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.

If high GI foods are bad and low GI foods are just less bad, then what does that leave that is good?  Protein and fat?  Sounds good to me!

I absolutely love this post!

So many people don't understand this basic concept.

I have had to expose several 'health conscious' individuals at various health food stores as to WHY that Agave Nectar is just nature's 'High Fructose Corn Syrup'. Along with the Ethanol poisoning from the Fructose, their insulin is spike through the roof for longer than if they just ate table sugar!

Thank you for continuing to educate the masses on the truth, instead of these horrific 'wives tales' that just don't seem to die!

I was diagnosed a type 2 diabetic 30 years ago.  Now at age 70, I've lost 60 pounds through exercise and avoiding processed foods.  My breakfast every morning is boiled oats-groats and whole barley.  My vision is 20/20 and my A1C is always under 6%.  My diet is mostly vegetarian except for salmon or mackerel in my salad.  I usually avoid wheat products except when travelling or on social occasions.

Health Test: I love the "agave nectar is just nature's 'high-fructose corn syrup.'" Well said!

What about Stevia? is stevia ok as a sugar substitute? please advise.

I don't disagree with your comments on GI in general, although as an Aussie I believe  it should be noted that Jennie Brand-Miller had a great deal to do with the develpment of the GI/GL concept.

As a type 2 diabetic I used the concept in a slightly different way. I used peak post-prandial testing to develop my own personal database of the effect of various foods on my own blood glucose levwels. In effect, a personal GL list.

My main reason for commenting was this: "Check your blood sugar after a low-glycemic index food like oatmeal. Most non-diabetic adults will show blood sugars in the 140 to 200 mg/dl range." Although I agree that oatmeal would do that to me - probably worse than 11mmol/L(200mg/dL) I have doubts that it would do that to a non-diabetic. In my experience testing friends and relatives I have never tested anyone who had levels that high after a meal who was not subsequently diagnosed as a type 2. The non-diabetics I have tested, regardless of the carb load of the meal (usually a feast like Christmas) have never reached 8(144), let alone higher numbers.

I would be interested to know if you have seen numbers like that personally in your clinical experience in non-diabetics, apart from those affected by medications like Prednisone. Or was the statement based on the experience of others?

This is one of the few published examples that I am aware of showing post-prandial blood glucose levels in non-diabetics:
http://www.diabetes-symposium.org/index.php?menu=view&chart=4&id=322

Note particularly slides 17 and 27.

Cheers, Alan
http://loraldiabetes.blogspot.com/

Why do you think the traditional extremely high carb Japanese diet
left its population almost free of obesity and diabetes?

Good post.
In the last few years there has been a better parameter, called "Glycemic load" (GL).
While GI is always the same, independent of HOW MUCH you eat, GL takes into account "portion size".
This is important because if you are eating half an apple or 2 apples it will have the same GI regardless, but not the same GL.  

Renfrew

Asians eat lots of rice, and they're skinny. Therefore starch is good for you and should be consumed in large quantities. Buy my ebook, "The Edgy Contrarian Hipster Diet"!

The Mercola mixed diet recommends eating occasional higher glycemic foods AFTER the rest of a meal...since this apparently blunts the insulin response.

I've been indulging in oatmeal...eaten dry as a snack.  Also fruit.  Shame on me.

Also beans as part of meals...not recommended (like wheat as far the effect on the gut?).  Not to mention the salted nuts roasted in hydrogenated oils.

Still have some work to do.....

I buy food only every 3 weeks or so...and I find that when I run out of "favorites" near the end of this period and am eating only lean meats...assorted veggies...olive oil...spices...I feel better.  Though I do seem to get a major itch to go buy some "junk food"...plus a kind of panic as far as running out of food.  

Wondering WHY this is...since I do feel better...do I have addictions?  Need to go to a clinic to recover?

I may be addicted to the sugar rush???  The oatmeal rush? The bean rush?  The hydrogenated oil/nut rush?  

Dependent on my food reactions?

Hi Dr. Davis,

If I remember correctly, in your book you recommend oat bran to decrease cholesterol.  Is that still the case?  (Many thanks for all the great work.)

Thank you so much for this -- the proof is always in the testing and I abandoned many "low-GI" foods early on.  

It sounds good, but ... I never had any success with it.  I thought it must be ME, and ended up feeling (more) sorry for myself.

"A slice of whole grain bread is really not that different from a icing-covered cupcake," except for the fiber, micronutrients, antioxidants, etc.

Alan--

Yes, I've seen many, many people with either "normal" (<100 mg/dl or 5.5 mmol/L) or slightly increased blood glucose (100-110 mg/dl or 5.5-6.0 mmol/L) with high postprandial glucoses.


Peter--

I believe there are a number of reasons, including the use of rice in place of wheat. Being part Japanese, I am well aware of their eating habits which are not as high-carb as often made out. There are confounding factors, as well, including iodine content of the diet.

Also, there are indeed fat, diabetic Japanese people, also. Diabetes is, in fact, a growing problem in Japan.

Dr. Davis is right about the Japanese diet.  Northeast Asians eat a bowl of rice or noodles at every meal, but that is the only high GI food at the table.  A typical Japanese, Korean, or Chinese meal includes fish or meat and non-starch vegetables.

Moreover, type II diabetes is common among middle-aged Asians, who get the disease at lower BMIs than non-Asians.  

I am wondering about the accuracy of identifying whole grain products as low GI.  The Easy GL Diet Handbook lists a GI of 37 for whole wheat pasta compared to 43 for regular pasta.  Likewise, brown rice and long-grain white rice have nearly identical GIs of 55 and 56, respectively.  Low GI is defined at around 55 or less, so pasta qualifies as low GI, but the difference between whole grain and refined varieties is not significant, especially when GI is converted to GL.  As the good doctor notes, it's best to avoid grains altogether.

I did the test today
And this are the results I had.

After wake up: 86

A bit over an hour after breakfast (rise with some vegetables, one egg, broccoli, and one cup of lapsang tea): 93

30 Minutes after lunch (Portion of papaya, bowl of 'auyama' soup, half chicken breast with tomatoes and green peas, one boiled potato and salad with olive oil, one cup of lapsang tea): 111

60 Minutes after lunch: 101

Afternoon before eating some oats: 94

30 Minutes after oats (quaker classics, soaked in water for 10 minutes with some almonds): 110

60 Minutes after oats: 121

30 Minutes after dinner (3/4 chicken breast same sauce as lunch, broccoli, salad, couple glasses of red wine): 109

60 Minutes after dinner: 116

90 Minutes after dinner: 92

This opens many questions to me, like how much the time at which I had the oats affects. Or the fat I just had them with some almonds instead than as part of a whole meal

Also as dinner seems to have more effect on my glucose than lunch even when lunch had  fruit and a potato I wonder if this is due to the black tea at lunch or to the time of the day.

Also I wonder how much effect had the wine at dinner.

I'll do some more tests when my fingers recover

I would add to this post the fact that fructose has low GI, yet is more toxic and screws up the metabolism more than most other carbohydrates.  (E.g. causing fatty liver disease and insulin/leptin resistance; increasing hunger rather than satiating it.)  Food companies are motivated to add fructose to their products so they can claim a lower GI (hence the agave craze), but the fructose does more harm than most higher-GI carbs.

I soon discovered that "low GI" foods, like oatmeal and other whole grains, still cause an unacceptable rise in my blood sugar.  Low GI may be a little better than high GI, but filtered cigarettes are a little better than non-filtered cigarettes.  Both are still bad.

Glycemic load, which also takes into accout the number of carb grams, is much more relevant.  Non starchy veg, meat, & fat are about as low GI/GL as you can get.

As for agave nectar, they still have to process it to extract it.  I'm not sure it's all that "natural."

Low-glycemic index foods trigger the very same responses as high-glycemic index foods—they’re just less bad. But less bad does not equate to good. Low-glycemic index foods cause weight gain, trigger appetite, increase blood pressure, and lead to the patterns that cause heart disease.

I eat oats with milk and 2 tbsp of ground flax seeds every morning, and since I'm doing that every morning I lost 10 pounds, and I feel great. I don't crave for sweet anymore. So, I don't understand how low glycemic foods like oats can increase your weight?
Few of my friends who implemented oats and flax seed in their diet had similar results.
No one mentioned very valuable fiber that oats contain.

Ivan
Male, 37 y.o.