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.

just came across this...thoughts?

http://thegearjunkie.com/the-runners-heart

Good article. One of the most common mistakes made by health conscious individuals is the idea that if study X says A is bad or good then one should adjust one's lifestyle accordingly.

If only it were that simple. A statistical analysis of a group is applicable to that group, not necessarily the specific individuals within that group; let alone those outside the studied group. We cannot determine individual risk on the basis of such studies yet time and again these studies are mentioned as "evidence" that we must accept. Sadly, too many health promoters, who should know better, tend to make the same logical error.

Very pleased to see that this error is highlighted here.

Real men aren't terrified of an entire macronutrient because of a poor understanding of science.

Then why do I have boys (later men) doubling testosterone when switching from a very low-carb to high-wheat, high-carbohydrate diet?  

http://180degreehealth.blogspot.com/2011/03/natural-testosterone-enhancement.html

Dr. Davis,

Can you explain why I remain lean eating 15 pounds of potatoes, 2 gallons of whole milk, and close to 2 pounds of butter every week? That's in addition to regular meat, eggs, other added fats, root vegetables, beans, occasional grains, and other carb sources like fruit and molasses. I'm 6'3", 175 pounds, have never dieted, and do not exercise. My weight has never gone higher than 176 pounds.

Thanks,

Mike

"Real men don't eat carbs."

Are you saying half a billion Chinese men and 70 million Japanese men aren't real men?

-DIANA

Prolactin secretion is held down by dopamine; with less dopamine turnover the prolactin self-regulation feedback loops are disturbed. Age has a role in the efficiency of prolactin receptors on the hypo-thalmic dopamine neurons.

Prolactin secretion is increased by seratonin, vasopressin, cholecstokinin, Beta endorphins, angio-tensin II, thyrotropin releasing hormone, enkephalilns Leu & Met, growth factors of epidermal and fibroblast, substance P, oestradiol 17Beta, and pituitary response to prolactin-releasing peptides.

Normal testosterone release has a  peak that inhibits prolactin for 9 -11 hours; when testosterone release is at it's lowest point in releasing cycle then estradiol gets active. Estradiol cycle is for 15 - 18 hours; and when estradiol starts to kick in the prolactin cycle of 20 - 23 hours gets going again. Estradiol in high amounts has a paradoxical effect; it lowers prolactin secretion instead of normally working toward increasing prolactin secretion.

Prolactin has a feed back loop with testosterone; it can act on the cognate receptors in the testes Leydig cells to raise testosterone. Testosterone, for it's part, can supress the synthesis of prolactin.

After the aged male ejaculation there is a secretion of prolactin that is sustained for about 1 hour; this is refractory, and if there is arousal without actual orgasm then that prolactin refraction does not occur. With healthy young males there is no post-orgasm prolactin perfusion; and thus their refractory phase is brief.

Where (in brain or in periphery) the prolactin is being considered has to be born in mind; as does the context (normal or altering). Chronic high prolactin in men is associated with poor sperm fertility.

Carb engendered insulin resistance I can see as down stream leading to more free fatty acids circulating; that, and the fact that as we age our sub-cutaneous fat cells tend to get less responsive to insulin anyway. The "freed" fatty acids cause blood albumen to release tryptophan, a substrate for synthesizing seratonin (and thus more prolactin). With age there is less need for tryptophan amino acids and so the ample western protein supply of dietary tryptophan might be a co-contributor (among others).

but who was troll?

Thanks Dr Davis for great advice as usual.

Dr Davis, have you noticed that humans somehow are arrogant enough to believe that they can eat whatever they want and still maintain good health anyway? It's like pretending a lion or cow can eat whatever it wants with no ill effect. Or maybe it's just my impression lately.

SSRI (seratonin selective re-uptake inhibitors) entail many formulations; a number of them are associated with loss of libido (reduced sex drive), ejaculatory anorgasm, +/- 25% men get erectile dysfunction  and sometimes impotence. Seratonin is a factor increasing prolactin production by the pituitary gland.

Carbohydrate ingestion is a popular  on-line recommendation to boost seratonin levels. The National Sleep Foundation states carbs make tryptophan more available to the brain; once tryptophan crosses the brain blood barrier we can then make seratonin from it.    

The journal "Public Health Nutrition" (Jan. 2007) details that our muscles will absorb amino acids except for tryptophan; the tryptophan builds up a "pool" in the blood to draw upon. When one is young &/or geneticly favored (among other exceptions) they are not plagued by the insulin resistance corollary of elevated free fatty acids causing their  albumen "pool" of tryptophan to head on toward excess seratonin synthesis.

Doc likes to post provocative snippets; not footnotes we can find by searching the internet (try "Yandex" search engine if getting poor pickings). I am not fixated personally on low/no carbs, so am not advising anyone here about diet. My unsolicited observation is that age and time often confound an individual's metabolism; what was once "great" may sometimes merit reconsideration.

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I think it would be more precise to say real men don't eat starches.  After all, vegetables are carbs, and I don't see anyone saying that veggies are bad for you....

WOW!  So much misinformation in such a short post.  

These kind of posts only undermine the nuggets of good advice you may provide.  

By your logic the human race should not even have survived agriculture!

Dr. Davis,
Please post my "Endothelial dysfunction ..." comment, your
Spam filter seems to have held it on 28th, following CarbSane's.

@Carbsane

Every statement can be verified. Which one is not true, i.e. misinformation?

As far as I can see, every one of those statements are true.

@Matt Stone

Congratulations, you have just discovered puberty (boy turns into man, doubles testosterone level in one year). You have also discovered the premature-puberty-triggering properties of wheat. It probably acts primarily through the insulin/IGF-1 pathway.

Um...actually, non-starchy vegetables are not a carb source for humans, they convert into fat in our gut through bacterial fermentation. Vegetables are actually very low in sugars. Ruminants like cows ferment grasses into fats; they are getting most of their energy from fats.

I am trying to de-program a friend that has been McDougaled.  McDougal is telling him all the scientific studies support hi-carb vegan diets.   Where can I find studies to counter these claims?  Especially about wheat.  I find Dr. Davis' articles on wheat quite compelling, but I need to show him studies.

Facts are facts.  A man with a testimony is not at the mercy of a man with an argument.    Sugar/Carbs raise insulin levels.

2 years lo carb hi fat.  30-50 carbs per day.  35 pounds lost.  Last VAP test was HDL 72, trig 52, LDL pattern A.  I'm 45 years old.  Exercise moderately.    I have discovered that FAT is your friend and sugar/carbs are the enemy.  Seems to work for me.

@Martin:  Perhaps let's start with evidence that carbs de facto  increase visceral fat.  So many of Dr. Davis' posts of late begin with either a false or unproven premise.  Some, like the recent battery acid post about oatmeal really take the cart over the cliff!

consider also: "life w/o bread" by wolfgang lutz, md, internist, wherein elevated insulin in response to carbohydrate ingestion is demonstrated to suppress testosterone and human growth hormone.  taubes also recognizes elevated insulin as a suppressant of t and hgh in gc,bc.  and sir, what a pity to see carb crank and her ilk here.  edit, please.

carb sane - why do YOU not respond to the others commenters here that are critical of your endlessly unsubstantiated comments (your nonsense, really)? Your insisting that  Dr Davis support HIS statements makes you look EXTREMELY hypocritical when you do not support your OWN statements.  

Please do better. If you do not like what Dr Davis posts, you can simply stop reading his blog, and stop making silly, inane comments (that make you look like a hypocrite!).

Dr. Davis,
Again request you to kick out of old Spam filter my  28th April post on this thread.  When I sent it your old blog format showed it in comments section right after CarbSane's 28th posting.
It  begins : "Endothelial dysfunction ...." and goes on to discuss particular  details related to  your premise that carbohydrates can contribute to male dysfunction.
I don't  have it saved to re-send and won't spend time trying to recreate it .  It wasn't "X" rated and maybe some of the  guys here might find it interesting.

CarbSane  shouldn't have to sing in the choir in order to participate and I,  for one,  hope she will continue to  comment  here.  I  request she stay on the island  ....
Unrelated:  
I just noticed this  blog format now  uses a  "Reply" to individual commentator's posts (ex: Tyson's 28th Ap. comment got a reply underneath from Steve on 29th Ap.).  Since I follow an entire thread this is annoying; because now I can't just go to the last comment I read (or date)  and keep abreast.
It's not like we are at a world events blog sounding of  on endless nuances.  Revisiting all the previous comments for   input is not  pleasant.  I will not use "Reply" and keep comments sequential,  like blog set up was before.

CarbSane has pointed out that carbs do not "de facto increase visceral fat";  she did not deny that carbs are implicated in de novo lipo-genesis.  In a sense the deal with carbs   relationship to internal fats  is location, location, location; and probably time complicates  the  functional impact.

High  carbohydrate diets increase triglycerides in the liver more than dietary fat does.  High dietary fat intake, in comparison, is what increases trigs in the plasma more readily (ie: chylomicron bound trigs) than ingested carbs.

Repeated high carb  intake can upregulate a  lipo-genesis gene, the sterol regulatory element binding protein 1c (SREBP-1c);  once  SREBP gets active this gene keys more activity of enzymes  fatty acid synthesase  and more mRNA of acetyl-CoA carboxylase .  The liver then goes on to make more triglycerides.  

A separate affect of high carb diets is the up-regulation of the enzyme pyruvate kinase, a glycolytic enzyme.  This involves the ChoRF (carbohydrate response factor) binding to a DNA ChoRE (carbohydrate response element) and then  the protein ChREBP (carbohydrate response element binding protein) complex hypes up the liver pyruvate kinase;  fostering a pre-disposition where mitochondria are set up  to burn glucose for ATP,  and not fatty acids nor ketones.

@Mito:  In humans, DNL is not a significant contributor to body fat accumulation.  It only becomes quantifiably significant in the context of massive carbohydrate OVERfeeding.  See studies linked in these blog posts of mine:  Excess carbs converted to fat?, Postprandial DNL, Nutrient Fates, Fat Futile Cycling of Carb Excesses.  

Paul Jaminet over at Perfect Health Diet had an interesting take on the subject of that last link:  How does a cell avoid obesity?.

Are high carb consuming cultures known for their moobs?

Well a priori, it's true. Carbs increase visceral fat. What makes you believe otherwise?

Actually, the opponents of the carb hypothesis always point out how fat cells always take in fat, and always put out fat. So do the proponents of the carb hypothesis incidentally. So in effect, any substance that causes fat cells to take in fat, increases fat cells. Thus, carbs increase visceral fat. De facto, sine die, that's it for that.

To say carbs don't increase visceral fat is to say carbs don't ever take a trip inside a fat cell at any time whatsoever never ever. How is that even more plausible?

Ian, since you have a better understanding of science, please explain what really happens when a man consumes "healthy whole grains".

No, a priori it's not true.  I didn't make the assertion, Dr. Davis did.  I'm asking for the evidence in support of that.  Why should I, or anyone for that matter, be tasked with disproving an assertion?  That's not how it works Martin.  To your other post, I didn't say carbs never cause fats to be deposited in visceral depots.  That would be ridiculous.  But I've yet to see evidence that they cause increased *accumulation* of fat in same.  Have you?  I'm interested in seeing this evidence.

@Mito:  It appears my response to you is in moderation limbo - links?

Here's the stripped version:  @Mito: In humans, DNL is not a significant contributor to body fat accumulation. It only becomes quantifiably significant in the context of massive carbohydrate OVERfeeding. See studies linked in these blog posts of mine: Excess carbs converted to fat?, Postprandial DNL, Nutrient Fates, Fat Futile Cycling of Carb Excesses.

Paul Jaminet over at Perfect Health Diet had an interesting take on the subject of that last link: How does a cell avoid obesity?.

Are high carb consuming cultures known for their moobs?

You sound like a sentient enough being (that's a little dig at the multiplication sentient being filter here ... not a dig on you!) to use the labels function or other search stuff to find the posts if you're interested.  All of those posts on my blog contain links to the full texts of some rather nice papers.

@Terrence:  When someone makes an assertion, the burden of proof is on them to back that up.  

@Martin:  It's pretty lame to conflate fat deposition - that we all agree occurs continually - with fat accumulation.  By your logic, everything causes visceral fat and all you fellas would be running about needing "Bros" or was that "Manziers"?  

Dr. Davis' claims all hinge on some special tendency for carbohydrate intake to lead to visceral fat accumulation.  It could be true.  I haven't seen much in the way of evidence though.

Back to Mito:  You said "High carbohydrate diets increase triglycerides in the liver more than dietary fat does."  I would point out the key word "in".  Are we talking elevated circulating triglycerides produced by the liver, or are we talking hepatic triglycerides?  Two different animals.

carb sane said "@Terrence: When someone makes an assertion, the burden of proof is on them to back that up. "
PRECISELY, carb sane PRECISELY!

Exactly WHEN will YOU "back up" your empty, meaningless assertions about Dr Davis's blog? WHEN???

Every assertion in this post hinges on increasing visceral fat.  Dr. Davis did not provide substantiation for his assertion that eating carbs does so per se.  That's his burden, not mine for pointing out his lack of substantiation.

Fat intake doesn't get a free pass;  depending on the amount (& type) of dietary fat it can contribute to obesity. At 10 - 20% dietary fat there is negligible contribution to weight;  it doesn't trigger intestinal gene expression related to lipid metabolism that promote  a metabolic syndrome.  

Constant intake of 20%  fat gets PPAR  (key lipid metabolism gene) busier; and by the time regularly consuming 30% dietary fat  gene alterations have more significant  potential to affect body weight. When the diet is 45% fat then fat absorption continues to occur even further down along in the gut as genes up-regulate there to handle the high fat intake.

Physically active people (ex: exercisers , agrarian ancestors,  hunter gatherers, youths) up-regulate AMPK  (adenosine mono-phosphate activated protein kinase); which  effectively counter-balances the effect of  regular high fat intake down-regulation of AMPK (a energy sensor in a cell when cellular energy is low) .  High fat diet retards  phosphorylation of  AMPK  gene and this stymies the mitochondrial Uncoupling Protein (UCP3);  UCP must  first activate in order to switch over to burning fat in our cells.

With AMPK down shifted the cell house- keeper recycling step of auto-phagy is inhibited; cells accumulate debris from oxidized fats and old mishapen proteins, with cell's attendant burden of ROS (reactive oxygen species, generated  from unchecked NADPH oxidase enzymatic activity).  Palmitate fat  (for example) can cause down-regulation of AMPK and downstream  activate inflammasomes (ex: NLRP3) that contribute to adipose tissue problems;  however,  adequate K+ (potassium) ions are able to nullify the inflammasome  spark.

Palmitate  (ex: lard = palmitate and oleate, et.al) generates ceramide molecules  ( a sphingo-glycolipid;   "sphingo" was an original typographical error instead of discoverers  chosen "sphinx-" prefix, relating to how molecule interacts biologically and enigmaticly flips it's own molecular orientation); ceramides work against insulin action in our muscles, and thus can contribute to insulin resistance (ie: risk of  pre-diabetes). Muscle ceramides are mostly made with the  fatty acids derived  from dietary fat;  in the muscle they (ceramides) increase insulin resistance . Oleic  acid, and other long chain fats,  get into intestine chylomicrons as triglycerides; their route is via mesenteric lymph transfer into the blood circulation at the left-subclavian vein (ie: don't go directly to liver).

So, ceramides in the liver are different because they are essentially  from de-novo lipogenesis; those ceramides are not considered to directly cause of insulin resistance. In other words,  if the individual has good insulin signalling in the liver  there is still the potential for muscle insulin signalling to be made worse by constant  high fat intake.

Lifestyle and genetics are not discussed here as mitigating factors; the dietetic strategy of eating fat to lose weight is not being parsed here .  The modern diet of abundance,  high in both fat and carbohydrates, probably  is more of a double whammy for weight gain than either die factor taken in isolation; protein is not factored in here either .

You ask why should anybody be tasked with disproving an assertion. Imagine if scientists had the same idea. Nothing would be done. If you disagree, _you_ are making an assertion. By your own logic, _you_ are tasked to prove your assertion. That's how it works miss sane.

You say it's ridiculous to say carbs don't cause fats to be deposited in visceral depots. This means you say carbs do cause fats to be deposited in visceral depots. However, you disagree that carbs cause increased accumulation of fat in same. In effect, you disagree that carbs cause any kind of dose response of the same. Now that's ridiculous.

As for evidence of all this, Gary Taubes Good Calories Bad Calories is as good a place to start as any. The key detail is insulin and the fact that visceral fat tissue is so much more sensitive to it than other fat tissue. To summarize, carbs drive insulin drive excess fat accumulation. Since visceral fat is more sensitive to insulin than any other kind of fat tissue, carbs drive more excess fat accumulation there than anywhere else. I'll try to find a more specific source for this if I can. But don't wait up, I could be late.

2 times got "server" error for comments here...this is a 3rd.
I miss the old blog set up.

Hi CarbSane,
13 women & 5 men with BMI = 35 +/-7 and fatty liver (non-alcoholic) followed 2 different diets (2011 study) for 2 weeks only. I think this might validate one of Doc's contentions; sorry comment seems brusque . (Unrelated: yesterday I  said "in" the liver, no circulating trigs were detailed ;  and  said "high" carbohydrate, whereas you classify "extreme" as game changer.)
Studied group 1, restricted calories to 1,200 & 1,500 daily for women and men, respectively. Weight loss after 2 weeks was +/- 4.3% and circulating triglycerides dropped 28 (+/- 23)%
Studied group 2, restricted carbs to maximum of 2o gr./d for both sexes and had no calorie restriction. Weight loss after 2 weeks was +/- 4.3% and circulating triglycerides dropped 55 (+/-14)%

edit correction from me CarbSane,  
The triglycerides  in low cal/low carb  diet comparison I cited were explicity  liver trigs,  and not circulating trigs as I skimmed from my notes; measurement of liver trigs was done by magnetic resonance spectroscopy.  I thought my synopsis was unlikely so  just traced the study back to Am. Jrnl. Clin. Nut.(ajcn.org/content93/5/1048); sorry about the error.

Hi, Might--

Sorry, but I can't find your lost comment. I don't know what's become of it.

I'm also just getting used to this new format.

There's much evidence that it's the lack of fat in the diet that leads to increased caloric consumption. We could still posit that it's the caloric surplus that causes obesity. But we can't discount the possibility that it's the lack of fat (and the surplus of carbs) that causes obesity, which we then compensate for by eating more, and that's what we see.

Considering many studies that show just that, that eating more fat leads to satiety which leads to eating less and losing weight simultaneously, and that hunger is an indicator of nutritional status (fuel partitioning for example: too much toward fat cells, too little toward every other cell), we can't just conclude that we grow fatter because we eat too much.

Add to this the fact that many drugs, which contain exactly zero calories, make us fatter by themselves (and some make us leaner, ha!), and it's clear that the problem can't be expressed by calories alone.

Ironically, you go on about physiological mechanisms to explain how fat can make us fat, but then proceed to posit that it could still be all about calories, i.e. abundance. Now that just doesn't make any sense to me. What's the physiological mechanism that controls "calories" then?

I enjoyed this post, but it begs the question: do real men look like Popeye?

Hi Martin Levac,
Just  saw your "reply" under my fat doesn't get a free pass comment; please tag me with new sequential thread comments (instead of as reply) to be sure I catch what you wrote.  I am not declaring excess weight gain is a clean cut factor of either  calorie, carb or fat intake;  genetics/epigenetics /age/pathology  will have a role in how susceptible one is to their  (carb & fat & protein) influence.  

I don't have  any  specific formula to promote for every one. Satiation at a meal is  well worth considering as a control  factor; unfortunately,  we are able (and many have access) to not only keep eating, but also to soon " graze" on food again irregardless of our abated hunger.

Fuel partitioning, as you mention it,  is a bit confusing to me. If your concept relates to how the body "burns" it's energy for functioning then that relates to one's underlying diet; we are set up to pump out energy in essentially distinct  mitochondrial steady states.

Our cells don't want to be oscillating , in real time, between burning fat and glucose;  slipping in & out of phase, in real time,  is normally prevented by a high threshold  that must be exceeded to switch mitochondria over to other fuel.  In this case there must be a relatively strong OFF signal needed to get out of  the already up and running mitochondria mode,  and into the ON for a different mode for burning the other fuel.  

The output of these types of cell signals (ie: Off/ On & On/Off  ) is a function of the previous history of trans-genetic activity (ex: genes key to burning fat or carbs and their respective cascades of genes that keep the process going) ; and this type of  threshold program is encoded on a chromosome  (like an epigenetic tweaking ).  That chromosome filters out other pulses of conflicting messenger RNA  (from typical gene transcriptions going on) that might otherwise cause other cascades leading to oscillation in the pathway of mitochondrial energy production.

With one predominant nutrient  the dynamic is inclined toward working on a gradient; it is based on a dose response (ie: gradient of how much nutrient is put into equation)  and not just positive feedback (ie:  not just  "x" induces "y" and "y" loops through "z" to  make the action of "x" worthwhile enough  to keep doing things that way ), because  concentrations of a nutrient fine tunes the feedback response.  Biologists now call this  "hysteresis";  when a nutrient  modifies the traditional  stimulus-response relationship according to the history of past usage, and then the stimulus-response sets a high threshold (on a chromosome) for switching OFF in order to achieve a self-sustaining steady state burning the "favored" fuel.

I have followed my own research since 2007. I started, via Dr Barry Peatfield, with Dr Broda Barnes (thyroid) and then Dr William McK Jeffries (adrenal).  Then, I found Carole Baggerly at GrassrootsHealth and Dr John Cannell at Vitamin D Council.  later still, I found Michael Pollan, Gary Taubes, Dr Mercola, Dr Kurt Harris, Dr Robert Lustig  and the wonderful Jimmy Moore with his podcast back library.  I also found Dr William Davis and this excellent blog.  

What makes Dr William Davis special is that he does not promote just one thing (i.e. vitamin D3); instead he integrates the latest knowledge and provides guidance for a healthy lifestyle (for heart patients) covering lipids, blood sugar control, thyroid (iodine, T4, T3) and adrenal hormones (DHEA), vitamins D3, K2 and niacin, fish oil, carbohydrate restriction and grain elimination.  Whats more, as a practicing cardiologist, we get the considerable benefit of feedback from his ongoing patients.  

I am pleased that the blog is concise and that it is not behind a paywall.  There are plenty of blogs which delve into every detail of every study, but thankfully this is not one of them.

So, thanks to you Dr Davis.

@Might-o'chondria-AL

Satiety seems to be the key factor for adherence. Like some say, hunger is not an option long term.

Fuel partitioning is the distribution of fat between fat cells and all other cells, i.e. storage or consumption. Nutritional status would depend on this. If too much fat is shunted toward fat cells, then all other cells don't have enough and call for more. Fat cells themselves can call for more in spite of being full through their own hormonal signals. Insulin is the primary determinant for fuel partitioning. It's also the determinant of which fuel to burn.

Incidentally, I thought that cells could switch on and off at will which fuel they burnt in their mitochondria. Since insulin is the primary determinant, and since cells can turn on and off insulin receptors, they can control their own choice of fuel. For example, if a cell contains its quota of glucose, it will turn off insulin receptors to prevent any more glucose from entering the cell. As it does so, it also causes a change in the signaling that would otherwise tell the cell to burn glucose, i.e. insulin. So while it is insulin sensitive, it burns glucose. But as soon as it's insulin resistant, it stops burning glucose and starts burning fat instead. This is normal insulin resistance, not pathological. But pathological insulin resistance applies to Dr Davis' post. Carbs cause this at some threshold.

@Martin:  I think you'll find Paul's article I linked to above (now published) rather interesting.

Martin Levac - do NOT expect miss sane to understand what you wrote - her mind is made up, and if anyone does not agree with her, they are wrong, wrong, WRONG, and  simply making assertions - as she endlessly asserts.

Hi Martin Levac and anyone still reading,
Thanx for the fuel partitioning orientation.   Maybe this elaboration will add to  your perceptions of fuel burning.

Lipids (a.k.a. fats, fatty acids) actively induce the metabolic mechanism to preferentially burn themselves ( technically speaking for researchers : dietary fat gene transcription factor PPAR downstream induces  the pyruvate dehuydrogenase kinase 4,  PDK-4; which then reduces the levels of the enzyme pyruvate dehydrogenase and thus restrict glucose burning).

Conversely, glucose triggers the mechanism to preferentially burn itself and by gene transcription stops lipid (fat)  burning (technically speaking for researchers:  insulin/glucose keep cell full of malonyl-CoA and this inhibits enzyme carnitine palmitoyl transferase, CPT;  fat can not get  shunted into the mitochondria fro burning). "Hysteresis"  ( explained previously and admittedly poorly)  is how there is chromosome threshold set up for controlling switching to burning one fuel vs. a different fuel;  potential to burn multiple fuels is not the same as getting to chose which fuel to burn.

Insulin, and not just glucose, boosts glucose burning (glycolysis) and stymies fat burning (lipolysis); yet not all tissue groups have the same insulin sensitiviy. This is additionally relevant,  since say +/-  half of glucose is used by us without any involvement of insulin.

Age is worth some precise discussion, especially since Type II diabetes is sometimes likened to advanced metabolic aging. With age the use of glucose for burning as energy increases, relative to the burning of fat & protein. This is notable in the heart, liver and brain;  while in the muscles the burning of glucose does relatively decrease compared to one's youth, but the burning of fat & protein decreases proportionately even more so.  In other words, post-prandial glucose favors burning glucose and due to hysteresis the mitochondria stay keyed to burn glucose;  even after the glucose levels drop back down to the pre-meal glucose level.

Again, age and genetic obesity,  engender a decrease in leptin hormone response  (technically speaking for researchers: there is less hypothalmic alpha melanocyte stimulating hormone being made by  POMC,  pro-oipo-melanocortin). The increased glucose burning  generates more age related metabolic problems, such as obesity;  and  so, what we did in our youth is not always what we can  do  with impunity.

When diet  relatively limits carbohydrates this  sets  the "hysteresis" threshold for mostly burning lipids (&/or protein) in the mitochondrial complex II;  this, however, does not mean glucose is not used as some fuel somewhere.  When blood glucose is low the atoms of Carbon from glucose burned  aren't burned in the mitochondrial complex I (technically:  don't make NADH from glycolysis); but rather, that glucose Carbon is put into the Pentose Pathway (technically:  makes NADPH ).

Age is notorious for oxidative stress  (oxygen radicals on the loose in cells) and having low glutathione  (key anti-oxidant our cells make); glutathione, for it's part get's it's oxidant reducing power from the pentose pathway's NADPH.  Age commonly expresses less of the enzymes  that drive the production of  glutathione  (researchers:  age depletes isocitrate de-hydrogenase, the enzyme  needed for mitochondria to make NADPH  via NAP-   which interacts with glucose-6-phosphate dehydrogenase, the  rate limiting enzyme needing to be upregulated to keep the pentose pathway going).  

In other words, age reduces our alternate pathway of glucose burning  and we get more oxidative stress  from using mitochondria complex I  for glycolysis;  mitochondria complex I burning for energy naturally spins off more  amounts of reactive oxygen molecules, these  can go on to potentially damage a cell.  A relevant example is that the shuttling of NAD+ to NADH from glucose burning in the mitochondria complex I has a potential oxidative  impact on the pancreatic Beta cells reaction over time;  youth and genetic fortune can keep cellular glutathione levels high to counter-act this Beta cell oxidative stress.

Low blood sugar, like hypo-glycemia,  upregulates  some cell's  gene activator of GLUT 1  (glucose transporters in a cell);  this indicates the carbon atoms from glucose are not being burned in mitochondrial complex I (ie: not doing glycolysis),  but rather the pentose pathway is burning the sparse glucose.  At this point a high enough threshold has been reached to switch OFF mitochondial complex I glycolysis and the body is switching ON to use mitochondrial complex II for getting  energy by burning  fat (researchers: Beta-oxidation has prepped lipid carbon atoms to burn ) .

@Might-o'chondri-AL

Thanks for the explanation. But I must admit that I will probably forget most of it pretty soon. I prefer to stick to simpler concepts. For example, heavy exercise depletes glycogen, which must be replenished. Cells open up more insulin receptors for this, they become insulin sensitive. If we don't eat carbs, this is done only as fast as the liver can put out glucose. If we eat carbs it's done as quickly as the carbs we eat. Considering that we can't store much more than about 2,000kcals of glycogen, mostly in the liver anyway, this is done _very_ quickly, a few minutes at most probably. As soon as that's done, cells close down their insulin receptors, they become insulin resistant. I'm just explaining what I understand, not necessarily how it really works. Anyway, as Taubes said, this effect lasts 36 hours at best, less if we eat carbs. So we could use this to prevent weight gain, but only if we don't eat carbs or not that much.

The weight gain can be explained by the shunting of glucose toward fat cells because all other cells are now insulin resistant since they are now replete with glycogen. Even if we believe that all cells will start using glucose for fuel instead of fat when we eat carbs, we still have to explain how the insulin receptors will be opened up when the cells are already replete with glycogen, and don't want to take in any more glucose. So basically, when we eat carbs all the time, we're not dealing with the choice of glucose/fatty acids in all cells, but only in fat cells. Because only fat cells now accept glucose. Then we end up with the associated problems Dr Davis talked about like higher estrogen and prolactin to name a few.

Does that fit in with what you know?

Erectile dysfunction relation carbs,  a re-constructed lost comment ....

Burning carbs (glycolysis)  for energy in the mitochondrial complex I  incurs super-oxide anions ( O2-) as  NADH generated .   Age  sees these super-oxides  anion levels increase and this can add &/or provoke pathological damage to the endothelial  vascular bed (for researchers: super-oxide locks up nitric oxide in the form of per-oxy-nitride); O2- + NO = ONOO-).

Once endothelial dysfunction is going on the extra cellular anti-oxidant SOD (super oxide dismutase) is decreased and this compounds the situation;  little super-oxide (O2-) gets scavenged and nitric oxide (NO) gets degraded even more. NO is the main signal gas for penile erection;  NO is a downstream vasodilator allowing the extra 50 - 90 mmHg blood pressure to get into the penis.

NO (nitric oxide  and nitric oxide  synthesase , NOS) works through a heme iron protein in hemoglobin  (researchers: via enzyme  heme oxygenase, due to NO affinity for FeII-heme protein) to act downstream on another enzyme (researchers: guanylate cyclase) to induce  a "second messenger"  inside the blood vessel's smooth muscle cells to relax and open. The "second messenger"  downstream from NO is the same molecule (researchers:  cyclic guanosine mono-phosphate, cGMP) targeted by Viagra; the drug works by stopping that "second messenger" from  degrading and thus vaso-dilation sustains erection.

In the male genital endothelium there are the  heme enzymes for NO to work through;  although with progression of  endothelial dysfunction  the NO is  less free, and more so if  always burning glucose in the mitochondrial complex I and spinning off oxygen radical (super-oxide, O2-) to tie up the NO  .  The erection's  status  is complicated by the fact that the "second messenger" (cGMP) that works to relax/vaso-dilate blood down there
is subject to degradation by another enzyme (researchers: phopho-di-esterase 5, PDE).

There is yet another key enzyme (researchers: soluble guanylyl cyclase,  sGC) that is part of the cascade leading from NO to the "second messenger" (cGMP) that normally keeps the levels of the "second messenger" (cGMP) degrading enzyme (PDE-5) from getting too high. Of course, with endothelial dysfunction and less NO involved in the erectile
cascade  there is less potential  ( less sGC)  to keep degradation enzyme (PDE-5) from knocking out the vaso-dilation;  then calcium rises inside the  blood vessel's smooth muscle cells,  less blood flows in and instead starts to flow out.

There is a parallel/back-up signalling gas produced in the endothelium for signalling; this is CO gas, it has a feedback  loop with NO gas and can entrain a cascade that also, downstream, produces the "second messenger" (cGMP) for vaso-dilation induced erection.  The draw back is , that,  CO has 1,500 times less affinity than NO for the early step of  connecting  with  iron heme in our hemoglobin; and, not only that ,  but CO will move off of the heme slower than NO would.

Using CO to drive the cascade  leading to downstream vaso-dilation  is  essentially  just plain slow in real time; and then too,  not enough of the intermediate enzyme (sGC)  that prevents degradation enzyme (PDE-5) is being made fast enough .  An  initial erection can be achieved in many instances through the agencies of CO &/or through a sequence of a little NO passing job on to CO;  unfortunately this erection fades and then can not be regained in a timely manner.

@Mito:  A loss of hepatic fat in a very short term carb restriction is a bit of a stretch to imply the reverse that carbs cause the fat accumulation per se.   There's also the problem with conflating hepatic fat with visceral fat.  Even all visceral fat doesn't appear to be the same - e.g. omental vs. retroperitoneal.

Oops hit post while a part of reply was highlighted so it got truncated.  Sorry so abrupt.  I believe this "reverse logic" is rampant and unfortunately used all too often to support certain contentions.  For example just because many lose weight cutting carbs doesn't make carbs fattening.  

I also added to that last sentence:  So many studies further confuse the subject because some show it's visceral, some subQ abdominal, some both, some none wrt various metabolic factors.

@Carb Sane

Yes, this "reverse logic" is rampant. But we call it "implication". Like so "this evidence implies that conclusion". Science is full of such "reverse logic". And, it's proof that scientists use their brains to figure out how things work. It also helps scientists devise tests to refute those implied conclusions. That's also how science works.

Incidentally, for the subject we're discussing here, there is _direct_ evidence that carbs cause excess fat accumulation. No need to refer to the previous evidence, or the previous implications, or the previous conclusions. In fact, there's about 150 years of it.

Now you're attempting to bring confusion yourself by pointing out how different fat tissue respond differently. We already know about that. It does not refute anything Dr Davis said about carbs. Carbs still cause excess fat accumulation, and all the other nasty stuff he mentioned.

Hi CarbSane,
Read me clearly:  I don't write that a carb automatically  always causes an iota of body fat;  and  I don't give a pass to dietary fat.    Doc, unlike me, has  a clinical practice to base his declarations on;  I am merely trying to understand any science that might validate his point(s).

Denmark " Inter99 Study"  of 3,164 adults with normal glucose tolerance tracked over 5 years data is interpreted in journal "Diabetic Medicine",, April 2009, vol. 26, issue 4, pg. 377-383.  Synopsis is:  2 hour post glucose (2hrPG; using oral glucose tolerance test as the glucose load) has  a relationship to overall degree of obesity; whereas fasting blood sugar has more of a relationship to larger abdominal/waist circumference.    

Doc's contention is carbs can raise the blood glucose and this contributes to getting fat;  which (2hrPG) the Inter99 study links to % obesity.   One  can argue  the issue from another direction;  namely that incipient obese fat, from any number of assorted causes  (ie: not carb induced) can , down the line,  cause the situation whereby 2hrPG ( blood sugar response) then goes on to predict waist circumference and BMI.

Omental adipose tissue is  considered as part of the  regulatory loop  of insulin sensitivity.  One of the causes of lipids (fatty acids, fats) going into the omental adipose cells (and liver cells) is when sub-cutaneous fat can't hold all the lipids presented to it (sub-cutaneous fat).

Size matters too, since large adipocytes produce more pro-inflammatory cytokines;  thus,  an individual with  factors  limiting pre-adipocytes from differentiating into functional adipocytes  is at risk of pumping up their  existing adipocytes.  This  is one way dietary excess  is modified by the metabolic coping  of each individual;  in other words not every obese person  is going to get Type II diabetes.

Omental macrophages, and their cytokines, are associated with greater liver inflammation; and an altered pattern of  fibrosis in the liver.  The omental macrophage risk to the liver exists even if there is no insulin resistance;  ie:   not only Type II diabetics but the obese  can have  liver risks.

Real men avoid grains (lectins, gluten, anti-nutrients), that's for sure. But that does not mean that they have to avoid all carbohydrates. Especially starches and glucose are, when cosumed in correspondence with your lifestyle, tolerated perfectly by the human body. It's time to get more specific doctor Davis. We cannot just keep advocating GCBC. VBR Hans

Martin, Dr. Davis made the specific assertion that carbs cause visceral fat accumulation (implied to a greater degree than fats or protein).  Where's the evidence for that?  Eating leads to fatty acids moving into fat cells and getting deposited.  That's not "fat accumulation" though.  Accumulation involves net deposition vs. mobilization and that is determined by how much carb, fat and protein someone consumes.   The statement "Carbs still cause excess fat accumulation, and all the other nasty stuff he mentioned." is unsubstantiated.  It is repeated over and over in the low carb echo chamber, but there's no evidence for it.

What has happened?!?  This comment section is ridiculous!  You trolls need your own site or forum to go nuts on and bash Dr. Davis there.  Or better yet, meet each other somewhere, throw your weight around in person, and claim your position as the smartest person in the world.

Hi Dr. Davis,

what is happening? No new post lately. On vacation? Sick? Tired?
I miss your musings and posts!
Cheers,
Renfrew

All - I think we should periodically go back to how our particular bodies evolved ..... (e.g Why/How do bears get fat before the winter).  Single season - meaning only available once per year - items are typically high in Carbs... Berries, Fruits, Roots, etc... Green leafy veggies are low in carbs... Grains from grasses are once per year.... highly processes they are acres of starch to our army of enzimes and produce huge insulin response... even Bears never had the availablity of wheat flour... otherwise they would have gotten fat enough, soon enough without having to go up and down all those mountain slopes looking for huckleberries and ants....

Man ... as usual ... is very efficient at what he does.....

You're an idiot and a charlatan.

Because on that list potatoes are pretty much the only thing listed that is actually bad and you probably burn more calories than you take in.

Anyone have any experience using krill oil, and how does it compare to fish oil?

As for other forms of omega-3s, isn't flax considered dangerous for men, due to ALA content? There are conflicting studies, but I recall at least one that said ALA caused a rise in the rate or prostate cancer.

Is there any way for a vegetarian to replace fish oil and get the same benefits?

I am definitely down with the fact that Fish Oil is vastly superior to Flax Oil. I've seen quite a few people touting flax oil lately so I'm glad you put that to bed.

Question: You mention recommended doses of EPA and DHA for those with elevated triglycerides. Can you offer any guidance for supplement levels when triglycerides aren't an issue? IE a level for good preventative nutrition? I've looked around and recommendations are all over the shop.

Thanks.

I've read a few other articles about the differences between fish oil omega-3s and other sources, but this article spells it out very clearly about how those differences apply directly to heart disease. I'll be printing this one for my family. Thanks!

S

Vegetarian DHA is available. It is cultured from algae. That's where the fish get. EPA may be available now too.

zubin:

There are vegetarian DHA/EPA supplements made from algae.

Zubin, when I followed a vegetarian diet I was able to find DHA supplements derived from algae, but EPA is harder to come by.  V-Pure is the only one I found that contained both EPA and DHA.  The capsules are costly, but might be a good option for you if you aren't comfortable taking krill or fish oil.

Thanks all, I will look into the algae supplements!

As a newcomer to your blog please forgive me if this topic has been brought up before.
There is a scathing attack in an article by Ray Peat,a noted Biology professor, on the damaging effects of fish oil.
A few people have stopped taking fish oil after reading the article.
Can you please comment?
http://raypeat.com/articles/articles/fishoil.shtml

http://www.westonaprice.org/knowyourfats/essentialfattyaciddef.html
A Reply to Ray Peat
on Essential Fatty Acid Deficiency

By Mary G. Enig, PhD

Ray Peat, PhD, is an influential health writer who claims that there is no such thing as essential fatty acid (EFA) deficiency. According to Peat, the body can make its own EFAs; furthermore, he claims that EFAs in the body become rancid and therefore cause cancer.

Unfortunately, Peat does not understand the use of EFA by the human body. He is trained in hormone therapy and his training in fats and oils has been limited to misinformation as far as the polyunsaturated fats and oils are concerned.

Research on EFAs is voluminous and consistent: EFAs are types of fatty acids that the body cannot make, but must obtain from food. We do not make them because they exist in virtually all foods, and the body needs them only in small amounts. The body does make saturated and monounsaturated fatty acids because it needs these in large amounts and cannot count on getting all it needs from food.

There are two types of EFAs, those of the omega-6 family and those of the omega-3 family. The basic omega-6 fatty acid is called linoleic acid and it contains two double bonds. It is found in virtually all foods, but especially in nuts and seeds. The basic omega-3 fatty acid is called linolenic acid and it contains three double bonds. It is found in some grains (such as wheat) and nuts (such as walnuts) as well as in eggs, organ meats and fish if these animals are raised naturally, and in green vegetables if the plants are raised organically.

Essential fatty acids have two principal roles. The first is as a constituent of the cell membrane. Each cell in the body is surrounded by a membrane composed of billions of fatty acids. About half of these fatty acids are saturated or monounsaturated to provide stability to the membrane. The other half are polyunsaturated, mostly EFAs , which provide flexibility and participate in a number of biochemical processes. The other vital role for EFAs is as a precursor for prostaglandins or local tissue hormones, which control different physiological functions including inflammation and blood clotting.

Scientists have induced EFA deficiency in animals by feeding them fully hydrogenated coconut oil as their only fat. (Full hydrogenation gets rid of all the EFAs; coconut oil is used because it is the only fat that can be fully hydrogenated and still be soft enough to eat.) The animals developed dry coats and skin and slowly declined in health, dying prematurely. (Interestingly, representatives of the vegetable oil industry blame the health problems on coconut oil, not on fatty acid deficiency!)

In a situation of fatty acid deficiency, the body tries to compensate by producing a fatty acid called Mead acid out of the monounsaturated oleic acid. It is a 20-carbon fatty acid with three double bonds named after James Mead, a lipids researcher at the University of California at Los Angeles who first identified it. An elevated level of Mead acid in the body is a marker of EFA deficiency.

According to Peat, elevated levels of Mead acid constitute proof that your body can make EFAs. However, the Mead acid acts as a "filler" fatty acid that cannot serve the functions that the original EFA are needed for. Peat claims that Mead acid has a full spectrum of protective anti-inflammatory effects; however, the body cannot convert Mead acid into the elongated fatty acids that the body needs for making the various anti-inflammatory prostaglandins.

Peat also asserts that polyunsaturated fatty acids become rancid in our bodies. This is not true; the polyunsaturated fatty acids in our cell membranes go through different stages of controlled oxidation. To say that these fatty acids become "rancid" is misleading. Of course, EFAs can become rancid through high temperature processing and it is not healthy to consume these types of fats. But the EFAs that we take in through fresh, unprocessed food are not rancid and do not become rancid in the body. In small amounts, they are essential for good health. In large amounts, they can pose health problems which is why we need to avoid all the commercial vegetable oils containing high levels of polyunsaturates.

Peat’s reasoning has led him to claim that cod liver oil causes cancer because cod liver oil contains polyunsaturated fatty acids. Actually, the main fatty acid in cod liver oil is a monounsaturated fatty acid. The two main polyunsaturated fatty acids in cod liver oil are the elongated omega-3 fatty acids called EPA and DHA, which play many vital roles in the body and actually can help protect against cancer. Furthermore, cod liver oil is our best dietary source of vitamins A and D, which also protect us against cancer.

Actually, Peat’s argument that polyunsaturated fatty acids become harmful in the body and hence cause cancer simply does not make sense. It is impossible to avoid polyunsaturated fatty acids because they are in all foods.

EFAs are, however, harmful in large amounts and the many research papers cited by Peat showing immune problems, increased cancer and premature aging from feeding of polyunsaturates simply corroborate this fact. But Peat has taken studies indicating that large amounts of EFAs are bad for us (a now well-established fact) and used them to argue that we don’t need any at all.

Finally, it should be stressed that certain components of the diet actually reduce (but do not eliminate) our requirements for EFAs. The main one is saturated fatty acids which help us conserve EFAs and put them in the tissues where they belong. Some studies indicate that vitamin B6 can ameliorate the problems caused by EFA deficiency, possibly by helping us use them more efficiently.

About the Author
Mary G. Enig, PhDMary G. Enig, PhD is an expert of international renown in the field of lipid biochemistry. She has headed a number of studies on the content and effects of trans fatty acids in America and Israel, and has successfully challenged government assertions that dietary animal fat causes cancer and heart disease. Recent scientific and media attention on the possible adverse health effects of trans fatty acids has brought increased attention to her work. She is a licensed nutritionist, certified by the Certification Board for Nutrition Specialists, a qualified expert witness, nutrition consultant to individuals, industry and state and federal governments, contributing editor to a number of scientific publications, Fellow of the American College of Nutrition and President of the Maryland Nutritionists Association. She is the author of over 60 technical papers and presentations, as well as a popular lecturer. Dr. Enig is currently working on the exploratory development of an adjunct therapy for AIDS using complete medium chain saturated fatty acids from whole foods. She is Vice-President of the Weston A Price Foundation and Scientific Editor of Wise Traditions as well as the author of Know Your Fats: The Complete Primer for Understanding the Nutrition of Fats, Oils, and Cholesterol, Bethesda Press, May 2000. She is the mother of three healthy children brought up on whole foods including butter, cream, eggs and meat.

IMPORTANT CORRECTION

In the Winter 2004 "Know Your Fats" column we stated that Siberian pinenut oil was a good source of gamma-linolenic acid (GLA). This was indicated from fatty acid analyses performed in Siberia. We have since performed further tests on the oil and found that it does not contain significant amounts of GLA but rather a fatty acid called pinoleic acid, an 18-carbon fatty acid with three double bonds but with the first double bond on the fifth carbon, not the sixth, as in GLA. We are sorry for any inconvenience this may have caused.

http://www.westonaprice.org/knowyourfats/essentialfattyaciddef.html

I'm a 57 year old grandma and have been vegan for over 6 years. I've run 3 marathons since turning 50, but took at 18 month hiatus to care for a grandson.  I was slowly trying to get back into running by starting out with 20 min. jogs and 3 minutes of jumping rope. Last October I developed painful tendinitis in my knee...my M.D. encouraged me to try O.T.C. painkillers (aspirin, acetaminophen, and ibuprofen) and take glucosamine all to no avail...he sent me to a physical therapist who gave me a few exercises said I shouldn't run at all, ever...that he quit running at age 30 and advises walking only. At that point my doctor wanted to prescribe some NSAID and give me a 2nd prescription for something that would allow my stomach to handle the prescription NSAID.   Without my M.D.'s recommendation I went to an acupuncturist for 3 months...no luck there.  Then a few months ago, again without my M.D.'s referral, I went to a chiropractor.  Since I was vegan, he prescribed flax oil, which seemed to help only a little, although the chiropractor said he really thought I would benefit the most from fish liver oil. Yesterday, in desperation, I took fish oil and felt much better.  I'm not pain free yet...but the improvement was quite dramatic.  I'll have to see how it goes.  I was vegan for personal, ethical reasons as opposed to health concerns...so even though this is a bit of a disappointment for me and my veganism...I think I will continue to use the fish oil and see if I benefit further.  By the way I had been taking vegan DHA for years from either "Omega Zen" or "Deva". Many, many years ago I heard that the playwright George Bernard Shaw had to take liver for a B-12 deficiency.  As the story goes someone said to him, "Is that liver you're eating...I thought you were a vegetarian."  Shaw replied "I am, this is my medicine."

Ah, This is exactly what I was looking for! Clears up
a few misnomers I've read

Dr. Goldstrich has proven especially adept at understanding how to incorporate new findings from clinical studies in our framework of coronary atherosclerotic plaque management strategies.

I have heard about acai berries and acai berry supplements containing sufficient Omega 3. I found out about this while I was looking for great alternatives for kids. Because for sure, they don't like fish oil supplements as they are huge and smelly, but I also believe they need the Omega 3 and all the good it brings. I found out about acai berry powder with Omega 3. I admit I am almost convinced.

I just finished cringing at today's Today Show w/Dr. Nancy S., and ran to see what you'd have to say.  Thank you for saying what you did (my LDL is higher than expected range and my Lp(a) is low).  I've watched and cringed before though (Gardisil vaccine for one): she touts mainstream's mantra, and is a great messenger/advertiser (subtle and not-so-subtle) for GE, parent company of NBC and maker of CT scanners.

I am so disappointed with Dr. Snyderman... she seems like such a nice woman. I think the interview was like a piece of Swiss cheese... full of holes (of information).  She has heart disease "because she ate too many cheeseburgers as a teenager"? Oh really...

It's been two years (!) since her CTA and she's not had symptoms like shortness of breath, so therefore she's better???  Oh, that's right... she's on a statin and eating better, so naturally she's better.  No proof there, but she's better...

OMG, how can such a bright woman, and a physician, too,  face her coronary artery disease with the equivalent of blinders and an eye patch?

It is tragic enough that her heart disease most likely has progressed with this standard treatment, but she also has a wide following who trust her advice... and they will likely think what she is doing is enough to reverse (and she did use the word "reverse") this type of heart disease!  It isn't enough, and she gave inadequate and poorly informed advice to millions of people. What a shame... a real opportunity missed.

So while Nancy Snyderman, M.D. is smiling, downing a statin, and wearing a Red Dress on Friday... I will be employing a host of TYP strategies ... and scheduling my next advanced lipoprofile analysis!  Real knowledge is powerful!

Thank you for Track Your Plaque and your spot on Blog, Dr. Davis!

madcook

She's obviously not much of a medical correspondant.  If she were, she would dig up the data showing statins provide no benefit to women.

She's probably right about blaming the cheeseburgers she ate as a teenager, but for different reasons.  It's the white flour buns, not the meat & cheese.

Speaking of heart scans, here's a negative article about them put out on today's NaturalNews.com newsletter: http://www.naturalnews.com/025535.html

It's frustrating, because NaturalNews.com has at least some good info (it's a real mixed bag), and a lot of people follow the stuff put out by that site. How many people are going to get turned off to CT scans because of this article, and suffer drastic results because of it?

David

Hi, David--

While I'm glad that the media is highlighting the excessive exposure of CT coronary angiograms, they are confusing these high-radiation tests with low-radiation heart scans.

We can only continue to try and educate everyone, including the media, on the important differences.

Well, in all fairness they do point out in the NaturalNews article that they're referring to the CT angiograms, but it still seems a bit misleading because they never really mention it in contrast to the safer, lower radiation scan. So it's likely that anyone reading that article without a trained eye will simply lump all CT scans together and write them all off as unsafe. It's unfortunate.