Low-carbs and lipids
Once again the dishonesty or maybe sheer stupidity of scientists bowls me over. I got an email from an old patient a couple of days ago who is following a low-carb diet while under the care of a skeptical (to say the least) cardiologist. The cardiologist sent the patient an email with a link to a Cardiosource (an online resource for cardiologists) commentary on an article in this month’s issue of the Journal of the American College of Cardiology.
The paper compared a standard high-carbohydrate, low-fat diet (HCLF) to a very-low-carbohydrate, high-fat diet (VLCHF) in terms of blood lipid changes. The Cardiosource commentary seized on the last two lines in the abstract of the paper.
…although both diets had similar improvements for a number of metabolic risk markers, the HCLF diet had more favorable effects on the blood lipid profile. This suggests that the potential long-term health effects of high- and low-carbohydrate weight loss diets remain a concern, and that blood lipid levels should be monitored in obese subjects with the metabolic syndrome.
As the commentator put in in his perspective:
The best diet for the metabolic syndrome is neither of these extremes. Rather, the best is a diet restricted in processed flour and simple carbohydrates, increased in complex carbohydrates and soluble fiber, and high in fish and monounsaturated fats. The results also support patient choice, with careful monitoring of the lipids. Of course, aerobic exercise and weight training should improve the outcome of any diet.
Jesus wept. Nothing in this paper leads to the Cardiosource guy’s pinheaded conclusion. In fact, nothing in this paper leads to the conclusion of the authors of the paper, at least not as they wrote it in the abstract.
Let’s take a look at what the data in the paper show and see how, once again, academic bias rears its ugly head.
A group of 88 abdominally obese subjects were randomized into two equal groups. One group went on a low-calorie HCLF diet; the other went on a VLCHF diet of the same number of calories. Both groups remained on their respective diets for 24 weeks. Researchers measured various blood parameters at the start and at the end of the 24 week trial.
Both groups lost a similar amount of weight over the 24 weeks (subjects on the low-carb diet were trending toward a greater weight loss, bt the difference hadn’t reached significance by 24 weeks). You can see in Table 3 below the results of any lipid changes in both groups over the 24 weeks.
Most of us here in the US are used to seeing these numbers listed in units of mg/dl instead of the mmol/l that are appearing more and more commonly in scientific papers. I converted the mmol/l units into the more familiar units and put them in the table below.
Let’s analyze to see what all this means.
First, we can see that total and LDL- cholesterol didn’t do much on the low-carb diet whereas both dropped on the low-fat diet. This is nothing that hasn’t been seen a thousand times before in other studies. It’s been known forever that reducing fat in the diet brings about a reduction in total and LDL- cholesterol. But it does so at a cost. The cost is that although the LDL-cholesterol level falls, the particles themselves convert to the smaller, denser type that are more atherogenic. Nothing new here – this has been known for a decade or more. More about this in a moment.
Second, the HDL-cholesterol went up by almost 20 percent and the triglycerides dropped by over 40 percent on the low-carb diet. These same values changed but slightly in those on the low-fat diet.
In my opinion (and the opinion of many others) the lipid parameters of most value in determining risk for heart disease are triglyceride levels and HDL levels. In fact an important index of risk is the triglyceride to HDL ratio (TGL/HDL): the lower the better. Looking at the data from this study we see that for the VLCHF diet the TGL/HDL dropped from 2.6 to 1.3. It halved. In those subjects following the HCLF diet the TGL/HDL dropped from 3.0 to 2.3, substantially less. (Now, these kinds of things matter if you’re a real believer in the lipid hypothesis, which, as everyone should know by now, I’m not. If you’re not a believer you think that these figures are markers for something else going on that probably causes heart disease, but are not the causative forces themselves.)
So, we’ve got a situation here where the lipid parameters improved more on the low-carb diet as compared to the low-fat diet, yet we’ve got the authors of the article, the generators of this data, telling us that the HCLF diet had “more favorable effects on the blood lipid profile.” Unbelievable.
But wait, it gets worse.
If you look at the first Table 3 above, you’ll see a category called ApoB at the very bottom. You’ll also notice that apoB didn’t change much in either group. But that is significant. Why? Because it means that the LDL-cholesterol particles really did get smaller in the HCLF group. Let me explain.
Cholesterol is a waxy substance that doesn’t dissolve in water or in blood. The waxiness of cholesterol is what makes it so important for providing structural support for the cells membranes and other fatty acid bilayers, but it’s also what keeps it from dissolving. In order for cholesterol to be ‘dissolved’ in the blood it must be attached to a protein, which will dissolve and carry the cholesterol along with it. Depending upon the protein it’s attached to and its density cholesterol becomes LDL or HDL or VLDL. One of the specific proteins making up LDL is called apoB. There is an apoB for each LDL particle (the particle is composed of the protein, some cholesterol and some triglycerides).
If we know the apoB count we can estimate the number of LDL particles. If the apoB number goes up, there are more; if it goes down, there are fewer.
Since the LDL-cholesterol measurement tells us how much LDL-cholesterol we have and the apoB measurement tells us how many particles we have, we can divide the LDL-cholesterol by the apoB number and get a rough estimate of the size of the LDL-cholesterol particles.
If we look at our two groups of subjects in this study, we find that in the VLCHF group the LDL-cholesterol didn’t change much and neither did the apoB. Therefore we can pretty much say that the diet didn’t really affect the LDL-cholesterol particle size. If we look at the HCLF group, however, we see a different picture. In the subjects following the low-fat diet LDL-cholesterol levels fell while apoB numbers stayed the same. This means that there are the same number of particles as before but they became smaller after 24 weeks of low-fat dieting. In other words, the low-fat diet converted the LDL-particles into the more dangerous smaller, denser type.
And these guys have the temerity to tell the world that low-carb dieting makes lipid numbers worse!
We could write it off to ignorance maybe. But not really. If you read the discussion part of the paper you will find the following statement:
It has been suggested [I would say it has been a whole lot more than suggested] that apoB, which represents the actual number of atherogenic lipoprotein particles, may be a more reliable indicator of CVD risk. Although there was some evidence for a reduction compared with baseline, apoB levels did not change significantly by week 24 in either group, suggesting that atherogenicity did not change despite a high or low saturated fat intake and the absence of an expected reduction in LDL-C with weight loss in the VLCHF.
Say what?
We know these folks know about LDL-cholesterol particle size and atherogenicity because they just described it. Then they go on to lay this smoke screen about there not being any change in particle size in those subjects on the low-carb diet. Duh! But they never mention the change in those on the low-fat diet. Unbelievable!
The disinformation presented in this paper goes to the very heart of the peer-review process. This paper wasn’t published in some low-rent journal – it was published in the Journal of the American College of Cardiology. A major journal. One assumes that the peers who reviewed this paper when it was submitted were cardiologists or at least scientists with more than a modicum of training in diseases of the heart. And one would assume that since these reviewers were cardiologists – almost all of whom are lipid-hypothesis moths of the deepest dye – they would be up on apoB and LDL-particle size and the putative atherogenicity of small, dense LDL-cholesterol particles. It beggars belief that a paper such as this one could make it through an intelligent peer-review process and wind up as it did in the pages of a major medical journal read by cardiologists all over the world.
Most of these cardiologists have their doubts about low-carb dieting, and, just as with the one who sent the email to my former patient, most will never read this paper critically, but will immediately use it as padding for their own anti-low-carb bias.
These are the kinds of shenanigans that go on all the time. They are the reason there is so much disinformation out there. And they are the reason that you should always be skeptical to the max whenever you hear this kind of idiocy bantered about. You must read the entire paper – not just the abstract.
Dr. Eades, many thanks for your work. It was your book, with Dr. MD, that got me into all this. But here’s a worrisome study that I don’t think you’ve covered:
Ketosis Leads to Increased Methylglyoxal Production on the Atkins Diet
http://www.blackwell-synergy.com/doi/abs/10.1196/annals.1333.025?journalCode=nyas
Any chance you could comment when your schedule allows?
gjl
Hi Gregory–
I have commented on this study but I did it in the comments section, which is one of the reasons I don’t like to put a lot of time into lengthly comment answers. Most readers of the blog don’t read the comments. I read a dozen or so blogs a day and I never read the comments (neither does MD. In fact, she doesn’t read the comments on my blog, nor do I on hers.) so I’ve got to assume that many other people do the same. The ones who get the posts by RSS (over 1000 people per day) don’t even get the comments I don’t think.
At any rate, if you go to the this post and look down through the comments to the exchange I had with a reader named Tim Lundeen you can see my take on the study you mentioned. I think there were four or five back and forths.
The short answer is: don’t worry about it.
Cheers–
MRE
A new year brings a new pro-carb campaign:
http://www.azcentral.com/arizonarepublic/food/articles/0109Carbs0109.html
Got to love the balanced reporting, too. We’ve got Cynthia Harriman, spokeswoman for the Whole Grain Council in Boston, Wade Moises, chef at Sassi, a high-end Italian eatery in north Scottsdale and Frank Muir, president of the Idaho Potato Commission all chiming in.
Maybe we should just give up. I mean, is diabetes, heart disease and [put your favorite industrial disease(s) here] really all that bad? After all, somebody has to support the pharmaceutical industry.
You gotta hand it to them. They never quit. Until they get fat and sick. And then sometimes they still don’t quit.
Thanks for the link.
Cheers–
MRE
If you get a series of comments like the back-and-forth with Lundeen, it might make sense to erase them and combine them into a post of their own.
Yes, it probably would. Maybe I’ll put it up.
Cheers–
MRE
I just finished reading Gary Taubes’ book (couldn’t put it down…read it in 3 days), so this kind of thing seems very normal to me.
My mother was an Adelle Davis acolyte, so I’ve been in the middle of this kind of controversy for 40+ years. And it’s been frustrating for most of that time. The good thing now is that with the internet, people like you on your blog, Dr. DeVaney, and others can get into the public conversation, decipher some of the bull, and perhaps get the other, correct, side into the argument and the public conversation. That was impossible when Ancel Keys, for instance, first started passing on his bit of misinformation.
So I think we should be happy for that, and optimistic for the future. Just as in politics, it’s not as easy to get by with shoddy claims and poorly-researched arguments any more.
Yep, the internet is a wonderful thing that lays waste to all kinds of BS. But it also acts as a vehicle for more BS as well. One has to be able to read and think critically to not be taken it, that’s for sure.
Cheers–
MRE
Doc
just seen this interesting piece that says researchers have found that people with low cholesterol levels find it harder to build muscle!
http://conditioningresearch.blogspot.com/2008/01/chlesterol-is-good-for-building-muscle.html
or
http://www.eurekalert.org/pub_releases/2008-01/tau-sc010908.php
The scientist is quoted as saying:
“Needless to say, these findings caught us totally off guard,”
Hey Chris–
I need to pull this paper to see how they came to their conclusions. I’m sure none of the study subjects ate pure cholesterol – they consumed foods high in cholesterol. So how do the authors know it was the cholesterol and not some other component of the food that caused the findings.
Cheers–
MRE
Do you have any thoughts on whether low-carbing to the point of ketosis (which is what I do and have done for years precisely because it keeps my triglycerides nice and low, my weight stable and my energy levels high) can increase the body’s production of Advanced Glycation Endproducts (AGEs)? I ask because someone on an IF forum I participate in posted a reference to the study link below regarding the Atkins diet increasing oxoaldehyde methylglyoxal which is an AGE precursor.
http://www.annalsnyas.org/cgi/content/abstract/1043/1/201
This study was quoted on a derm site — link is below — skip to the question of whether avoiding sugar will help skin:
http://futurederm.wordpress.com/2007/10/07/can-excess-sugar-age-your-skin/
I realize you did a terrific post on ketosis not too long ago but this is the first time I’ve read anything about ketosis increasing AGEs. Thoughts?
Hey Annie–
Go to this post and scroll down to the comment section. Take a look at the 4-5 comment exchange I had with Tim Lundeen. He asked the same question and I answered there.
Cheers–
MRE
It’s only slightly related, because it involves cholesterol, but I thought you might be interested in this report on a study that found that cholesterol plays a role in muscle gain (http://dmc-news.tamu.edu/templates/?a=5549&z=15). It seems that cholesterol is so vilified that even scientists are gobsmacked when it turns out to have benefits.
Hi Susan–
Same way they were (and still are) gobsmacked that low-carb diets have therapeutic benefits.
Cheers–
MRE
Great post Dr. Mike!
Just wanted to add a funny anecdote. I’ve been on Protein Power for 18 months and have been exercising a lot and really enjoy it. I’ve had great results.
After about 12 month on PP I needed to get private medical insurance. They required a blood test, and since I had just had one by my doctor, the results of which were excellent, I had no worries.
I was shocked to get a rejection letter from the insurer for poor lipids. My LDL was 98, which is optimal, but they flagged my HDL of 112 as ‘high’. How can you have too high of HDL? You can’t as far as I know. Then they added the two numbers together and said my ‘total cholesterol’ of 220 was ‘high’. My triglycerides were 55.
I thought it was really funny and exasperating, this is a major health insurer, they didn’t know what the different numbers meant. It worked out OK, I wrote them a letter disputing their findings and explaining the numbers, and they eventually wrote the policy. You would think they would understand this stuff without me as a layman having to explain it to them
Keep up the great work! Love the blog
Truly unbelievable. The depth of their dumbth is sometimes unfathomable.
Cheers–
MRE
Hi Dr Eades,
Thanks for examining the paper and explaining it on your blog in understandable English. Would you have time to have a look at an article (http://well.blogs.nytimes.com/2007/12/26/the-risks-and-rewards-of-skipping-meals/) and the two studies it comments on (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17998028&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum and http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17291990&ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum)? The part of the NY Times article that I am especially curious about is: “The researchers found that skipping meals during the day and eating one large meal in the evening resulted in potentially risky metabolic changes. The meal skippers had elevated fasting glucose levels and a delayed insulin response — conditions that, if they persisted long term, could lead to diabetes.”
There is a third study that appears to support regular meals as opposed to intermittent fasting (http://www.ncbi.nlm.nih.gov/pubmed/15220950?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus
.
Thank you!
Alicia Zhuang
Hi Alicia–
The studies under discussion involve different groups of people, different meal schedules, different caloric intakes and different foods. It is certainly not comparing apples to apples in comparing the outcomes of these studies. Questions abound. Do intermittent fasting regimens work the same way in young, lean healthy people as they do in older, obese people. Do they work the same in people with underlying disease, i.e., asthma?
When the first studies came out about intermittent fasting, the results seemed to be uniformly good. Now that more labs have gotten into the act, and humans are being used as subjects, we’re seeing some results that aren’t as uniformly positive. It will take require many more studies before it’s all sorted out.
Best–
MRE
Dr. Mike, your comment on my TAG is funny, because I haven’t been on a low-carb diet at all. I’m considering starting one and doing all the research I can. (At least I wasn’t trying to eat low-fat. But oh, yes, lots of carbs. Mostly home-made.)
Can TAG drop too low? Because if it drops on low carb, and it’s already pretty low, maybe I should worry.
Has it been demonstrated that it’s the statins causing the birth defects? I mean, it seems pretty obvious, but correlation is not causation, even if the correlation is so strong it breaks the heart. From what I can’t tell, they aren’t even trying to research it, but I just tried following up on the papers that cited the 2004 letter.
Other than a couple of papers I’ve seen, I’m not all that up on the statin-birth defect science. At this point I suspect it’s a correlation, but with these kinds of things it may not get beyond that. Who’s going to do a controlled study?
Cheers–
MRE
Hi Dr Mike,
Another dodgy scientific paper on nutrition. It makes me despair, especially with people like my cousin who is a doctor and married to a very rich property developer. She believes all the mainstream stuff and has no hesitation in prescribing statins. My opinion doesn’t count because I’m not a doctor. (I could have been one, just chose not to.) I mean, she’s actually a very nice person and all, but I thought she had better critical faculties than that. Never mind that before I went low carb, my trigs were through the roof, had an enlarged fatty liver and kidney stones. Why don’t I have these any more?? Couldn’t be the way I eat, could it! The lack of kidney stones alone — passing one is a charming exercise — is enough to keep me on the restricted carb straight and narrow. A couple of months ago said cousin was nonplussed when I said that the way I eat will be mainstream in 5 year’s time. Yes, I am an optimist.
Now for the actual reason I’m posting this comment: I get RSS feeds via a Firefox toolbar bookmark. When you look up an item you sure do get the comments. It’s probably the reason why I read the comments, being a lazy kind of guy.
Finally, the usual irrelevant stuff: Am currently on dial-up because the whole family plus my kids’ friends are on summer holidays. Wifeypoos and the kids have been eating junk, junk, junk. I’ve been a bore eating the right stuff. Except that the town we’re staying at has the best oysters in the country, possibly the world, and oysters do have quite a lot of carbs. Mmmmm…..
I’m on the net now because of beach sunburn and because the seas have been huge, like 4 metre waves. (But fun!!!!) Only been able to make it to the beach the last couple of days due to rain and really rough weather.
But before we left Sydney, I caught MD’s Messiah excerpts. Fantastic. I bet She Who Must Be Obeyed had fun working up to those high Gs in the Halleluiah Chorus! The American accent seems a bit strange to me in this music, but then I guess Handel’s original performance was with an Irish lilt or brogue.
Michael Richards
Hey Michael–
Enjoy your time at the beach. Sounds like fun.
You and a couple of others let me know that the comments come through on RSS. I didn’t realize that.
MD doesn’t mind the high Gs – but the B flats in Beethoven’s 9th nearly killed her.
Cheers–
MRE
In one of your comments above you said, “The ones who get the posts by RSS (over 1000 people per day) don’t even get the comments I don’t think.” As well as the RSS for articles, there’s a feed for comments – which I use, and which is how I saw the comments on this post. I find it very helpful, because, as you say, interesting stuff often comes up in the comments, and sometimes it’s long after the original article was posted. I’d never go back over all the old posts looking for new comments. So, thanks for setting up the RSS feed for them, even if you didn’t know you’d done it.
Hi Janet–
I certainly didn’t know I had done it, but I guess I’m glad I did.
Cheers–
MRE
Hi Dr. Mike,
I have two questions for you that don’t really fit this post, but hopefully you’ll find interesting enough to be worth your while:
1) I’ve always been skinnier than I’d like to be. I’ve been low-carbing for about a year, and had up til recently gained a healthy-looking layer of subcutaneous fat for the first time in my life. I’ve recently lost it again (along with almost 10 lbs), and I suspect this may be due to my holiday-season sweet tooth, but I simply can’t make heads or tails of the biology behind what might be happening. Would you be willing to offer any insight into the inner workings of those of us on the opposite end of the metabolic spectrum?
2) Do you have any opinions on conjugated linoleic acid (CLA), and whether supplementation with it might be a good or bad idea?
Thanks for your always entertaining blog, and happy new year to the Eades family.
David Godot
Hey David–
Sorry it’s taken me so long to get to your comment, but for some reason you got hung up in my spam filter. I’ve got to apologize, but I’ve just got to say it: Godot has been waiting for me.
The problem of inability to gain weight is as frustrating to those who have it as is the inability to lose weight to the rest of us. As I’ve pointed out before, and as Gary Taubes makes much of in his book, the calories in/calories out side of the energy balance equation are not independent variables. When you decrease calories coming in, the calories going out (i.e., energy expenditure) don’t stay the same: they tend to go down as well. Which makes it difficult to lose weight for most people. Overfeeding studies have shown that when calories are greatly increased, so is energy expenditure so that the people consuming the increased number of calories tend to dissipate more of them than expected, and, hence, gain less weight than simply the caloric intake would predict. In your case and in the case of most of those who can’t gain weight, this system works efficiently.
As to your gaining a nice layer of sub Q fat on the low-carb diet…about 20 years ago Wolfgang Lutz, a German physician, wrote a medical textbook in German (subsequently translated into English) about the use of low-carb diets to treat a multitude of disorders. The book contained a number of photos of patients who had gone from being underweight to being normal weight on low-carb diets. I think a low-carb diet will tend to normalize weight: it reduces excess fat and puts on fat when there are inadequate amounts.
CLA is not a single fat but a conglomeration of various isomers. Studies have shown many different effects from the administration of CLA. But most CLA supplements contain just one of the many isomers, which leads me to believe that some are probably beneficial while some others are maybe harmful. Until it’s all sorted out, I would prefer to avoid CLA supplements and confine my CLA consumption to that found in meat from animals that are grass fed. Grass feeding increases CLA content of meat and dairy products considerably.
Cheers–
MRE
Hi Dr. MRE, Thank you for your blogs — I’ve lost myself 45 lbs on low carb for the last several yrs and really appreciate the info and ideas that share here! the ADA shortly may not be on everyone’s target list b/c their practice guidelines will advise ‘low carb diets’ for wt loss x1yr (not for glucose control, read, wt loss only ). see diabetes.org (under publications) just fyi! I’m a CDE so I counsel many T2DM patients — I’ll tell you this will make the job 400% easier finally.
I’m glad to see that you’re getting into TYP — I’ve been investigating it since Sept (I wish that I found the light sooner!) and have found studies that back up nearly every strategy (I just haven’t had the time to look e-v-e-r-y-t-h-i-n-g up yet ;-/ ) and have personally seen it work in a secondary CAD individual (ie, cessation of stable angina). I’ve just had another guy tell me yesterday that his ED is ‘TWO TIMES better’ (translation: he stopped using Cialis). DO you see any changes such as this?
I was curious, how protein power affects CAC scores? I imagine it would improve it significantly but would it dramatically reduce CAC score 10-30% CAC annually as some people are achieving on TYP (conventional TYP *ha* in case you know what that is)?
Have you been on Oprah yet? How do we get both you and DR. D and MD on that show? (get Oz impeached?)
guess who is Vit D deficient (which triggered her hypothyroidism, I conjecture)? probably Oprah… wonderful Oz, think u missed that one…
THANK YOU IN ADVANCE FOR YOUR INSIGHT and humor! g
Hi g–
You wrote that you were glad to see that I’m getting into TYP…I suppose I would be glad, too, if I only knew what it was. And CAC scores. What are those?
Haven’t been asked to be on Oprah yet, and I’m not waiting by the phone.
Cheers–
MRE
There you go:
http://news.bbc.co.uk/2/hi/health/7180733.stm
“Statins for all diabetics urged
People with diabetes should receive cholesterol-busting drugs regardless of whether they have signs of heart disease, UK researchers say.
Statins cut the risk of heart attack, stroke and death in diabetic people even in those with low cholesterol levels, analysis of 14 trials shows.
It means hundreds of thousands more people could benefit from treatment, the Lancet report said.
There are 2.5 million people diagnosed with diabetes in the UK.”
Jesus wept.
Bawled his eyes out more like.
Cheers–
MRE
Reminds me of my new favorite quote..There ae lies, damn lies and there are statistics”
Wow, no, certainly no controlled studies (aiee!). But more followups. I’ve hardly found anything. Do they just not want to know?
No, I don’t think they do.
In response to Janet,
I, too, get RSS comment feeds. It is the primary way in which I’m alerted to new comments, but also a primary way in which I’m alerted to new posts (by way of comments).
I completely agree that sometimes comments show up weeks, months, or even years after the original posts, yet they are worth reading (and even commenting on
).
Anyway, wouldn’t it be funny if anthropologists of the future lamented the lameness of Total Cholesterol and LDL particle size?
Of course, anthropologists of the future would need an adequate brain to do so… uh oh!
Darwin weeps. And Homo sapien sapien regresses ever more…
Or, the other scenario: the Darwinian one, suggests that the Ornishes shall become extinct, and the low carbers (the meek) inherit the Earth?
I’ll settle for just the Ornishes becoming extinct.
Cheers–
MRE
Hi,
You wrote earlier in response to Dr. Davis and his plaque reversal tome “Track Your Plaque”
‘Good to hear from you. I read your blog from time to time and read your book Track your Plaque over the holidays. I was already pretty much sold on the idea of calcium scores, but your book really convinced me of their merit.’
CAC scores are calcium scores on EBT/CT scan (calcium is pathognomic for plaque). What are your experiences and insights on plaque regression with Protein Power? I would imagine that the potential to reduce small dense LDL is there, but does it have any effects on Lp(a) or Homocysteinemia (as Track Your Plaque does)?
THANK YOU IN ADVANCE FOR YOUR TIME!
Much respect, g
Hi g–
I’ve not worked much on reducing calcium scores because when I left active practice these things were just getting started. I do know that a Protein Power style diet drastically reduces triglycerides and increases LDL particle size because I have measured those directly. And the increased saturated fat in such a diet markedly reduces Lp(a), another phenomenon I’ve seen first hand. The work on homocysteine was also just becoming known – at least to me – when I stopped practicing, and I didn’t have enough patients whom I had checked homocysteine levels on to really get a feel for whether the diet worked for that as well. I would assume that the program as we administered it would have worked because the patients got plenty of vitamin B12 from the diet and plenty of folic acid and vitamin B6 from both the diet and additional supplements.
Cheers–
MRE
Hi,
Today, we had a lecture by one ‘eminent’ doctor (who heads the diabetes treatment division in a big hospital at Bangalore-India) on prevention of diabetes through diet and exercise. He appears to have published a lot. When I asked him about low carbing, he had the guts to say that it is irrational and there is no published evidence showing that it works. When I mentioned about my lab values (after an year of LC, that too falling off the wagon every three weeks-for two weeks) the only thing he pointed out was that my Triglycerides are high due to low carbing. I had got it checked two years ago and it was 175. While I know that he was bluffing through his hat (since I have personally read many papers on LC benefits-thanks to your books and blogs) my high! TG and VLDL put me to a great disadvantage in front of the gathering which did not want to believe me anyway. Am I doing something wrong to have those TG numbers?
My wife is in US (NJ) since one week and we (2 kids with me) will be joining her in March hopefully by the time the 6 Week cure.. gets out. Could we be fortunate to get your signatures on our copies?
My lab work:
HBA1C- Jan 2008: 8.5, Jul 2008: 6.9 and Jan 2009: 6.5. I am on 1000 mg Metformin for a year
Lipids (Jan 09)- TC 189, TG 220, HDL 41, LDL 104, VLDL 44
Could you please suggest something for staying on LC continuously? I am doing it typically for 3weeks – 2weeks of mindless eating – 3 weeks LC again… pattern.
Regards,
Ram
The ‘eminent’ doctor is an idiot if he thinks your triglycerides are high because of low-carbing. Triglycerides always fall on low-carb diets. I suspect your triglycerides are high because of the two weeks of backsliding you do after every three weeks of low-carbing. I’m planning a post soon on how you can maybe prevent that.