but it appears that Ancel Keys' hypothesis is still very wrong. It has nothing to do with cholesterol, but the effect of lipids (that compose lipoproteins) tendency to oxidize. Anyone in here on a diet shouldn't be worried about saturated fats. If anything they are healthy if they substitute too much PUFA.
In this study they compare the accuracy of predicting coronary artery disease between Global Risk Factor Assessment Score (GRAS - traditional lipid hypothesis) vs oxidized LDL.
http://atvb.ahajournals.org/cgi/content/full/21/5/844
They found that GRAS was 49% while oxLDL was 82%.
http://atvb.ahajournals.org/cgi/content-nw/full/21/5/844/T3
Another study finds that oxLDL is a good indicator in otherwise apparently healthy men:
http://www.circ.ahajournals.org/cgi/reprint/CIRCULATIONAHA.104.529297v1
This study attempts to explain why the oxidized LDL is bad. Apparently macrophages gobble it up and become inflammatory.
http://www.jlr.org/content/38/1/101.full.pdf
This study demonstrates how a powerful antioxidant is antiatherogenic.
http://www.ncbi.nlm.nih.gov/pubmed/1466646
This may explain why these statin studies aren't consistent. If statins indiscriminately reduce all LDL, but the problem is small, dense LDL with a tendency to oxidize, then sometimes statins would help and other times harm. But it doesn't have to be this way if a drug is developed that targets the cause of oxLDL, or if people eat fats that aren't rancid.
What causes oxidized LDL isn't as clear. There is some evidence that it is n-6 fatty acids, or too much n-6 AND n-3. I'm beginning to see why Dr Harris recommends elimination of n-6 as opposed to balancing a ratio by adding more n-3. So DominoTheory take note. As an amateur scientist (and not an MD), the more I understand biology and nutrition, the more this list makes sense - I think you should consider applying it to your mother:
http://www.paleonu.com/get-started/
I'm not sure if VLDL is the same thing as the stuff that typically becomes oxLDL.
Some evidence on PUFA increasing oxLDL.
http://atvb.ahajournals.org/cgi/content/full/24/3/498
Here EPA was found to mitigate oxidized LDL:
http://www.ncbi.nlm.nih.gov/pubmed/18252023
Looks like this stuff is making it into schools:
http://cmbi.bjmu.edu.cn/www-learn/labmeeting/labmeeting_014.pdf
More research is needed, but it appears that Ancel Keys' hypothesis is still very wrong. It has nothing to do with cholesterol, but the effect of lipids (that compose lipoproteins) tendency to oxidize. Anyone in here on a diet shouldn't be worried about saturated fats. If anything they are healthy if they substitute too much PUFA.
teh_pwn, have you ever considered starting a thread to put this unconventional nutrition science in? It's obvious that you are very passionate about it, and you demonstrate that by proselyting about it in every health and/or food thread.
I see two problems with this. First, the information that you have accumulated is fragmented and sometimes incoherent when spread over many threads. Your message would be better served by having it all in one place, carefully organized and clearly laid out.
Second, this sometimes overwhelms threads with pages of links. You'd create a better forum for discussion if that was the explicit purpose of a thread.
Just food for thought.
I see two problems with this. First, the information that you have accumulated is fragmented and sometimes incoherent when spread over many threads. Your message would be better served by having it all in one place, carefully organized and clearly laid out.
Second, this sometimes overwhelms threads with pages of links. You'd create a better forum for discussion if that was the explicit purpose of a thread.
Just food for thought.
D
Deleted member 17706
Unconfirmed Member
grumble said:
According to his book:
grumble said:
Maybe one day, but I'm trying to avoid doing it. There are so many comments in the real world that refer to the conventional wisdom that I really need to just learn to tune it out. That part is my fault - how I constantly bring it up in threads. It's also time consuming, and I really don't want to create a thread and have the lesser half of gaf post 300 1 liner replies. Hopefully I'll gradually disappear over the next couple of months if my girlfriend and I get more serious. The subject is starting to get boring anyway. I'll probably study architecture next. I want to design my own house.
hockeypuck
Member
I'm pretty sure at this point because currently there is no published prospective trial showing that treating VLDL/HDL ratios is effective, period. I'm going to stick with the stuff that has been tried and true, not stuff that has yet to move from the lab.BronzeWolf said:
What you still haven't answered is, how do you know that treating VLDL/HDL is even effective in the first place? You don't have prospective data.
The remainder of my replies to your quotes are going to be purely logistical and to point out the fact that you still do not understand how to read a clinical paper, as you still haven't produced any type of contrasting evidence on par with a prospective trial. Think of my critiques as basic lessons in epidemiology.
I have no idea what you just said. Make a conclusion. Stronger apoB/apoA relationship in the placebo group means what, exactly?BronzeWolf said:
The fact that you included a block quote seems to make you proud, as if apoB/A ratios were better clinical predictors. But then again, this showed that you did not read the study carefully. If you had read the methodology of this study you would find out that the exclusion criteria included anyone with a LDL > 190. I.E., the investigators specifically and purposefully excluded the typical patient population who would at baseline would be prescribed a statin in the first place. Secondly, if you had read between the lines and understand the implications of this study you would realize that the authors of this study are trying to justify even MORE aggressive use of statins than is currently recommended by finding other SECONDARY lipid markers if the LDL is below the threshold for treatment.BronzeWolf said:
Finally, you should also know that the apoB/A portion of this study was a SECONDARY analysis and was not the PRIMARY goal of this study. This was apparent within the first three sentences of the entire paper. Hence any conclusion drawn from that should be not be as highly regarded. Moving on...
Bullshit. Show me your reasoning why you think apoB/apoA is stronger than TC/HDL, which by the way isn't even my claim to begin with. Since you're so sure, explain your reasoning. I don't have a PhD in biostatistics, and I'm guessing you don't either, so show me your reasoning.BronzeWolf said:
Again, like the study above, this study is to find more secondary markers to justify further statin use after the LDL target has already been reached.BronzeWolf said:
Your point being? If it doesn't even mention apoB/apoA ratios, why even mention the study?BronzeWolf said:
You're not explaining your point clearly. I don't understand why you're trying to state.BronzeWolf said:
When compared to treating the LDL, yes.BronzeWolf said:
You seemed to have forgotten the original point of this debate. You stated, "LDL does not correlate as well to actual diseases as the HDL:VLDL ratio." It was this statement I challenge. How did you respond? You provided a bunch of studies where the authors looked for secondary markers after treating the LDL to below the recommended upper limit.
Every single study you've linked above has a definitive statement supporting the primary treatment of lowering LDL for dyslipidemia.
That you failed to recognize this means you didn't carefully the entire paper and/or you do not know treatment guidelines, which are important to drawing conclusions from these results.
And therefore any rational clinical scientist would place more weight on treating the LDL over the VLDL/HDL ratio. It's common sense.BronzeWolf said:
That's a pretty cocky statement from someone who has shown in plain view that he can't analyze an epidemiological paper. So you can predict the future now, eh?BronzeWolf said:
The evidence you've thus far brought to the table only supports my (and mainstream medicine's) claim. The consensus to treating LDL levels first has been reached for years.BronzeWolf said:
My original point still stands. You cannot produce a single prospective trial testing efficacy of VLDL/HDL ratio, which you now freely admit ("there isn't any clinical trial that directly assesses VLDL:HDL ratio treatment"). Hence you used suboptimal data, not even correctly, to try to form an argument which you lost before you even began.
And since you can't produce any such trials, you should stop posting links. That was my original point.
BronzeWolf
Banned
Hockeypuck, here are a couple of points that need to be clarified before going on further.
1. No one (and by no one, I mean me) here or IRL is treating people with or without statins.
2. No one (and by no one, I mean me) is denying that statins work and that they do so by lowering the apoB proteins in circulation.
3. No one (and by no one, I mean me) is trying to say that TC/LDL are faulty markers or that they do not work.
That said, your lack of scientific curiosity in general is astounding. I am appalled and a little disappointed by how you tackle the questions that are being brought. You asked for a clinical trial that is focused on HDL/VLDL ratios. I know and you know it doesn't exist so you are asking for a standard of evidence that hasn't been really set out. That wouldn't be a problem with me, because what I have been trying to do is not prove to you that HDL:VHDL ratios are the best way to treat people. Yet you try so hard to put those words in my mouth.
What I have tried to do is show that HDL:VHDL is not some microbiology mumbo-jumbo and it does have a strong, although incomplete, evidence instead. IE HDL/VLDL is not homeopathy. The truth of the fact is that when measured, HDL/VLDLL are as good if not stronger markers than TD/LDL markers. Which is what last time we checked is what we are doing here. Are we treating people? NO! Are we giving drugs to improve HDL:VHDL? NO. I don't think the disclaimer was necessary, but apparently it is.
The evidence for HDL:VHDL stands now as follows:
1. When measured reliably (which is what I meant with unreliability of measurement, not many trials and case studies measure apoB/A reliably, doing it only at baseline or not doing it at all), apoB/A in the wild has been shown to be better markers than TC/LDL in good observational studies (INTERHEART and AMORIS).
2. It is supported by animal models.
3. In the few clinical trials that published apoB/A, it has been found to be as equal or stronger marker than TC/LDL, such as the AFCAPS/TexCAPS, IDEAL, 4S and CARDS. This is after the LDL treatment worked, but that doesn't counter the notion that apoB/A is a useful tool. I know more studies actually tested apoB/A but didn't publish it, which might be of great help if a retrospective analysis is done.
That said, I do acknowledge and concede your point of HDL:VHDL not being a valid treatment for the time being.
We can from this, do some conclusions, with some side comments:
1. Statins work. This was never disputed by me. Statins also have nasty side effects
2. TC/LDL is a good marker. This was never disputed by me.
3. HDL:VHDL might be better markers encompassing points 1 and 2. HDL:VHDL are standardized and do not require fasting
I don't think we are really breaking new ground here and we are not having a professional discussion either. As such, this is an informal educational debate. Now, as an informational debate, I really appreciate what you bring to the table in terms of epidemiological knowledge, but you could really give more if you could switch from "I am right you are wrong" to a more pedagogic discourse.
EDIT: sorry for all the edits, I try to not say stupid stuff if I can help it
1. No one (and by no one, I mean me) here or IRL is treating people with or without statins.
2. No one (and by no one, I mean me) is denying that statins work and that they do so by lowering the apoB proteins in circulation.
3. No one (and by no one, I mean me) is trying to say that TC/LDL are faulty markers or that they do not work.
That said, your lack of scientific curiosity in general is astounding. I am appalled and a little disappointed by how you tackle the questions that are being brought. You asked for a clinical trial that is focused on HDL/VLDL ratios. I know and you know it doesn't exist so you are asking for a standard of evidence that hasn't been really set out. That wouldn't be a problem with me, because what I have been trying to do is not prove to you that HDL:VHDL ratios are the best way to treat people. Yet you try so hard to put those words in my mouth.
What I have tried to do is show that HDL:VHDL is not some microbiology mumbo-jumbo and it does have a strong, although incomplete, evidence instead. IE HDL/VLDL is not homeopathy. The truth of the fact is that when measured, HDL/VLDLL are as good if not stronger markers than TD/LDL markers. Which is what last time we checked is what we are doing here. Are we treating people? NO! Are we giving drugs to improve HDL:VHDL? NO. I don't think the disclaimer was necessary, but apparently it is.
The evidence for HDL:VHDL stands now as follows:
1. When measured reliably (which is what I meant with unreliability of measurement, not many trials and case studies measure apoB/A reliably, doing it only at baseline or not doing it at all), apoB/A in the wild has been shown to be better markers than TC/LDL in good observational studies (INTERHEART and AMORIS).
2. It is supported by animal models.
3. In the few clinical trials that published apoB/A, it has been found to be as equal or stronger marker than TC/LDL, such as the AFCAPS/TexCAPS, IDEAL, 4S and CARDS. This is after the LDL treatment worked, but that doesn't counter the notion that apoB/A is a useful tool. I know more studies actually tested apoB/A but didn't publish it, which might be of great help if a retrospective analysis is done.
That said, I do acknowledge and concede your point of HDL:VHDL not being a valid treatment for the time being.
We can from this, do some conclusions, with some side comments:
1. Statins work. This was never disputed by me. Statins also have nasty side effects
2. TC/LDL is a good marker. This was never disputed by me.
3. HDL:VHDL might be better markers encompassing points 1 and 2. HDL:VHDL are standardized and do not require fasting
I don't think we are really breaking new ground here and we are not having a professional discussion either. As such, this is an informal educational debate. Now, as an informational debate, I really appreciate what you bring to the table in terms of epidemiological knowledge, but you could really give more if you could switch from "I am right you are wrong" to a more pedagogic discourse.
EDIT: sorry for all the edits, I try to not say stupid stuff if I can help it
betweenthewheels
Member
Are you taking any supplements? It's good to take at least a multivitamin during induction.Fina1e said:
Also, make sure you're drinking plenty of water.
That's all I can think of. I've never had any (noticeable) carb withdrawal symptoms myself, perhaps it's WHAT you're eating? I'm sure some of the other guys on here could give you some advice.
betweenthewheels said:
Yes, I am taking a multivitamin along wish fish oil and have been drinking a lot of water (I always do). As for the food, I am eating things that shouldn't give me too many problems: bacon, chicken, almonds, fish, olive oil, butter, pepperoni, etc. The headache was gone when I woke up this morning and I am hoping there aren't any more like it down the road.
betweenthewheels
Member
Fina1e said:
From what i've read, the induction 'flu' typically lasts around 3 days, the lethargy and headaches should subside. Good luck!
hockeypuck
Member
I never mention TC/LDL in my arguments. I never propounded any ratios in my arguments. I only talked about absolute levels of LDL.BronzeWolf said:
Again, your original statement
The only evidence I've provided studied lowering the absolute LDL level, not any ratios. I'm not sure why you changed the debate from "LDL versus VLDL/HDL" to "TC/LDL versus VLDL/HDL."BronzeWolf said:
BertramCooper
Banned
After digging my car out from under a foot and a half of snow, I treated myself to a piece of cake from my local bakery. And now I'm mad at myself for it.
You'd think after losing over 70 pounds in a year, my mind would grasp the fact that I'm not going to gain 10 pounds from a single piece of cake. The fear of falling out of my diet and exercise regimen really messes with my head sometimes.
You'd think after losing over 70 pounds in a year, my mind would grasp the fact that I'm not going to gain 10 pounds from a single piece of cake. The fear of falling out of my diet and exercise regimen really messes with my head sometimes.
betweenthewheels
Member
BertramCooper said:
I'm the same way. Even though I KNOW a cheat isn't gonna break my diet it still makes me feel guilty.
I think it's cause indulging in sweets can lead to cravings and i'm in the mindset of "I'm over my carbs for the day, may as well pack my face full of crap for the rest of the day"
infiniteloop
Member
Finished my Whole30 this week, ended up doing 32 days in the end. Really enjoyed it, ended up eating a lot of stuff I wouldn't have tried before. Went from 169.2 to 160.8, very little exercise and no counting. Yesterday I ate a cheeseburger and fries, tasted like crap and I felt really ill afterwards. :/
BertramCooper said:
THIS...A Thousand times THIS
I can't even allow myself a packet of chips or a bar of choc without feeling like my diet is over and i'm going to put it all back on, and I lost 115 or so pounds since march. I really need to relax a bit. One bar of choc is not the end of the world.
and so I begin the end of this wretched journey.
I've been dieting on and off a.k.a not dieting at all since summer 2010. During the past 12 months or so ( again on and off ) I've gone from weighing 240lbs to my current 175lbs.
I've "got" 100 days to lose 20lbs so I reach my goal weight, 155lbs. It's gonna be fun to compare the before & after pictures.
I've been dieting on and off a.k.a not dieting at all since summer 2010. During the past 12 months or so ( again on and off ) I've gone from weighing 240lbs to my current 175lbs.
I've "got" 100 days to lose 20lbs so I reach my goal weight, 155lbs. It's gonna be fun to compare the before & after pictures.
good luck corky! you can do it
and i'm the exact same way as far as the occasional snack food. i simply won't do it. i'm afraid that since i'm losing weight, eating anything out of my routine will stop or sloooow down any progress i've made thus far. i have one cheat meal a week, always on saturday for lunch. and that's it when it comes to cheating. at work, if i'm offered a single piece of starburst candy or anything like that, i turn it down. we're even having a catered dinner in the next few weeks and i'm debating if i want to eat that for my cheat meal or just leave when the food shows up.
i've lost a total of 47.5lbs and i'm afraid of gaining it back. i know how i felt and looked at my heaviest and i simply don't want to return to that - ever. i'll stress over any amount of weight increase. it's a mental hurdle i'll have to get over. but at least i recognize the problem. that's half the battle =/
and i'm the exact same way as far as the occasional snack food. i simply won't do it. i'm afraid that since i'm losing weight, eating anything out of my routine will stop or sloooow down any progress i've made thus far. i have one cheat meal a week, always on saturday for lunch. and that's it when it comes to cheating. at work, if i'm offered a single piece of starburst candy or anything like that, i turn it down. we're even having a catered dinner in the next few weeks and i'm debating if i want to eat that for my cheat meal or just leave when the food shows up.
i've lost a total of 47.5lbs and i'm afraid of gaining it back. i know how i felt and looked at my heaviest and i simply don't want to return to that - ever. i'll stress over any amount of weight increase. it's a mental hurdle i'll have to get over. but at least i recognize the problem. that's half the battle =/
betweenthewheels
Member
How often (if at all) do you guys hop on the scale?
I really like the encouragement of seeing the weight loss, but what if I don't lose one week or lose as much, it can be very discouraging.
Maybe i'll just get out the measuring tape once a month.
I really like the encouragement of seeing the weight loss, but what if I don't lose one week or lose as much, it can be very discouraging.
Maybe i'll just get out the measuring tape once a month.
spindashing
Banned
Messi said:
LOL, I actually love the feeling. I feel real shitty eating even one CHIP. Hell, I felt bad eating two crackers a few days ago. Although the feeling sucks, it's a great reminder to not fall off track.
betweenthewheels said:
I hop on the scale once a week. I used to do it once a day but I felt that was too frequent. It's so hard staying away from the scale. It's tempting but it's rewarding seeing some weight loss, but it sucks when you've seen no change. I've hit a plateau too...
Measuring my waist is also every once in awhile. I sometimes forget to do this. Last time I checked, my waist was at 37.5 inches! Sometime last year it was around 41. =(
ScrabbleDude
Member
I weigh myself every morning. It can be discouraging if the numbers go up a bit, but it's natural to have a daily fluctuation.betweenthewheels said:
infiniteloop
Member
every morning.
I like graphs
I like graphs
Domino Theory
Crystal Dynamics
betweenthewheels said:
Every Tuesday with measurements every 1-2 months.
BertramCooper
Banned
Once every month or so.betweenthewheels said:
I stopped stressing out over numbers a while ago. I was weighing myself weekly and it became far too discouraging.
These days, I just go by how loose my pants feel. At my heaviest, my waist was a 52 (ugh, I get sick just thinking about it). Now I'm at a 38. And to me, that's more satisfying than the number of pounds I've lost.
entremet
Member
Wow congrats. That's a quite a loss there.BertramCooper said:
I second the notion to forget about the scale. Especially if you're doing any weight training, because muscle weighs more than fat. Measurements are more accurate in regards to improving body composition. Get a tailor measuring tape and use that instead of just a scale.
goldenticket
Member
BertramCooper said:
ive had similar weight loss as you and i feel the same way. i can be hard on myself
betweenthewheels said:
every day. i wake up, use the restroom and hop on the scale right before taking a shower. i can understand people not wanting it every day. when i first started losing weight i didnt have a scale and didnt want to know but i reached a point after losing some weight i wasnt sure if i was losing anymore or at what rate so i got a scale to keep track. i got
from amazon for like 29 bucks. I like it because it has the decimal point so you can lose .3 of a pound and feel good about it. the flip to that is when you are working hard and eating right and dont lose any it can be frustrating. also i keep track of my weight (and what i eat) in fitday.com (its free) and when my weight changes i enter it in and you can see the graph and look at your progress which is nice.speaking of weight loss this shitty weather (texas) has kept me inside (my exercise is doing a lot of walking) the last time i got to walk was monday. i started in july and before this the longest stretch on not walking was two days and that only happened once. and today i was tired of being forced to stay inside by the cold weather so i walked to the store and bought a big bag of chips, hopefully it wont mess me up too bad. i need to get back on schedule. having more time at home with nothing to do i think about food much more. when im exercising and stuff its easy to stay on my low carb diet but this week has been tough