What am I missing here? Has it not been proven that Statin + Niacin combo is like 90% affective in stopping plaque progression in its tracks? Why does that not say that LDL reduction AND particle size reduction,(Niacin for LP(a),works best? Its not just LDL, I developed heart disease with a 90-100 LDL before my Dr discovered  high LP (a). Treated with 10mg statin,1500 Niacin, diet,I am at a30/30 count. OVER&OUT

Let's just summarise. First there was Keys with his total cholesterol. This turned out to be garbage. Then there was LDL vs HDL. But LDL is calculated and, as we know from this site, tells us nothing about anything. Then we have LDL particle size. Small dense is bad, big fluffy is good, noting that big fluffy contains lots of cholesterol per particle and can increase your calculated, or even absolute, LDL. Two factors, most studies use calculated LDL. The bin is there, file promptly.

The second is that something controls your LDL particle size. How, on a practical basis, does Dr Davis control LDL size and density? No wheat and no sugar. Does wheat and sugar elimination alter anything in the body? Wheat contains both an insulin mimetic and two insulin potentiators, plus starches and sugars both increase blood insulin levels per se. Perhaps there is a message here. It's been known for decades that insulin drives the proliferation of the arterial media we call arteriosclerosis.

If insulin also controls LDL particle size (I have no information on this, but I'm willing to bet it does) then Yudkin and Stout are correct, Keys is wrong and the cholesterol hypothesis, what remains of it, describes the effects of insulin on blood lipids. While insulin and glucose do the damage to the arteries.

Just a cholesterol skeptic view.

Peter

Statins are anti-inflammatory, antioxidant, anti-proliferative and probably anti other things too. Unfortunately they drop cholesterol levels (in humans anyway). Zetia, like torcetrapib and clofibrate, does the cholesterol dropping thing without the anti everything else that statins bring along. No wonder they killed so many people in the clinical trials. Clofibrate. Torcetrapib.

If a drug company develops a drug which converts small dense LDL to light fluffy LDL without affecting insulin sensitivity or glucose, I predict it will go the way of clofibrate and torcetrapib. There's the bin.

I especially find it interesting that, among the so-called pleiotropic, or non-lipid, effects of statin drugs is a modest rise in 25-OH-vitamin D3 levels.

I think this just once again shows that statins DO reduce heart disease but NOT because of the reduction in LDL. I'm always amazed at the Dr. who say you don't need to be on a statin your LDL is fine. Statins have been proven to reduce death rates in cardiovascular disease by 30 to 40% and yes with niacin by 90%!!!!!!!! Anybody worried about heart disease should be taking them. And save me the "side effects" alarm of statins that is so over blown. The fact is we invented a drug to reduce LDL, it does that but thats not why it reduces heart attacks and we're still not sure why they do. We accidently created a great class of drugs.

I remember in Taubes reading that small LDL are the result of particles being formed in a high-triglyceride environment--if so there is a more direct link to diet than through insulin.

About the merits of statins, can't we at least say that through reducing the number of all LDL particles and hence the number of small particles arteries are protected?

Keith

The drug company slanted this study so that they'd get a wonderful result, that they didn't and the lengths that they went to hide or misrepresent the data that came out of the study has to make you suspicious of what ELSE they have learned.

Did you catch that they also suppressed other study results showing liver damage from Zetia?

Also, did you catch the BMJ story today about the calcium supplementation trial that lowered LDL raised HDL and increased cardiac and stroke events in older women?

While that too isn't a death blow to the LDL hypothesis, it certainly doesn't bolster it.

Peter,

Good post; you have an impressive grasp of the literature on this!  I have a question for you, though:  Besides the epidemiology (which I know you don't buy), aren't there still tons of animal studies linking atherosclerosis to dietary saturated fat?  In fact, to promote atherogenesis in lab animals so they can study it, don't they feed them a diet rich in palmitic, stearic, myristic and lauric acids from animal and tropical plant fats, which works predictably?

Drug companies are actually scrutinized fairly closely, though plenty of shenanigans still go on.

What scares me even more is what may have been going on BEFORE the intensified scrutiny began a few years ago.

Nowadays, the return on investment for treatment of chronic diseases like cholesterol, osteoporosis, and hypertension are so substantial that it is causing them to see a blur between right and wrong.

Yes. I believe that the evidence for that effect of statin drugs is quite confident.

When I question the Lipid Hypothesis, what I really mean is that I question the wisdom of the simple "high cholesterol means more atherosclerosis" philosophy, a belief that is clearly oversimplified, though it contains a germ of truth.

For anonymous,

Of course statins reduce cardiac mortality and obviously it's nothing to do with LDL cholesterol lowering. But before you pop one on the off chance (they are available OTC in the UK) go very carefully through this paper.

You need the full text, the abstract tells you nothing, so here's a summary:

There were 2913 patients in the placebo group. A total of 306 died during their 3 years of not taking a statin. That is 10.5% died. In the treatment group there were 2891 patients and 298 died, that's 10.3%. Bear in mind that these were high risk cardiovascular patients, the sort for whom statin therapy is supposed to be effective in saving lives.

There was undoubtedly a significant improvement in cardiac mortality WITHOUT improvement in overall mortality. To sum up the PROSPER trial, you can have the cause of death changed from heart attack to cancer, but not the date on the death certificate. You choose. Perhaps you're too young to be in the PROSPER trial, but live long enough and you won't be!

PS if you EVER see a statin trial without the overall mortality figures, just assume there was no benefit or worse. If there is even a miniscule benefit it will be broadcast far and wide.

Keith,

Thanks for the pointer. Obviously high triglycerides are a classic marker of hyperinsulinaemia and insulin resistance. I'll follow that one when I get that far in to Taubes' book. Seems it's looking good for Yudkin.

bad_crc,

Yes, there are thousands of papers like that. They usually use D12451 or something like it. High fat alright, 45% calories from lard. As the rest is? A bit of corn starch, a mass of maltodextrin and an even bigger mass of sucrose!!!!! But of course it's the lard that kills....

Whereas using a real high fat diet you get this paper. I would suggest the 60% of calories from fat us a little low for a rodent. Choosing for themselves they can go to around 80%, get plump but don't develop insulin resistance.

Peter

My understanding is that studies show that statins are effective in reducing heart attacks ONLY in people who have already HAD heart attacks. Not in the general population.

This would confirm the growing suspicion that statins work by limiting the inflammation associated with heart disease. Not through their effect on lipids.

To get back to Zetia/Vytorin, what Dr. Nissen pointed to, which IS in my mind worth noting, was that while the variation in individual endpoints did not rise to statistical significance every single endpoint measured went in the wrong direction. That argues against random effects in my mind.

Beyond that, we know that in most people heart disease develops over a longer period than that spanned by this study, which only lasted 2 years. If all these parameters measured were trending negatively at 2 years, what happens at 5? Or 10? This is one of those drugs that once they put on on it, you take them forever. So the 5 or 10 year result could be devastating if this turns out to be a significant finding.

My suggestion would be continue testing this drug in small studies involving people who are very well informed of the risks, but end the writing of the current 1 million prescriptions a month. That's a LOT of guinea pigs, and if there turned out to be an accelerating pace of problems with it, a lot of people could die unnecessarily.

Statins reduce the number of LDL particles, which is very poorly represented by the conventional (Friedwald)calculated LDL cholesterol.

More importantly, when someone with heterozygous hypercholesterolemia (as in this Vytorin study) has a high number of SMALL LDL particles, then statin drugs, in my view, do provide benefit. But a superior effect would be to specifically reduce the number of small LDL particles, best accomplished with such strategies as elimination of wheat, weight loss via low carbohydrate diet, fish oil, vitamin D, and niacin.

This raises the question of how well the two groups in this study were matched for the number of small LDL particles. To my knowledge, this was not measured.

Let me also remind everybody that the measure obtained and used for comparison was carotid IMT, not carotid plaque.

I'm certain I'm not alone in feeling bewildered that such a dominant theory of the disease could turn out to have been so wrong for so long at such great cost in lives and treasure.

Just as a question of historical interest, how far back in the history of science do we have to look to find this kind of reversal of understanding of what the facts are with such broad and great consequence?

Hi, WC--

I'm not sure, but it's not the first time.  

Is the earth still flat?

Hi Dr. D.

I was thinking of Galileo also and his remarkable discovery that the earth orbits the sun.

But then I thought "surely we don't have to go that far back do we to get to such a broad and consequential paradigm shift?"

Maybe we do.

Could zetia be interfering with the absorption  of simvastatin?

Hi wccaguy,

You may enjoy this discussion article from PLoS. The authors intend it to be provocative, put it does pose the question "on which day did medicine stop making mistakes?"

Peter

In response to Jenny, not all studies on reducing heart attack death havwe been done on people who already had a heart attack. The reduction of 30 to 40% is whether you've had one or not.

Our saturated fat question keeps coming up, but the current common wisdom is that saturated fats are "neutral" in the sense that they raise both LDL and HDL. But do we know what they do to the number of small particles? Of course, if LDL is raised by making particles fluffy then saturated fats are clearly protective.

Keith

Hi, Richard-
No, there was indeed a substantial further drop in LDL with Vytorin over simvastatin.

There is a very modest shift from small to large LDL.

Zetia dropped my very high, inherited LDL to normal, BUT I afer a couple months on Zetia my post-menopausal body stopped making estrogen--my gynecologist remarked on it.  

I also started having a problem with persistent visual afterimages which the ophthalmologist said might also be from having too little cholesterol.

Both problems went away when I stopped the Zetia. I have very high LDL but I also have the "longevity" cholesterol gene which makes for big fluffy LDL as well as very low Apo(b). My doctors--including the cardiologist I saw--are ignorant about the implications of both findings and just obsess about the high LDL.

Since naturally produced estrogen seems to be protective for heart disease, I wonder if some people with inherited high LDL are like me have the large fluffy LDL molecules which give a deceptively high LDL value on tests. For them lowering it with Zetia drops LDL TOO low, so that the body doesn't have the cholesterol it needs for important functions, like making the naturally produced female hormones that may be protective against heart disease.

Hi, Jenny-
Keep in mind that conventional LDL is a flagrantly inaccurate number. In my experience, LDL of 150 when accurately measured (we use the NMR LDL particle number as the "gold standard"), the true number is between 80 and 270 mg/dl.

In my view, conventional LDL is a silly number. It is also the basis of a $23 billion (annual revenue) industry.

In Dec 05 I had a heart scan score of 145.  I went from 10 mg of Lipitor to 80mg of Vytorin and 1000 Niacin, 1 fish oil.  At that time my particle number was 1325 and small particle # 977.  A year later it went to 1503/1277.

In Nov 07 my heart scan went to 291. I then went to 2000 mg of Niacin and 150 COQ10,4 fish oil, 500 mg C, Vitamin D.

My new liposcience profile taken Dec 27 07 shows small particle down to 249 and particle number down to 279.

I dont know why my plaque increased so much but the new lipo profile is impressive in reduction.

Is there anything here that seems weird or is it just the plaque grew fast and is likely now under control with the much improved scores?  All other factors on the profile were great and my Vitamin D is very good and CRP excellent too.  My homosistine was 15.7 is the only thing a bit high.

Thanks!!

Sorry, but I do not assess entire programs on this blog.

I would invite you to participate in the conversations in the Track Your Plaque Forum for detailed discussions like this. There is also a free report on "10 steps to take if your heart scan score increases" on the www.trackyourplaque.com website.

I would not automatically conclude that Zetia causes carotid plaque. This is absurd. And I am definitely not one to come to the rescue of a drug or drug manufacturer. I am simply after understanding and truth.

Probably probably the most helpful in addition to up-to-date info I came across on this topic. I am positive fortunate that I noticed your article by chance. I¡¯ll be subscribing to your individual rss feed in order that I can have the most recent posts. Take pleasure in all the pieces here.

Probably probably the most helpful in addition to up-to-date info I came across on this topic. I am positive fortunate that I noticed your article by chance. I¡¯ll be subscribing to your individual rss feed in order that I can have the most recent posts. Take pleasure in all the pieces here.

I could see this might be a problem if gut health was compromised; exogenous AGEs would then have a pathway to get into our tissues.  Assuming someone is on a low carbohydrate paleolithic style diet, what evidence is there that the exogenous AGEs do anything other than merely pass through the digestive system?

Hi August, I echo the same question. Is there any research on exogenous AGE's absorbing in to our bodies?

Dr. Davis,

Are palm oils/hydrogenated oils a significant source of AGE's like butter?

What about clarified butter (ghee)?

Dr. Davis, now you're delving into the unknown with your suggestion of an anti-AGE diet. You don't know. You're suggesting we eat that diet but you haven't any data to support such a suggestion. Don't do like they did with saturated fat. Think of the alternative we adopted then that brought us here. Think of the alternative we will adopt now that will bring us who knows where.

If the advice of the day is to avoid AGEs in food, what kind of food will we eat then? Since meat contains a boatload of AGEs, that's out but what will replace it, soy? See how your advice is already turning on itself?

Stick to what works on the TYP program as a good doctor should and leave the speculation to the speculators.

Martin, there have been numerous studies connecting the association of AGEs with various health issues. There is nothing novel or or new about this.

Avoiding AGEs doesn't mean you can't eat meat. All you have to do is eat good fresh meat and don't over cook it until it is well done or overbrowned. If you like your meat chared and well done, then you may have to make a sacrifice.

Yes even properly prepared meat has some AGEs in it. But no one food or diet is perfect. You just do the best you can and try to avoid the big mistakes. Just my opinion for what it is worth.

Doc - with regards to exogenous AGEs, it sounds like this could be the new cholesterol-is-bad-for-you theory. My apologies if I have overlooked something in your post, but I don't see any logical argument leading to the conclusion that exogenous AGEs affect your health. Your previous post on butter also makes you sound like an alarmist. Of course, if you have a diet coming up, this is understandable.

what do stomach acid and bile do to ingested ages?? ...and the rest of the digestive process? sss

One of the primary AGE components of milk products is pyrraline:

Glycation in food and metabolic transit of dietary
AGEs

Here are some quotes from this study:

"Given the data for pyrraline excretion, it
can be concluded that dietary pyrraline is nearly completely
released and resorbed during digestion, followed by rapid
elimination via the kidneys, thus leading to nearly complete
recovery of dietary pyrraline in the urine. This indicates that,
in contrast with Amadori products, of which only up to 5%
are recovered in the urine [24,25], pyrraline obviously is not
metabolized within the body."

"Above all, however,
it has to be realized that the term ‘AGE’ comprises a large
number of individual amino acid derivatives, of which only a
minority have been identified and quantified either in foods
or in vivo."

Now that everyone is speculating in the last two posts, is it possible that some AGEs are much more harmful than others? (As the previous study indicates?)

Are we distinguishing the types of AGEs when we measure them? (Or are we lumping them all together like what was done with cholesterol?)

Are food derived AGEs eaten as part of a meal less harmful then analogues produced in a lab and fed in isolation? (Like most AGE studies I've read?)

Again, if butter is as bad as these measurements indicate, why hasn't it been identified epidemiologically as such a bad food? Those with the highest butter consumption tend to be the healthiest (although I suppose because it displaces margarine).

I can understand why all AGEs might be harmful to someone with compromised kidneys, but I agree with Martin Levac that we're really delving into the unknown.

"Martin, there have been numerous studies connecting the association of AGEs with various health issues. There is nothing novel or or new about this."

Please give us a study. This sort of broad statement is hard to counter argue otherwise!

I'm not really convinced AGEs you eat are a problem. But if you're enamored of low temperature cooking, looking into Sous Vide cooking. It yields delicious results by cooking at much lower temperatures than normal.

Speaking of endogenous AGEs, caused by high blood glucose levels, here is an interesting factoid - blood glucose levels in birds are very high yet their HbA1c levels are low:

http://healthcorrelator.blogspot.com/2010/10/blood-glucose-levels-in-birds-are-high.html

There are a few possible reasons for this. One of the most interesting mechanisms is vitamin C synthesis. Not only is vitamin C a powerful antioxidant, but it also has the ability to reversibly bind to proteins at the sites where glycation would occur.

All humans cook food and have done so for thousands of years. This is natural for us. If you've ever cooked meat on a camp fire, you know that the some of the meat becomes very crisp. Paleo people didn't have temperature gauges so I'm very sure there were plenty of exogenous AGE's. In fact, I would suggest, since these pieces of foods tend to taste very good to humans that they are an important piece of our nutrition not the opposite.

"High blood glucose (any blood sugar above 100 mg/dl) will permit glycation"

I would love to know some research that backs this claim. I have seen it numerous times but have not been able to find any research that specifically deals with it.  Also, just guessing, but I would bet that damage occurs at considerably lower blood sugar levels for those eating a conventional, nutrient sparse diet as compared to those replete w/ vitamins, minerals, phyto-nutrients etc who eat a diet containing very large amounts of "real food" particularly non-starchy vegetables

Has anyone ever taken an A1C of a grain-feed cow?  Maybe that high AGE butter was from a diabetic cow!

I don't know if AGEs are harmful either, but a pressure cooker is great for low-temperature cooking. It's also much faster and keeps in the juices better than oven roasting.

Re: sausage (from the last post), the list of ingredients from the chorizo I eat is pork, water, salt, paprika, spices and garlic powder. "No nitrates, MSG, preservatives, sugar or soy," reads the label. I don't understand why this is worse than any other meat.

Sausage could be a problem because,

1)The meat is ground up so more of the surface area was exposed to oxygen. More of the meat is oxidized.

2)Sausage unlike unground cuts of meat must be cooked through because of bacterial contamination. The more you cook meat the more you get AGEs.

3)Some sausages as with hot dogs are pre cooked. Then you cook them again. This should also increase AGEs.

There are indeed studies that 1) measure serum levels of AGEs in humans after consumption of exogenous sources, and 2) relate AGE levels to biologic effect, e.g., endothelial response.

There is no question that the exogenous AGE conversation requires more exploration. I've followed this conversation for some years, but I believe it is gathering real momentum and looks and feels like a genuinely meaningful issue.

We need more info, no doubt. The notion of endogenous AGEs already fits quite nicely into our observations of the benefits of a low-carb diet. But  exogenous AGEs have potential for taking us one step farther in crafting an ideal diet. Recall that the "Paleo" approach is one reconstructed to mimic ancient behaviors, not necessarily one to achieve a new set of modern goals, such as reversal of coronary disease or osteoporosis.

It's clear that in the US we eat lots of carbs and get lots of heart disease and diabetes.  But there are lots of traditional cultures that eat even higher percentages of carbs (cassava, beans, rice and others) but that don't get those diseases.  How does the AGE theory explain that?

Dear Dr Davis,

I know your opinion against butter, but disagree, based on a lifelong experience, as a skin chronic healed by milkfats and (land)animal fats.

For the first 40 years of my life I was never free of allergic reactions and imflammated skin symptoms. Raw food helped not, vegetables and salads helped not, and the official healthy lifestyle helped not either. 10 years ago, when the stsart of Zonish lowcarb (much like your style) finally helped me incredibly much... Yet my skin has healed fully only after I switched to very, very buttery and egg-yolky diet close to Jan Kwasniewski.

I live far up North, but have no symptoms of vitamin D deficiency, in spite of not eating the pills and not having much sun for the better part of the year. Furthermore, I cannot eat fish, and do no longer supplement with fish oil either, due to problems induced by it. Yet my skin has never been as good as now, fully without irritation or other symptoms. And unlike my frends and colleagues, I no longer seem to catch seasonal colds, either.

So far the only thing I can blame for the last few years of well-being is increased use of milkfat and non-muscle parts of animals (fat, marrow, liver and skin collagen). Of these the milkfats make up a major part of the daily calories, often more than 50 E%.

I'm interested to hear your thought on possible causes, which make this butter strategy work the best of all that we've ever tried; both for myself and for others in our family

With regards,
LeenaS

I am a Type 2 Diabetic with normal blood sugar who takes -0- drugs and -0- insulin.

I experienced tremendous benefits from going low carb primal. I won't detail them here but I have not been sick in 20 mos.

This summer I performed a one week dairy fast (I'd been off milk for almost a year) and then added back butter.

Butter was very inflammatory. I no longer eat it. Clarified butter or Ghee and Cheese are not inflammatory and I eat it occasionally.

So for me, I agree with butter.

Anonymous, thanks for the info on sausage. I buy raw sausage and I'm careful to avoid over-cooking any meat, mostly because it gets like shoe leather.

Another question: is cream high in AGEs? Does the churning action required for butter contribute to oxidation or AGEs?

What's the consensus on carnosine ? I've read some articles claiming it helps with AGE factors.

Dr. Davis, it's fine to have data on a diet that contains AGEs, but where's the data on a diet that avoids AGEs? Where is the justification for adopting such a diet? Avoiding something leads to adopting something else. What will that be? You can't predict. Nobody can predict. This is the danger of advising to avoid something just like that was the danger of advising to avoid saturated fat and pretty much all animal fat altogether in one big swoop.

If we can't eat fat, we must eat sugar. There's no other alternative. If we can't eat meat, we must eat some other form of protein. What will that be, soy, wheat, any other grain, legumes? If we can't eat meat, we must eat some other form of those essential nutrients like B12 and EFAs. But where can we get such a high quality source of those nutrients but in animal flesh? The quick answer is nowhere.

When you advise to avoid AGEs without giving us a safety threshold, the safe course is to avoid all AGEs, not just a little bit. When you give a safety threshold, it doesn't matter because the substance has been declared bad entirely anyway so the safe course is the same.

We can see this with animal fat and pretty much any kind of fat. Fat is bad, so any fat is bad, so less fat is good or better, but no fat is best. That's how it works in spite of having some form of safety threshold we can abide by like say 10g of saturated fat per day maximum. Why is that? The safety threshold is declared as a maximum with no minimum.

So tell us Dr. Davis, what is the maximum and the minimum amount of AGEs you advise we eat? But more relevant to the discussion, how can we find out exactly how much AGEs is in the food we eat every day so that we can make an informed decision on exactly how much AGEs we eat every day? Is there a tool that will allow me to find that out? The point is that even if you give us a precise number on how much AGEs we can and cannot eat, we can't even control how much AGEs we eat. Accordingly, the best course of action is to avoid all AGEs and not just a little bit just to be safe because the contention is that lots of AGEs is worse than none.

With endogenous AGEs production due to high blood glucose and other simple sugars like fructose, the problem is much simpler. That's because this AGEs aspect of sugars is merely the last installment of How Sugars Kill Us Slowly. We already know that sugars kill us slowly and we already know just how much of it will do it and how long it will take and etc. But until you find out exactly how much exogenous AGEs we must avoid and exactly how much we can get away with and how to measure the AGEs in the food we eat, this problem will remain unresolved and unresolvable.

In other words, the best course of action with exogenous AGEs is to just ignore them outright. After all, we've been ignoring them outright for the past couple million years without so much trouble.

Bill,

Butter is high in AGEs? Wow - why? What about Ghee?

Do you know what the AGEs are in smoked meats like smoked trout?

Does the canning process increases ages as in canned wild caught salmon?

Hi, Fred-

I believe that smoked fish tend to be moderately high in exogenous AGEs.

One of the difficulties with quantification of AGEs in foods is we have limited data on the AGE content of various foods. It's not like grams fats or carbohydrates listed in plain sight on the label.

I find the AGE conversation a fascinating new potential insight into helping us decide how to best manage food choices, as well as food preparation.

As with all new ideas, it will cause upheaval in preconceived notions.

Given some of the previous blog posts, the largest preconceived notion might be yours toward butter. So, it's no big deal if you aren't up to the challenge of defending what you posted. That's okay. Trying to be coy about it, not so much.

Count me as a skeptic on this one.

Very good review on AGEs. Dr. Davis is 100% right to be concerned.

http://biomedgerontology.oxfordjournals.org/content/65A/9/963.full#ref-109

Chris Masterjohn has the skinny on AGEs in butter:

The Daily Lipid: Is Butter High in AGEs?

People are confusing exogeneous AGEs which are generally harmless compared to the dangerous endogenous AGEs.

Endogenous AGEs are created by proteins in our bodies reacting with reducing sugars.  Practically the only sources of dietary reducing sugars are fructose (table sugar, HFCS) and  cooked starches. The obvious solution is to eat far more meat and butter and drastically reduce carbohydrates.

Humans have been eating cooked food for 1.8 million years and are very well adapted to them. The novel foods in the human diet are large quantities of plant proteins, starches and sugars.

I'm surprised you think kale and spinach are so wonderful. Renowned toxicologist Dr Bruce Ames says that there are considerable amounts of natural toxins and carcinogens present in all food plants.
http://www.fortfreedom.org/n16.htm

Any potential benefits from eating kale is likely to be due to hormesis.

In fact there is absolutely nil direct scientific evidence that eating fruit and vegetable has any health benefits whatseover. The benefits of vegetables have only been found in a few poorly designed population studies. Any observed 'benefits' of eating vegetables are probably just due to confounding variables - people who eat vegetables smoke less, drink less alcohol, are more active and eat less sugar and junk foods.

Gary Taubes is skeptical of the claims about exogenous AGES

http://www.healthcentral.com/diabetes/c/36758/17729/gary-taubes

Hi Apra,

In 'The Diet Delusion' Gary Taubes says that the natural diet of humans is almost purely carnivore with a few berries. Taubes studied physics at Harvard and aerospace engineering at Stanford before becoming a journalist. Because he was properly trained in using rigorous scientific methods he can readily see the flaws in nutrition research.

I've read the sole paper that lists butter as a high-AGE food: "Advanced Glycoxidation End Products in Commonly Consumed Foods" (2004, Journal of the American Dietetic Association, via Google Scholar cache).

The data is in Table 1, which refers to "foods prepared by standard cooking methods" (these include frying), but the table says nothing specific about how the butter was processed. I am willing to bet that the butter in question had been treated at high temperature (maybe used in frying).

Consider these values:

Milk, cow, whole .... 0.05 kU/mL
Butter .............. 265 kU/g

Expecting high AGEs in uncooked butter -- over 5000 times the level in milk! -- would make little sense.

Would you consider revising your post in light of this?

The data table lists butter as 100 gm serving, or over 3 ounces (23,000 - 26,000).  In the serving size database, the amount of AGEs normalize a bit, at 1100 - 1300.  I wish they had done organic vs commercial butters, but maybe next time we can see that data.  No surprise on pan fried bacon at 91,577 for 3 ounces and 11,905 for the serving size (2 slices is the norm).   As with all foods, moderation.  And thank you for your blog - it is very informative!

Your blog entry appears to have been truncated.

How are Stan's blood sugars?

Sounds like Stan is screwed. Of course, there may be other factors mitigating his lipid pattern because he avoids the neolithic agents. Stan would be more susceptible to heart disease than ollie on the SAD, but not when they both have good diets?

Is it possible that a different diet might work for Stan? I don't know what it would be, I just wonder if it's possible.

So Ollie and Stan BOTH show substantial improvement on their LC diets.

The difference between them may well be due to genetics, but where is the evidence that Stan needs to avoid saturated fat?

Did you advise Stan to increase sat fat and then watch his sdLDL get worse?

If they accomplished this with "oils" at the expense of saturated fats (oils are liquid due to the paucity of saturated fats in them), then it looks like they both have a saturated fat deficiency, and one could speculate that Stan is even more deficient than Ollie.

Swap out the nasty oils for more butter and beef fat and coconut fat and maybe Ollie will have sdLDL of 0 (like I do on 35% of calories from sat fat) and Stan will improve even further.

Hi Dr Davis,

You describe a fascinating scenario.

Ollie has clearly lost weight. He has lost 55 lb in 6 months. That is nearly 10 pounds of "lard-equivalents" each month. This has not evaporated. It is exactly what he has been running his metabolism on. Whatever nuts and vegetables he has eaten can have been nothing in comparison to the 4 times half pound blocks of lard he has "eaten" from his own adipose tissue, every week. Result: Metabolism runs on lard and sdLDL plummet.

Stan has lost minimal weight so has run his metabolism on  his food alone. If this is low in lard he may well be running his metabolism on vegetable derived carbohydrate and nut derived omega 6 PUFA. It's possible he has NOT been eating 2lb of lard a week in his diet, because obviously this might raise his LDL. So he has NOT used lard to fuel his metabolism, he has used nuts and vegetables when Ollie has used lard from his adipose stores.

Before I would blame genetics I would get rid of the nuts and unlimited vegetables from Stan's diet and replace them with exactly the same the adipose tissue derived fuel that Ollie was using. If Stan cannot spare it from his butt (he certainly cannot at BMI 21), it's going to have to go on his plate. Two pounds of lard a week.

Then compare sdLDL values, when you have similar metabolic situations... Until then Stan just has nut and vegetable poisoning showing as sdLDL.

There do not have to be any genetics involved. There might be, but let's keep it simple for the time being... Ollie is on lard while he is losing weight. Mimic that.

Peter

Stan did improve.  Maybe he will improve further, the longer on diet?

I think it's somewhat telling that you advise your patients to eat "oils."  What kind of "oils" are they eating?  Why are your patients eating unlimited nuts?

Until you get off the Omega-6-loaded "heatlhy" polyunstaturated fats bandwagon, it's hard to take your clinical observations on "fats" very seriously.

Dr. Davis,

Help me understand the part about not eliminating meats or fats.  First, here is my blood work 15 days apart.

Total cholesterol 295 - 15 days later 156
LDL 200 - 15 days later 102
HDL   46 - 15 days later  32  (have added 1500mg of niacin since then)
Triglycerides   242 - 15 days later 109
VLDL  49 - 15 days later 22
Vitamin D was 28 – 15 days later it’s 56 (using 10,000 of Carlson’s D3)

FYI my heart scan was 899 (54 year old male)

I started on all the main nutrients you recommend here plus a few.  I dropped dairy like a hot potato including 6 or more ounces of cheese a day.  During those 15 days I ate only plant based foods (have since added some salmon and egg whites)

The only oil I use now (sparingly) is olive.  I have a couple of gallons of coconut oil I assumed would have to be tossed sooner or later.

Guess you could say I became fat paranoid and downright phobic about any saturated fat.

Am I understanding I could add back Grass-fed beef (omega-3) pastured chicken and Omega-3 whole eggs?  Coconut oil?   If so, is there some safe percentage of a person’s diet to include those proteins/fats?

By the way, my doctor wouldn’t let me out of his office without a copy of your book.  He’s one in a million as are you!

Steve

Doc, would you say family history could be a clue towards small-particle tendencies?   I have zero family members with heart issues yet I was given pause by your recent post on saturated fats having a disproportionate affect on these genetically challenged folks.  I ask because I eat a ton of rib eyes and bacon.

I have indeed had many people with presumed "genetic small LDL" load their diets with oils and fats with only minor improvement. Loaded with saturated fat, however, and there seems to be deterioration.

I know this flies in the face of the "saturated fat is great" dogma, but I don't make this stuff up. Just as I don't make up the deterioration of postprandial triglycerides and chylomicron remnant effect when saturated fats are loaded heavily in the diet.

The persistence of small LDL is also long-term, i.e., it persists for years despite continuing efforts.

Oils = olive oil, flaxseed oil, canola oil (yes, yes, I know), avocado, almond, oils from raw nuts and meats.

No polyunsaturates here. You've go the wrong guy.

On Doctor's orders, Ollie did indeed lose a massive amount of weight.
http://www.youtube.com/watch?v=IYAeYj8-G4w

@Peter, fascinating...eat lard when slim in attempt to reduce sdLDL.  Doc D thanks for 'splaining 'genetic' tendency to sdLDL & why numbers not reduced on sat fat & only reduced mildly on mono sats.  Great info guys!

"Oils = olive oil, flaxseed oil, canola oil (yes, yes, I know), avocado, almond, oils from raw nuts and meats.

No polyunsaturates here. You've got the wrong guy."

But Dr. Davis, those all chock full of PUFAs

Linseed oil (flax oil) is 71% LA and ALA

Rapeseed oil (Canola oil) is 33%  LA and ALA

Almond oil is about 25% PUFA

Even olive oil can be up to 20% PUFA

And all of these are mostly Linoleic acid.

All best left as industrial lubricants and paint additives rather than eaten.

So, you have a fat guy, who has been living on (his own) saturated animal fats, and he has improved a lot.

Then you have a skinny guy, who has been living on "healthy vegetable fats" with surprisingly much LA in them, and he has not improved that much.

So, it seems to tell that without saturated fats LDL improvement is much harder in LC, to say it kindly.

And it sounds as if butter and saturated animal fats would be advantageous for the latter guy, too. Have they ever tried this, under your coucelling?

With regards,
LeenaS

Dr. Davis,

While body composition certainly isn't a prerequisite for being part of a classic comedy team, I couldn't help but notice that Stan had the makings of a skinny-fat bean pole checking in at 5' 10" and only 148 pounds. Those stats make him sound like a diehard distance runner or a chain smoker.

While it was clearly just for illustrative purposes, I couldn't help but think that, if "Stan" exercises at all, he must not be exerting himself very much. I'm not advocating that every older gentleman suddenly attempt to impersonate Mr. Olympia, but I have to wonder seeing such a lightweight. That's not to say that I think sufficiently intense exercise would remove the problem that is genetically-based small LDL, but it is enough to make me raise an eyebrow when I see that type of weight for a male listed as 5'10".

Dr. Davis,

Would a take-home point simply be to let the numbers from proper testing be the guide versus what we "think" is right based upon generally-sound dietary advice that may apply to many, but not all, situations?

Bill Lindvall

Olive oil is monounsaturated but flaxseed oil, canola oil, avocado oil, almond oil, and oils from raw nuts are all polyunsaturated oils!  Yes, flax oil is omega 3 and canola has more omega 3 than omega 6, but both omega 3 and omega 6 are polyunsaturated.

Do you know how much saturated fat was eaten?

Maybe too much mono-unsaturates?

In another post, you said that blood sugars parallel small LDL.  Do Stan's blood sugars follow the pattern you would predict for someone with a lot of small LDL?

http://heartscanblog.blogspot.com/2009/12/to-track-small-ldl-track-blood-sugar.html

No polyunsaturates?
Because olive, flax, canola oils, nuts have no polyunsaturated fats?
I found something different.
Even avocados have 10 % PUFAs.
http://curezone.com/foods/fatspercent.asp

So what about epigenetics? Any way to modify this unknown gene or set of genes?  Pomegranate, etc?

Please guys, find so other monounsaturated (MUFA) fats with less PUFA..

I eat almonds, walnuts, extra virgin olive oil as fats and my diet is low in Omega 6, 10% or 20% of Omega 6 PUFA is nothing compared with 70 or 85% of MUFA.

My experience taking a lot of saturated fats with low carbs is bad, I prefer a diet high in MUFA and low carb.

Maybe the mental stress of having to worry about what to eat is a factor.
I do find my self stressing about that often and wonder if just enjoying the food would give me a longer nicer life quality which is in then end what matters.

Which reminds me somehting I have never read in this blog is about cortisol.
Have you ever tracked cortisol levels in your patients?

A yea ago, i went off niacin and zocor due to elevated liver enzymes.  Before I restarted niacin, an NMR lipoprotein analysis showed:
LDL particle number - 2197
Small LDL-P - 1614
LDL Particle size - 20.3
Saturated fat (% of calories) - 21%

Six months later, after radically increasing the amount of coconut oil I consumed, the results were:
LDL particle number - 896
Small LDL-P - 466
LDL Particle size - 21.6
Saturated fat (% of calories) - 45%


Five months after that:
LDL particle number - 946
Small LDL-P - 120
LDL Particle size - 21.1
Saturated fat (% of calories) - 52%

Carbohydrate consumption has held fairly steady at 10% of calories.

I agree 100% with these comments.  Not a drop of dogma in them; pure science.  Yes, omega-6 is evil; avoid foods with any of it. No nuts, no seeds. Soy -- dangerous.  Milk -- cavemen didn't drink it and it's possibly dangerous too.  Vegetables -- no, no, goodness no, they're mostly made of dreaded carbohydrates, have little fat, an fiber isn't important!  Saturated fat?  I don't know about you, but I'm too scared to go hog wild on it.

I know, I know!  Let's not eat at all.  That would drive small LDL to 0!  That would end heart disease -- and everything else -- in a flash.

Or, just maybe, we could be moderate and sensible.  Take some fish oil to balance whatever omega-6 you get in the olive & canola oils and in nuts.  Eat some, but not too much, animal protein, and mostly fish and lean meats at that, because saturated fat isn't out of the woods yet. (Just because saturated fat's risks have been over-hyped doesn't mean that we should eat all meat all the time, because the evidence is not in yet that saturated fat is a panacea.) Eat some, but not tons, of fruits, because they have antioxidants.  And for goodness sake, eat your vegatables -- lots of them, and all kinds of them -- because your mother was right to make sit at the table until you finished them.

"I couldn't help but notice that Stan had the makings of a skinny-fat bean pole checking in at 5' 10" and only 148 pounds. Those stats make him sound like a diehard distance runner or a chain smoker."

I'm 5'10" and under 145 lbs., and I'm neither.

Kurt G & Lightcan,

I think when Dr. D said no "No polyunsaturates here. You've got the wrong guy."...he probably meant to say "No (high omega 6) polyunsaturates here.".

Lastly...I have a question for Dr. Davis:

Dr. D., is this "genetic small LDL" the same as when you talked about people with ApoE4 in your November 17, 2008 post? If so, do you think it would be helpful to test ApoE before experimenting with diet??

Thanx!

John M.

Aren't most nuts full of N-6 PUFA?

Hi Dr. Davis,

and what is happend with the triclycerides of Stan. Are they high too?

This is usually when the good doctor stops answering comments.

Come on, Dr. D, prove me wrong!

You have really great taste on catch article titles, even when you are not interested in this topic you push to read it

I'm going to steal a page from T. Colin Campbell here (yechh!)

Dr Davis, you say that

"I have indeed had many people with presumed "genetic small LDL" load their diets with oils and fats with only minor improvement. Loaded with saturated fat, however, and there seems to be deterioration."

Campbell makes the contention that studies showing that low saturated fat intake is beneficial (never mind whether they actually exist or not, just for the sake of argument here) might actually have nothing to do with the type of fat in the diet, and everything to do with the protein which accompanies the fat; most animal fat in our culture comes attached to meat (protein.)

Adding plant fats and oils to the diet, including nuts, would tend to increase total percentage fat in the diet at the expense of both carbohydrate and protein. Adding animal fat, attached to meat might increase total protein percentage even as it increases total saturated fat.

Understand, I'm not saying "protein bad," I guess I'm just echoing Peter, really, Stan may be trying to live off of a protein/fat mix that's too rich in protein, entirely aside from the whole issue of saturation.

Don't tell me no one picked up on the Laurel and Hardy reference! Brilliant!

Could all you saturated fat mafia people please stop polluting the comments section?

Maybe recommend Stan use only sat fats and no poly oils and then see if there is a change.

Drs. Davis and Harris,

Googlemaps indicate you two practice your medicinal arts about 154 miles away from each other.

May I respectfully suggest a summit meeting in Manitowoc to resolve these matters?

Flax oil, canola oil, any nut oil (except macadamia nut oil), and all of those nuts -- these are all rich with polyunsaturated fats. I never eat these oils, and my Lp(a) is 2, as last measured a few months ago.

I always recommend nuts as a very moderate snack because of their high PUFA content.  Macadamia nuts are the ONE exception, with a fatty acid profile similar to olive oil.  Basically, I never recommend any food with a PUFA content greater that 12 percent.  That means canola oil is right out!

Dr. Davis, perhaps try putting a few of these presumed "genetic small LDL" people on a real low PUFA diet for a while (with more coconut oil and butter--but no nuts during this period) and see if there's improvement.

I'd bet there is.  Nothing really to lose by giving this a shot.

If it works to your satisfaction, I'll donate $1000 to your Track-the-Plaque program, or a charity of your choice.

Some other features of the presumptive "genetic small LDL" pattern:

1) It occurs in the minority of people with small LDL, likely less than 20% of people who start with substantial small LDL.

2) It is associated with insulin resistance and a tendency towards diabetes

3) It can occur independent of ApoE genotype. However, if it occurs with ApoE2, it means a very potent carb-sensitivity/diabetic tendency.

4) The "floor" of 600 nmol/L can be broken. We've had success achieving really low body weight and inconsistently with several supplements, e.g., phosphatidylcholine.

This area is fascinating, though very poorly explored. "Genetic small LDL" is truly one of the problem areas in gaining control over heart disease risk.

I currently consume coconut oil and butter  I do not use any lard or pufas  I consume a moderate amount of almonds a day ( nine) and some ground almonds as a meal replacement about 10-20gs as a meal about two or three times a week

I eat avocados maybe twice a week  about two-three

I have started to show my abdominal muscles after two months where before I looked as if I were pregnant of about a 5 month pregnancy

I have dropped half a stone  My BP is controlled by a sartan

I consume a moderate amount of frozen blueberries and raspberries May be about 1 kg of each a month

or less

I am living on saturated fat and loving it

My body works better on it but then I have blood group B

You have to eat right for your blood type perhaps?

I would like to add support to Dr. Harris' hypothesis. LDL (no NMR in our country) and TG both rise on low carb, high sat fat diet. No weight problem ever. No high protein no high PUFA for me. Pre-diabetic fasting glucose (110-120). Only complication is I had my gallbladder removed (but my brother didn't). Will increase coconut oil and olive oil on account of double cream. Feel so good on low carb it can't be wrong. Also wonder if under healthy low carb diet LDL and TG have atherogenic effect (My calcium score is low)
In summary I think Dr. Davis is onto something but I would love to know if LDL status corresponded to increased calcium score in the said patients.

Choline deficiency can lessen hyperglycemia in rodents with fatty livers. Maybe the inconsistent effects of phosphatidylcholine have something to do with that?

To the person who mentioned the saturated-fat mafia; we have limited information going in here. Trying to guess at alternate explanations isn't the same as insisting that saturated fat is good in all situations for everybody, no matter what. Proper skepticism demands that we question even the most respected sources.

Dr. Davis, this recent article seems congruent with some of your observations:

http://jn.nutrition.org/cgi/content/abstract/jn.109.115964v1

To all these nutty omega-6 fatphobes - I eat lots of nuts of all sorts, probably 40% of calories, including... peanuts, which I am aware are a legume.  I have no small LDL, undetectable CRP, and lp(a) of 4, high hdl and low homocysteine, HbA1C of 5.2.

Dr. Davis,
You said "Some other features of the presumptive "genetic small LDL" pattern:

1) It occurs in the minority of people with small LDL, likely less than 20% of people who start with substantial small LDL."


So, based on a minority of people with small LDL, you are recommending the same diet to everyone?

Please don't misunderstand: I am NOT saying that saturated fat increases small LDL in most people.

What I am suggesting is that there is a genetic minority in which saturated fat increases small LDL. These people seem to be the unusually slender, high HDL, low triglycerides, yet diabetes-prone who show apparently intractable small LDL.

I don't know for a fact why this happens, but I speculate that it is a genetically-determined trait.

This pattern responds best to a high-protein, high-fat, very low-carbohydrate diet. But saturated fat is the exception in this group.

Hello Dr Davis

I am only persisting in this as the implications might be important.

I asked, "Did you advise Stan to increase sat fat and then watch his sdLDL get worse?"

You later said, "Loaded with saturated fat, however, and there seems to be deterioration."  and ..

"What I am suggesting is that there is a genetic minority in which saturated fat increases small LDL."

and...

"This pattern responds best to a high-protein, high-fat, very low-carbohydrate diet. But saturated fat is the exception in this group."

Can I assume when you say "seems to be deterioration" and "there is a suggestion that saturated fat increases small LDL" and "saturated fat is the exception" that this is based on the observation of  serially increased sdLDL NMR values after increasing only saturated fat intake in these 100 or so patients?

If this is what you have, serial NMRs that show increased sdLDL with increased saturated fat intake, why not say so explicitly?

Or is it just a reasoned (perhaps correct, perhaps not) guess of what would happen to sdLDL in those 100 or so who have this presumed genetic pattern of persistent sdLDL?

Dr. Davis wrote:

"I know this flies in the face of the 'saturated fat is great' dogma, but I don't make this stuff up."


The way that Peter described the scenario you presented, it seems to support the health benefits of saturated fat rather than deride them

Ollie is mainlining saturated fat from his gut.  Stan is not.  Ollie's sdLDL drops like a rock.  Stan's doesn't.  

It seems like if this phenomenon of high sdLDL specifically affects low BMI people, their lack of saturated fat intake, whether through their mouths or from their love handles, could be the culprit.

Dr. Harris,

I'm a fan of your blog, but I can't help but notice that you have completely ignored Dr. Harris's questions in this entry as well as the other recent entry about saturdated fat and LDL.  I find his questions to be pertinent.

I'm actually a little surprised no one's brought up this blog, that indicates polyunsaturate consumption over 4% of calories can be detrimental:

http://wholehealthsource.blogspot.com/2009/05/eicosanoids-and-ischemic-heart-diseas.html

Eh. Took me long enough to find. At any rate, 10-20% polyunsaturates, especially if they come from omega-6, is a huge amount for a human.

Imma going to go away and let you argue now.

Hear Hear throwing cows out of windows...  It blows the polyunsaturates out  of the window

I have the printout of the Rose et al Paper..

Corn oil increased the death rate

My family has a history of high colestral and plaque build-up in the blood.  Should I stay on my Lipator and stay on a low-carb diet ?  Your article brings up some red flags for me.  Maybe I should talk to my Doctor, but my low-carb friends tell me the doctor will tell me to get off the diet !  I would like some advice.

How did that happen? Is it possible? Different diet will work to Stan? I am curious about that. I will visit this blog again. I am hoping for an update.

Obviously another great blog about eating and living right, but at some point we have to take a step back and live.  Food avoidance and constant stressing about food seems it could negate any benefits of just eating a sensible, well balanced, moderately low carb diet.  

To me, all these nutrition blogs are fun to read at work. But have you ever noticed the incredible difference in opinion from one to the next?  I take all that with a large grain of salt, pun intended.

Oh my god, I ate a walnut, surely I will be in the cath lab tomorrow getting my LAD stented;)

You might not find yourself in the cath lab from eating the random 1/2 cup of oatmeal, but you might find yourself there from stressing about it too much.

Read all the blogs, use all the information to help guide you.  But don't get in line with the zombies and wander off the deep end too far.

Just a thought.

Here's a stumper. I just had my VAP done and the results surprised me. Some background: I'm not on any medication and never have been. Never had a weight problem, body fat below 20%. I exercise regularly (CrossFit 4x/week). Never smoked. Rarely drink. I eat mostly a primal diet w/plenty of grass-fed/organic/cage-free/wild-caught meat/fish and lots of fresh veggies. Some dairy, but only hormone and antibiotic free. Hardly any grains or processed foods. Low fasting blood sugar (76 as of two weeks ago.) Here are my VAP results:

Total cholesterol: 200
HDL : 79
LDL: 106
VLDL: 14
Lp(a): 7
Triglycerides: 43

With all that I'd expect to have Pattern A LDL. Yet the VAP test says I have Pattern B! I'm not aware of any history of heart disease on either side of my family. But if it's true that my LDL is small and dense, all I can figure is that it must be genetic. I'm not really sure what to make of it! Any ideas?

Liz Stanley - while my HDL and LDL aren't as good as yours (63 and 185 respectively), I also just received VAP results that stumped me for a similar reason.  I exercise frequently, am not overweight, don't smoke or drink, eat low carb, etc., yet I have pattern B as well.  To add to the confusion, my cCRP is 0.7, which my doctor said was excellent and basically renders my test results a wash as I have zero other risk factors.  I don't know what to make of any of this when you put it all together, and I stumbled upon this post because I'm hoping to find some answers online.

While body composition certainly isn't a prerequisite for being part of a classic comedy team, I couldn't help but notice that Stan had the makings of a skinny-fat bean pole checking in at 5' 10" and only 148 pounds. Those stats make him sound like a diehard distance runner or a chain smoker.

Amen, brother! This is the dirty little secret that proponents of the lipid-hypothesis of CAD continually try to sweep under the rug. Looks like the cat's out of the bag, though, thanks to the internet.

But what can be done about post-meal elevated triglycerides?  Would it be best to avoid fats too, and just eat fruits and vegetables, if one had the will power to do it?

Perhaps we should just give up eating altogether.

I think that worrying about post-meal elevated triglycerides is probably shortening your life more than post-meal elevated triglycerides.

so what does this mean?

"It also remains true if you chronically consume fats."

my understanding is that it is actually in support of normal metabolic functioning for us to "chronically" eat fat. low carb eating, in my lay-person's opinion, means therefore eating good fats (and i am of the un-pc standpoint that saturated animalfats are a-ok) , not just green veggies alone. low-car and low-fat would be no fun! but that's just my 2 cents.

I've had two non-fasting cholesterol tests performed in the last year.  My fasting triglycerides are around 40.  My triglycerides three hours after eating a meal with 10g carbs and 59g of fat were 91.  The time prior to that, they were 79 eight hours after breakfast and three hours after lunch (both were high-fat meals).

Yeah, they go up, but not that much.

So what about the other side of the equation? Decreasing the absorption rate of fat (or spreading it out over more meals) might not help any. But if you can optimize the deposition of fat where it really belongs, in subcutaneous fat tissue-- that is, if fat is deposited in fat tissue where it belongs until needed, at a rate close to the rate at which new dietary fat is absorbed into the bloodstream-- then there shouldn't be a problem.
Interventions that raise HDL generally increase adiponectin. Eating less wheat, beer, fructose, or adding in fish oil, niacin, vitamin d, even being born a woman. And they also associate with less wheat belly.

http://www.springerlink.com/content/dpy09vbc0r8jxnm9/

-----------------------------------
Conclusion/interpretation. These data suggest that adiponectin concentrations are determined by intra-abdominal fat mass, with additional independent effects of age and sex. Adiponectin could link intra-abdominal fat with insulin resistance and an atherogenic lipoprotein profile.
--------------------------------
Maybe they've got cause and effect reversed here? I read a study in mice that were leptin-deficient. Adding extra adiponectin made the mice fatter. So adiponectin is probably not so much a reaction to deposited fat as it is a promoter, maybe a facilitator of proper fat storage.

?

Thanks, interesting post. Just wondering: what about proteins?

So if I eat cheese slices with butter as snacks all day, my triglys will be chronically high and I can get heart problems?

Does this mean that intermittent fasting is very important if you eat low carb/paleo style?

Where Oh Where can I find a Doctor like Doctor Davis in the New Jersey area?

My doc who is a cardiologist referred to by local medicenter when it was found out my Trigs were 235 and Total Cholesterol were 295, LDL 195, HDL 57, promptly put me on 5 mg Crestor to lower trigs and LDL, never discussed diet or anything with me. His office plastered with Pfizer Lipitor posters and Crestor bags given by pharma reps.

Heres the kicker, this was all done with blood work that was NON-FASTING. I had blood drawn an hour after I had eaten eggs and bacon. This was also around halloween time too when I was over indulging on ALOT of Sub sandwiches and bread and lots and lots of candy. I love peanut butter cups. But I know 5 a day is excessive, which was my intake.  Was I getting a DOUBLE Whammy increasing my Trigs?

Since I found this blog, I've been taking my Crestor which I don't want too. But have taken up the no wheat diet and HFC out of my diet that Dr Davis suggests. Dropped 18 pounds in a matter of weeks.

Took my own cholesterol with one of those home machines after 4 weeks of Crestor. Doctor wants to test after 3 months. But my Total Cholesterol was 151, calculated LDL 87, HDL 50 and Trigs 69. I wonder how much was the Crestor doing the change or the change in my diet and 18 pound weight loss?

Sorry for the rambling, but Dr. Davis your blog does give great info and brings peace of mind to me.

Anonymous,

Absolutely not. Having elevated triglycerides immediately after a meal is not a dangerous thing. It's only when they are chronically elevated that you are in danger. Same thing with insulin. Chronically elevated levels are the problem.

Both of these are caused by excessive sugar/carb consumption.

-Bryce Lee

Bookmarked this. Sometimes non-standard due to you after sharing. Positively value my time.

Dr. Davis: a friend of mine recently had triglycerides trending up to 700 and more. I pointed him to your blog, recommended low carbs and fish oil, and after *one month* his TGs are around 200.

Kudos to you.

Interesting series of posts. But keep one thing in mind: Excess blood glucose is converted to palmitic acid by the liver...a saturated fat.

(This fact alone should give the anti-saturated-fat crowd pause...if the body could have evolved to convert glucose to any type of fat, why did it evolve to produce a saturated fat? Can't be too bad for you...)

Anyway, if the body through DNL produces a saturated/healthy fat after only a very brief (and normal) spike in blood glucose - after which the glucose returns to a normal fasting level - then high starch (not fructose) diet appears to be quite healthy. This would answer the question of why a rice-base culture can maintain good health while consuming a diet high in starches...in effect, they are eating a high saturated fat diet.

If they don't eat continuously, allowing their bodies time to eliminate the excess blood glucose and the attendant insulin spike before the DNL triglycerides (palmitic acid) hits their blood stream, then there is no insulin-driven storage of the fats. Instead, they have elevated blood-borne fats that remain available for a consistent energy source of over time, of a type that their body prefers and has evolved to produce.

Can you get the same effect from eating saturated fat in the first place? Yes. But to assume that this is better than the starch-driven approach you have to accept that higher levels of ANY saturated fat in the bloodstream is unhealthy. Which runs counter to the viewpoint of paleo and low-carb eaters.

As Stephen has pointed out, there is no evidence that post-prandial glucose spikes are dangerous to someone with a healthy metabolism (i.e. not a type I or II diabetic). So, if there is no evidence of danger from a post-starch-meal spike, why would your body care where it got its saturated fat? Either dietary or liver-produced, it’s all the same once it is in your blood.

Following the chain of reasoning further, a high-starch diet that leads to DNL production of palmitic acid would be healthier than a high fat diet composed of vegetable oil or other undesirable fats.

We have to be very careful about quickly latching onto bits of "evidence" that confirm our biases. Remain scientific, think it through. The human body is an amazingly complex organism; when we begin to isolate its responses to prove our points, we can start down a path that leads to conclusions that may satisfy our dietary worldview, but are not entirely accurate.

Scott W

Note: If we are being carefully scientific in our approach, we should be careful to distinguish our descriptive terms for non-fat and non-protein calorie sources. "Carbohydrates" is too general. It encompasses fructose, which as a much different effect on the liver than glucose. My discussion above focuses on starches for a reason; they break down to glucose, which the body has evolved to handle efficiently, even in large quantities. It can handle fructose, too, but did not experience it in large quantities prior to modern times. Even using the term "sugar" is inaccurate, since it is half fructose and half glucose. By extension of my discussion above, eating pure glucose powder (dextrose) would be as healthy for a rice-based culture as eating white rice itself. You are simply giving the body the end product of rice digestion (glucose), from which it can produce palmitic acid.

There's no question that postprandial triglyceride-rich lipoproteins are causally related to atherosclerosis, regardless of whether they were fat-driven or carbohydrate-driven.

However, these brief posts are NOT meant to endorse low-fat diets. They are meant to show that a simple low-fat vs. low-carb approach is too simple-minded. There are other aspects of diet that count for substantial effects. Postprandial phenomena are one important class of effects that cannot be fully controlled by just controlling carbohydrate or fat content of the diet.

You still haven't explained why the chart in your previous post (Di Novo Lipo-what?), where normoinsulinemic people have lower DNL on a high-fat diet, is in marked contrast to the chart of Gretchen in the post before that (Gretchen's postprandial diet experiment II) when she was eating high-fat.  From those two posts, it seems that peoples' postprandial triglyceride level is dependent on the amount of insulin they produce (and obviously how sensitive they are to that insulin).  Therefore a high-fat diet is not problematic unless one is also hyperinsulinemic.

"They didn't teach that to me in medical school (back in 1980)!"

Unfortunately vitamin d is not mentioned in med school nowadays except for osteoporosis prevention...

Dr. Davis -- thank you for your blog. I am a med student interested in REAL evidence based medicine (which makes me a bit unpopular between my teachers).

I researched vitamin D after reading your blog, and decided to mega-dose on it. It's been 4 weeks now and my "inespecified mood disorder" (never met criteria for depression, but have never been really "well" since I was 16) is GONE. Like a "veil" has fallen or something. PMS is gone as well.Now I have discovered that the periods of my life in which I felt truly well were when I spent outside most of the day (I live in the mediterranean coast).

I also had a single attack of MS some years ago, so vitamin D will help to prevent full blown multiple sclerosis.

My comment is in no way related with atherosclerosis, but I just wanted to thank you, and congratulate you for having found a way to help people outside conventional medicine. I feel greatly inspired by your work.

Regards,

Angela Nicolas

"primary care physicians are completely in the dark"

For the record, we aren't ALL in the dark. In fact, I stumbled across your website a few years ago as I was looking for supportive testimony from other practitioners who saw things clearly. In fact, I watched as you "caught up" with the idea of adding Vitamin K2 to your regimen - presumably based on the results of the 2004 Rotterdam Study.

I hate to sound defensive, but such a sweeping generalization is uncharacteristically irrational of your posts up to now. Perhaps you haven't known any primary care "grunts" without a cranial suppository.

Now you know at least one.

I guess it's just a matter of time until someone breaks the record again?

I know you have talked highly of vitamin K2, I'm wondering if you've made it a staple of the TYP program already? I think there's all reason to do so.
Below two studies using high doses of K1, but it should work via conversion to K2 (the epidemiology of K2 hints at the same phenomenon).

Am J Clin Nutr. 2009 Apr 22. [Epub ahead of print]
Vitamin K supplementation and progression of coronary artery calcium in older men and women.
Shea MK, O'Donnell CJ, Hoffmann U, Dallal GE, Dawson-Hughes B, Ordovas JM, Price PA, Williamson MK, Booth SL.

One of THE most impressive studies I've ever read:
Thromb Haemost. 2004 Feb;91(2):373-80.
Beneficial effects of vitamins D and K on the elastic properties of the vessel wall in postmenopausal women: a follow-up study.
Braam LA, Hoeks AP, Brouns F, Hamulyák K, Gerichhausen MJ, Vermeer C.

Over the last year, I have seen about a dozen physicians (for a reason other than heart disease).

Be they a GP, cardiologist, pulmonologist, oncologist, or hematologist, they all tell me the same thing; we all "naturally" develop coronary plague as we age and that it can only be minimally "managed" by lowering our cholesterol with -insert your statin drug here.

Every time I reply with; there is nothing natural about having calcified plaque build up in our coronary arteries at any age and that it can be very effectively managed by following Dr. Davis' "Track Your Plaque" protocol. (As I pull out your book to show them.)

The physician then usually looks at me like I have two heads and dismisses me by standing up to signal that the visit is over.  Except for one physician, honestly, who responded by reaching for his script pad and saying that he would like to start me on an antidepressant medication right away... lmao.

I have now given up looking for any local physician who would be willing to help me in any way with the heart scan/track-your-plaque program.

Antidrugrep--

Actually, that generalization was intended principally for the sorts of primary care docs who wouldn't read a blog like this. You are clearly the exception.

If you had responded that most cardiologists are knuckleheads out for a buck, I would have agreed, too.

Kismet--

Thanks for the references. I hadn't seen the Shea study; the findings are interesting.

We haven't had enough people have pre-K2 and post-K2 heart scans, so it's hard to know what effect it ADDS to the existing battery of strategies. Nonetheless, K2 is definitely on the list of most promising. Given its benign nature, I do encourage people to add it, though dosing remains entirely uncertain.

I seem to be developing atherosclerosis at age 26 and I've been doing a lot of research. B12 and Vitamin D are related, but you should also be aware of magnesium. See the study at Comparison of Mechanism and Functional Effects of Magnesium and Statin Pharmaceuticals. In this study they basically explain how magnesium works as a natural statin and calcium channel blocker. If you do further research online you may become convinced, as I am, that magnesium deficiency is just as widespread as Vitamin D deficiency.

You need to take a chelated form of magnesium, such as glycinate, because other forms (like magnesium oxide) are poorly absorbed by the body and not worth the money.

I would predict that the cardiologist is among the conventionally-thinking, "statins drugs are the only solution" group who follows his patients over the years to determine when a procedure is finally "needed." In fact, I know many of these cardiologists personally. The primary care physicians are completely in the dark, usually expressing an attitude of helplessness and submitting to the "wisdom" of their cardiology consultants.

Worst thing you can do is use the tobacco drug, either by smoking or through spit tobacco.

Also, being exposed to toxic tobacco smoke (sometimes called second-hand or environmental tobacco smoke) is EXTREMELY Dangerous! Make sure you work to BAN SMOKING EVERYWHERE, INDOORS OR OUT!

Better yet, BAN THE TOBACCO DRUG, NOW!