Atkins Horror!

viviennem

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borofergie said:
RoyG said:
RESULT!!!! RESULT!!!!!! all hail borofergie :clap: :clap: :clap: Just told the wife to shove the low fat **** back in the dogs cupboard, and to break out the Butter, double cream and 16oz er's again :D :D steak for tea wah hoooooooo.

Thanks Roy!

Not just steak. It has to be fatty steak. You can stick your filet - I always look for the most marbeled piece of ribeye I can find.

I love fillet steak! Locally we have a proper butcher who hangs his meat well, and who sells rare breed beef and pork. He saves me the fillet steak when it gets so black that no-one else will eat it. I cook it in a very slow oven with olive oil, butter, garlic and a few mixed herbs, and sliced mushrooms go in towards the end. It just melts in the mouth.

In fact I might just get some for today . . . or for tomorrow to celebrate after my blood tests :p

Viv 8)
 

NewdestinyX

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Be careful, folks, that we don't miss the forest for the trees in the issue of the Lipids profile. First - Viv -- I think it was you-- Trigs are 99% genetic in nature. Most all of the diabetics I've interviewed over the years - and Borofergie and you are great examples too - show clearly that regardless of your diet - your Trigs don't move much. When I was eating high carb an had an A1c of 10.9 my Trigs were 85 (sorry for American numbers). When I transitioned (for 1 year) to <50g carbs a day - my Trigs were 84. Borofergie said the same (he ate high carb and had the same trigs as now) and you've said the same - that yours tend to be on the high side even eating as LCHF as you do.

The same is the case for the other numbers of the lipid profile. Though we CAN have an effect on our HDL by the diet we choose - we can rarely make huge differences without massive changes. And then what's MORE important is again those nasty genetic predispositions. The most important test any person can ever take to predict their risks for CVD, diabetic or non diabetic, is the VAP test where they measure the amount of VLDL (small dense particles) and the ratio of A to B particle size. A - fluffy - okay.. B-small dense -- BAD!!. Anybody who comes back with A-B ratio 1:1 or more B than A should be on statins tomorrow. No amount of changing your diet will ever change the A-B particle size. That's almost pure genetics from what the studies show.

Then the even larger question - if you really want to 'beat the system' and avoid statins and you have the bad genetic predisposition - is to read about 'inflammation' in the body. It's inflammation that's responsible for the dense particles of LDL gathering in your arteries in the attempt to PROTECT the heart and arteries. So even bad old LDL is trying to PROTECT you from the results of the inflammation. The entirety of the Heart Disease research is really turning toward this now. Slowly. The establishment is still in power and we're getting OLD data from the docs. But it's all about reducing inflammation in the body. You are genetically predisposed to have certain levels of cholesterol/trigs and particle size ratio. Diet doesn't even directly affect that. What diet affects more directly is the level of inflammation. With lipids - the end game is all about reducing inflammation. NOW if you have mostly A particles - fluffy LDL - then in a way you're 'home free'. Statins will never be needed.

So everyone 'force' your docs to give you a VAP test.
 

viviennem

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I'm not going to disagree with you on inflammation throughout the body causing all sorts of problems, including in the pancreas; and while I don't know much about your genetic data (and you haven't offered any links to peer-reviewed papers), I probably would pretty well agree with you. I don't like 'averages' that everyone has to fit into - thyroid is a case in point but I won't get into that here!

I can give you anecdotal evidence about my triglyceride levels, based on my medical records:

I first did Atkins from April 2004 to November 2005, 5 years before I developed Type 2; I lost 77lbs in that time.

My HDL went from 0.9 to 1.65 (that's in our 'money'. Target is above 1.2, so that should give you a comparison)

Trigs went from 1.09 to 0.65 (target - below 1.7, and the lower the better). That's a big drop if it's 99% genetic?

Didn't get LDL's in those days, but my Total:HDL ratio went from 5.9 to 3.3 (target : below 5, preferably around 3.5). Interestingly, over the same time period my total cholesterol went UP, from 5.3 to 5.4.

Over that 18 months 3 things changed in my lifestyle: I ate Atkins Induction the whole time - as you know, 25g of carb per day. Possibly I got up to 30g daily, but no more. I cut down my alcohol intake considerably; and I walked about 25 miles a week, dog-walking, an increase of about 10 miles a week. No other exercise. My back wasn't as bad then as it is now.

Now, as I understand it (but I'm no expert) when you have insulin resistance, the excess glucose from carbohydrate intake is turned into triglycerides so that it can be stored in the fat cells. When you get into ketosis, you start burning off that excess fat. This can lead to an initial increase in blood triglyceride levels, but then it settles down and your trigs continue to drop as you continue in ketosis. Alcohol stops ketosis 'cos our bodies can run on alcohol. (Simplistic I know, but it does for me).

Obviously I had inflammation before because of my alcohol intake - a bit excessive, and regular; no binge-drinking. Stopping drinking almost completely would obviously have improved the inflammation throughout my organs. On the other hand, I have been on anti-inflammatories for the back problem for about 25 years, and I was taking them then.

The most significant change in my lifestyle during that time was going from a very high carb/low fat diet to 30g or less of carb per day, and a corresponding increase in fat intake. I really don't see how that massive change in diet could have had no input whatsoever to the vast improvement in my lipid profile. Nor that cutting out alcohol would have been the sole factor in the drop in my triglycerides.

I've never heard of a VAP test over here; possibly we call it something else. As for "forcing" a doctor to give me one, with the prsent eagle eyes they have on finances - well, I can ask! I certainly can't afford to go privately for one. Maybe I could bargain - give me a VAP test and I might reconsider my refusal to take statins. I'll ask tomorrow. After all, I eventually got my Vit D test :D .

Isn't Vit D involved in the inflammation process too?

Just goes to show how complex the whole thing is.

Viv 8)
 

borofergie

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Some great points Grant, I think that I agree with most of them.

  1. I like the idea that my lipid profile is mainly gentically determined, because it poles even more fire on the lipid hypothesis, which I firmly believe is still the single largest obstruction to wide scale acceptance of low-carb diets for T2 diabetics
  2. I am almost certainly predisposed to low-cholesterol, every test I've ever had has come back abnormally low.
  3. However, I've been eating an extreme diet, 80% fat with a much as possible saturated. If the "sat fat is bad for you" brigade we're right, then I should have been able to shift it upwards a little bit. I think I've demonstrated that fat in your mouth doesn't equal fat in your blood stream.
  4. The actual result is that my lipid scores are chronically low, and are probably bordering on the unhealthy. I'm actively trying to see what I can do to increase them.
  5. I agree with Viv, I also hang out on Paleo Hacks, which sometimes looks like an extreme competition to see who can get the biggest HDL (this is the less attractive side of the Paleo scene). These guys definitely move their scores through low-carbing and supplementation.
  6. I think that lots of the numbers are meaningless and have no real impact on CV health. none of the correlations included people on VLC diets, so it would be naieve to think that our low numbers mean that we are safe.
  7. Low trigs are a good proxy measure for LDL pariticle size.
  8. I agree 100% on inflammation.
 

borofergie

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Here is (occaisional forum viewer) Dr John Briffa's analysis of the "shocking Swedish 'science' " behind the paper:
http://www.drbriffa.com/2012/06/12/shoc ... h-science/

Anyway, the researchers point our attention to the fact that fat intakes fell from 1986-1992. At this time, by the way, and through the study period as a whole, average weight was climbing. So what does that say, on the face of it, for the effectiveness of low-fat eating for weight control?

But then fat intakes started to rise in 2002 for women and 2004 for men. The concern that comes loud and clear in the paper is that this was paralleled by a rise in cholesterol levels which the authors describe as a ‘deep concern’. However, by their own admission, cholesterol levels didn’t start to climb until 2007. The inference is that increased fat intake led to the rise in cholesterol. But are we really expected to believe that it took 3-5 years for cholesterol to rise in response to an increase in saturated fat intake? That doesn’t seem quite right to me.
 

viviennem

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IanD posted:

. . .had a ham salad for lunch, with an orange for afters. A chicken & cheese salad for evening meal. No carbs.
Check my BG after all that energy expenditure - 6.7.

I just spotted this. Ian, there are about 16g carb in an average orange, and there would be a few in whatever veg you made up your salad with. About 3g in a large tomato, for instance, and 1.8g in an 80g serving of Iceberg lettuce (that's a lot of lettuce :shock: ).

On Atkin's Induction, you get almost all the 25g of carbs from the vegetables, salad or otherwise.

So you could have had as many as 30g or even 40g carb in those 2 meals - depending on the size and make-up of the salads.

Viv 8)
 

ShottleBop

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Not everyone experiences a reduction in their cholesterol levels after going low-carb. I was diagnosed as "pre-diabetic" back in February, 2008 (very borderline: A1c was 6.5, and my FBGs were 127 and 123; it was that 123 alone that kept me from being diagnosed as a Type 2). I found Dr. Bernstein's book, The Diabetes Solution, within a couple of months thereafter, and have maintained a low-carb diet since then. (No grain, virtually no fruits, other than avocados and limited amounts of tomatoes and berries, no milk, no starchy vegetables--40-60 total carbs per day, 25 or so of them from fiber.) My A1cs run 5.3-5.5 (most recently 5.4), and my monthly meter average (7-8 tests a day) is--and has been, since late 2008--in the low-to-mid 90s.

On January 28, 2008, my lipids were (sorry, folks, but most of these are 'Merkin numbers, my understanding is that our recommended LDL level of 100 corresponds to something like 2.6 in the system used in the UK (at least, using spacedoc's converter tool, at: http://www.spacedoc.com/converters.html):

TC: 281
LDL (direct) 215 [5.6, in the UK]
HDL: 40
Trig: 142

By August, 2008 (down 55 pounds, A1c at 5.5) my lipid profile looked like this:

TC: 269
LDL (Direct): 194 [5.0 UK]
HDL: 48
Trig: 77

Between August and November, 2008, I lost another 15 pounds (total weight loss: 65 pounds, from 220 to 155, on a 6-foot frame). My total cholesterol soared 100 points:

TC: 369
LDL (Calculated): 287 [7.4 UK]
HDL: 65
Trig: 85

In March, 2009, my A1c was 5.3, but I didn't have another lipid panel until September, 2009 (A1c 5.4):

TC: 337
LDL (Direct): 219 [5.7 UK]
HDL: 79
Trig: 41

It's stayed more or less in that neighborhood since. I had an NMR assay done in September, 2011; it showed that more than 92% of my LDL was the light, fluffy kind. Still, my LDL particle concentration (LDL-P) was 1793, as compared to a recommended high of 1,000, and, that summer, I began to experience chest discomfort while doing my daily exercise (climbing 24 flights of stairs on my way back from lunch; riding a stationary bike). In mid-December of last year, they did an angiogram, found a 90% blockage in one of my coronary arteries, and inserted a stent. So, low Trig/HDL ratio, high HDL, low trigs, decent TC/HDL and LDL/HDL ratios, large, fluffy LDL particles cannot guaranty elimination of risk.

It's looking, in fact, like mere cholesterol concentration measurements--the typical LDL-C, for example--do not indicate actual level of risk as well as the particle number measurements you can get with an NMR test, and, since 2009, at least, there have been reports in the medical literature to that effect:

  • http://www.cardiovascularbusiness.com/index.php?option=com_articles&view=article&id=26891:jcl-ldl-p-levels-may-better-predict-cvd-risk-than-cholesterol ("JCL: LDL-P levels may better predict CVD risk than cholesterol")

    http://www.diabeteshealth.com/read/2009/07/29/6293/considerable-risk-of-cardiovascular-events-may-linger-despite-achieving-target-ldl-cholesterol-level/ ("Considerable Risk of Cardiovascular Events May Linger Despite Achieving Target LDL Cholesterol Levels with Statins in Patients with Metabolic Syndrome: LDL Particle Concentration More Closely Related to Risk of Cardiovascular Events than is LDL Cholesterol")

    http://www.theparticletest.com/uploads/pdf/Otvos_MESA2011.pdf ("Clinical Implications of Discordance between Low-Density Lipoprotein Cholesterol and Particle Number"):
When LDL-P and LDL-C were discordant, LDL-P was more strongly associated with the risk of CVD events and with atherosclerosis as measured by carotid IMT than was LDL-C. This finding has potentially important implications regarding our understanding of the etiology of atherosclerotic cardiovascular disease.

According to Dr. Thomas Dayspring, Director of Cardiovascular Education at the Foundation for Health Improvement and Technology, an acknowledged expert in lipidology, many of these issues can best be dealt with by eating a low-carb diet: http://www.thelivinlowcarbshow.com/shownotes/6371/585-lipidologist-dr-thomas-dayspring-explains-the-truth-about-cholesterol/ ("585: Lipidologist Dr. Thomas Dayspring Explains The Truth About Cholesterol"). Even so, it is possible to eat a low-carb diet and still have a concentration of LDL-P that--at least, according to much of the research--places you in the "high risk" category.
 

borofergie

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Hmmm, sorry to hear of your problems. Hopefully those arteries are nicely unblocked now...

Doesn't what happened to you show kind of indicate that LDL is a symptom of CVD, rather than the cause?

Hope you're all fixed now man.
 

ShottleBop

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Back to climbing stairs and riding my stationary bike, thanks. Still fighting with my cardiologist over whether statins would be of any benefit.
 

NewdestinyX

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ShottleBop said:
Back to climbing stairs and riding my stationary bike, thanks. Still fighting with my cardiologist over whether statins would be of any benefit.
Me too.. But all medical science now purports that "inflammation" is the reason any small dense particles stick to artery walls. People eager to avoid statins should be reading up on how to decrease inflammation in the body. Sadly - stress is one of the main causes of inflammation.

Statins have wonderful anti-inflammatory properties which is a main reason docs want us on them. I'm told aspirin can't give the same protection. Still not on them but I fear that I already have blockage. Just no symptoms yet.


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