Hi Dr. Davis.
I’m actually both pleased and troubled with the link to Dr. Diamond’s presentation that you’ve provided.

On the “pleased” side, Dr. Diamond’s analysis is:
•  An excellent/very well done presentation
•  Fact based (e.g. cites numerous studies, documented references, named experts, etc.)
•  Spans the test of time (e.g. references from the 1800’s thru the present day)
•  Ferrets out the major drivers of our present-day obesity epidemic & debunks other commonly held beliefs
•  Synchs with some of the Track Your Plaque (TYP) tenants (e.g. TYP guidance on triglycerides, diet, sugars, etc.)
•  â€œFlags” potential issues like conflict of interest which might have a tendency to creep into the science on occasion (e.g. the Keys report, the errant conclusions resulting from the NCEP report and supporting studies, etc.)

On the “troubled” side, Dr. Diamond’s analysis seems to:
•  Fly in the face of some of the foundational tenants of TYP
•  His analysis/conclusions, and that of other experts he cites, is that cholesterol of any kind is NOT correlated with Coronary Heart Disease (CHD) – at least as a root cause of heart disease (see Myth #2 and Dr. Diamond’s related analysis)
•  That LDL cholesterol – and although not stated by Dr. Diamond I’m inferring – the “sticky kind”, i.e. the small particles that actually adhere to artery walls (not the fluffy LDL particles that bounce away), are actually good!! On his “Final Issues 2” slide, and later in his related pictorial slides (entitled “What Causes Coronary Heart Disease?”), he makes reference to [LDL] cholesterol as a “Misunderstood Hero”?
•  That small, sticky LDL particles actually help the body recover from the damage created by the real culprits… sugars that work in concert with certain bacterias to create micro-tears in our artery walls
•  That small, sticky LDL actually results in the belt-and-suspenders, Rube-Goldberg “spackle” [which again I infer from Dr. Diamond’s presentation ultimately becomes plaque], that fixes (admittedly in a suboptimal and too-late manner) the damage already done by the artery-tearing, sugar/bacteria combo.  Plaque caused by LDL is actually the ‘finger in the dike’, last ditch effort, to fix the artery tears!  Kind of the last line of defense. [see slides on page 53 and Dr. Diamond’s related YouTube discussion.]

As a result, just curious about your thoughts on Dr. Diamond’s hypotheses.  
1.  Am I getting Dr. Diamond’s message(s) right?
2.  If yes, do you concur with – or tend toward – the theory(-ies) supported by Dr. Diamond and other cited experts about the role of cholesterol in CHD?  I gather from your blog post that you sympathize with his glycation theory(-ies), but how about the rest?
3.  If yes again, does that change some of the TYP direction?  For example, a significant part of the TYP approach is to reduce, as much as possible, small LDL particles. If LDL – and thus the resulting plaque – is indeed a suboptimal last line of defense, does reduction of LDL particles lead to a sub-optimization of the body’s last-ditch defense/“back-up plan” to deal with arterial microtears?
4.  Also, knowing that plaque/“spackle” is admittedly a suboptimal last ditch effort, what consequence does reversing plaque ultimately have given that the real damage – the tears in the artery walls (the seemingly real CHD culprits) – has already occurred. Are we pulling the finger out of the dike… without addressing the real root cause of the problem?  â€¦and if yes, what’s the back-up plan to the body’s back-up plan? If we reduce LDL and plaque, and the arterial damage is already done due to years and years of sugar abuse, what plugs the dike then?  I’m not talking about the preventive approaches of avoiding glycation in the first place… obviously that seems to be the real, preventive answer. I’m referring to those of us – for whom preventative measures are too late because the microtears are already there – who might be already living with the consequences of years of potentially errant diet/health guidance (by Keys, NCEP, etc.) and thus “spackle” in our arteries?  If the "spackle" is removed, does the dike start leaking again?

Although I thought I was “on the path to CHD righteousness”, I’m now confused again as a result of Dr. Diamond’s insights. Thanks for any clarifications Dr. Davis!

Dr. Davis,
I'm also anxious to hear what you think of the "hero" role of LDL in plaque.  I'm hoping he didn't go too far off the reservation on this point because the entire hour long presentation was so well done (comprehensive, well-explained, and credentialed) that it will be a powerful aid in spreading the word on both carbohydrates and how messed up the typical GP is with cholesterol treatment (not their fault - but the ATP-III as you say).  It was the tipping point for me.  I'm going off Lipitor now, which I"ve been on for years and will look into your TYP program to ensure I'm doing the right thing.

HI, Joe--

This "hero" thing, to my knowledge, is extrapolation and supposition. It is an interesting notion. I, too, was impressed with his presentation, but I think that the "hero" thing paints LDL as an entirely innocent player and I don't believe it is. We have only to look at people with heterozygous familial hypercholesterolemia who can have heart attacks in their 30s with pure large LDL to know that there is more to LDL's behavior than a protective function.

Hi, G--

By providing the link to Dr. Diamond's wonderful talk, I didn't mean to suggest that everything he says should be taken as gospel.

Virtually everything he said up until the "spackle" I do agree with. The spackle argument is pure supposition. It makes sense, but only to a degree and ignores the quantitative (e.g., heterozygous familial hypercholesterolemia) and qualitative (small, oxidation- and glycation-prone LDL particles with unique conformations that differ from larger LDL) differences in LDL particles.

Nonetheless, Dr. Diamond's recounting of how this mess was created was enlightening and well-presented and I still enjoyed it.

Dr. Davis,

I watched Dr. Diamond's presentation in its entirety.  I agree that he's done some great investigative medicine, especially looking into long-established research on carbohydrate intake, and, more recently, digging into questions of research funding and conflicts of interest.

His presentation leaves me with a major question about the role of cholesterol.  Diamond claims that high cholesterol levels are not harmful, so long as they are below 300 mg/dL, and that cholesterol has a helpful role.  It is used by arteries to repair themselves after the arterial lining is torn, infected by bacteria, or otherwise damaged.  This is why, he says, we find cholesterol in atherosclerotic plaques, together with white blood cells and dead bacteria.  Yet, we know from your reports and others that an elevated LDL particle number *is* correlated with coronary events.

What's going on here?  Is cholesterol itself harmful, or is high particle number just another symptom of high carbohydrate intake, which causes glycation and loss of elasticity in the arterial walls, leading to damage?

I just read the other comments, so the above question has been answered.  Thanks for all the info!

Hi Brian--
While I truly enjoyed Dr. Diamond's presentation, I think this particular path leads us down a dead end.

I don't think cholesterol per se is harmful; I believe that the particles that contain, among many other things, cholesterol can be harmful, especially small, oxidation-prone, glycation-prone LDL particles. I believe it would be an incredible stretch to say that small LDL particles are somehow protective.

I have inherited cholesterol and just learned from my health store guy that all the grains I have been eating are likely responsible for the high numbers of my small LDL(527) particles.  I thought oatmeal and other whole grains would squeege-mop the bad guys out of my system.  This news is also likely why I haven't  lost any weight (I eat lots of veggies and apples, fibrous fruits and protein.)  I do not use processed foods at all.  I walk a mile to work each day and I am still 10-20 # overweight (and yes it is right in my middle.)  My health guy is the one who directed me to this blog.  Any other information is most welcome.  I am trying to figure out what to fix everyday (supper/dinner) is the hardest.
Joan phillips

Doc Davis,

Thank you for all of your generosity and energy.  You've 50 posts on fish oil and 84 or vit D.

I'm sending people to your site, but sometimes they're overwhelmed.

Since these seem very important topics to you, would it be possible to summarize them in a definitive, proscriptive pair of posts.

Thank you,

DG

Spino-cerebellar Ataxia (SCA) researchers claim to be associated with 28 (29?) variations of gene positions (loci) on human chromosomes; with gene mutations in 17 of those loci. Hereditary neuro-degeneration becomes clinicaly symptomatic in due time, not neccessarily when young.

Gluten/gliadin responders who make anti-bodies to tissue trans-glutamin-ase (enzyme) have this anti-body implicated in ataxia syndrome. Spino-cerebellar ataxia is a category encompassing more than stumbling (SCA clinically includes psychiatric symptoms, etc.).

Serum from humans with ataxia and the tissue trans-glutaminase anti-bodies was injected into normal mice, and the mice temporarily got ataxia. And then serum from humans who did not have ataxia, but did have tissue trans-glutaminase anti-bodies (ie: gluten sensitive)injected into normal mice also gave the mice temporary ataxia. In other words the gluten anti-bodies, irregardless of person having pre-existing ataxia or not, were enough to trigger ataxia in the mice.

Doc cites study with average age of 48 as development of ataxia; this is explainable as fitting classic pattern of genetic neuro-degeneration. What I do like about Doc's linkage is the  concept that the gluten/gliadin anti-bodies may be a trigger of some sort.

As for people "without positive celiac anti-bodies" who get spino-cerebellar ataxia (including any SCA associated symptoms)at the study's average age of 48 I am  skeptical. "Idiopathic" anything is a fancy way of saying something just so happens to be; as in patient Q has idiopathic XYZ and nobody knows for sure why, it just is XYZ.

Doc has me thinking that if SCA genetic tendencies occur in an individual along with sensitive gluten genetics then cutting out the one risk factor controllable makes sense. Since genetic tests for SCA isn't readily done the no gluten tactic had to be tried out, and Doc seemingly noticed a % of encouraging results.

Hi, DG--

Point taken.

Perhaps a "Best of the Heart Scan Blog" would be in order.

Thanks for the excellent suggestion.

Hi, Mighto-o,

You've got some wonderfully unique insights.

I'd like to see more of your ideas chronicled. Are you blogging or writing in some form?

Recently there have cases of four people in the TV entertainment/news on air business that for some reason start speaking in gibberish...the latest being Judge Judy.
http://vigilantcitizen.com/latestnews/judge-judy-the-4th-to-talk-gibberish-on-air/

Do you suspect we may be seeing some brain atrophy from consumption of wheat?  I wonder how many times this may happen to ordinary people and they don't seek medical help because it passes.

Hi Dr. Davis,
I am not qualified to practise medicine, nor claim to be a true
expert on things I discuss. Most of my work has been in developing countrys, which challenged my perspective and what pick-up on.

The only other blog I read (and comment)is Whole Health Source.
No personal blog or publication until another 1/4 century proves my advice worthwhile.

How can it prove, if there is absence of digital forms ?
You should express your thought, definitely, in whatever form.
Bring open source to medicine !

Cheers.

Hi, Dextery--

Interesting thought.

Making the connection between wheat/gluten consumption and a neurological syndrome can be tricky. The most confident means to establish probable cause-effect is brain biopsy or autopsy. Most people would not submit to such things, so we rely on indirect measures like HLA DQ genetic markers and the reversal of the syndrome with elimination of wheat and gluten.


Might-o--

Well then, keep your wonderful insights coming!

"Recently there have cases of four people in the TV entertainment/news on air business that for some reason start speaking in gibberish...the latest being Judge Judy.
http://vigilantcitizen.com/latestnews/judge-judy-the-4th-to-talk-gibberish-on-air/"

Some of my more paranoid friends think this is from "EMF mind control experiments" being performed by our govt, NSA, CIA, etc.

Geoffrey

well that certainly proves brain atrophy, if not in those 4 tv anchors but somewhat in your friends!!



PS

While there is more to wheat's adverse effects on human health than celiac disease, studying celiac disease provides important insights into why and how wheat--the gluten component of wheat, in this case--is so destructive to human health.

Disheartening, but facts are facts.  It's somewhat mind-boggling to fathom how much wheat is consumer everyday, and the amount of adverse effects that can inflicted among the population.  The best thing is to stay informed-It should be a priority for everyone to understand at least fairly well what we are ingesting daily.

It saddens me that a gluten-free diet for six weeks isn't recommend for a whole host gastrointestingal, neurological, and automimmune diseases. Celiac markers are just numbers. Exclude gluten from the diet and see if there is improvement. That's the best way to assess wheat's role.

Hi Mitochonri'Al!

I love your commentaries!  Anyway, just wondering, a hypothesis of mine, given your citation about the human blood serum and mice experiment above, can trans-glutiminase anti-bodies be present in grain-fed meat and dairy products (pasteurized)?  Would that be another argument in favor of grass-fed beef and dairy (and the raw dairy of that group, if wanted)?

Just a hypothesis, as i notice a lot of people that eat very low carbs to zero carb paleo eating start to have issues that are arthritic and ataxiatic (sic) and conditions that seem neurologic (incontinence, lower back pains, and other inflammatory issues) even from heavy whipping cream consumption.  And anecdotal journals, they tell of self-experimentation with and without dairy, and the pains depart, return and then depart again almost to a tee...

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Dr. Davis,

Can someone have a good HbA1c but still have an undesirable amount of small particle LDL? ..Like perhaps someone with FHC that has their LDL particles floating around longer in the bloodstream and hence exposed longer to oxidants.

Thank you.

John M.

I love your blog but I have to clarify on this point. Check out the post by chris kresser: http://chriskresser.com/blog/why-hemoglobin-a1c-is-not-a-reliable-marker/

a1c is not reliable for many people because of the variation in RBC life length. healthy people's red blood cells may live as over 4 months whereas diabetic's live only as 60 days. This results in vast discrepancies.

For example my fasting BG averages 77 and postprandial peak is 85-90, but my hemoglobin A1c is 5.7

This doesn't make sense unless you account for differences in RBC lifetime.

I'm wondering what your opinion is of glycation and aging.

I've been reading that a major part of the aging process might be caused by glycation of proteins in the body, mostly caused by elevated blood sugar.

Do you believe that practically, one could expect a longer life expectancy to correlate with lower blood sugar levels?

The other day on the tv show, "The Doctors", they profiled a young woman concerned about her FBG.
She said that Diabetes ran in her family.
They did a bloodtest and announced that her FBG was 111.
The scary part was when they told her that reading was okay.
With that FBG, one can assume that everytime she eats, her post-prandial FBG is heading into dangerous territory.
But they told her not to worry.
She was right about her concern...as Diabetes will continue to run in her family.
Especially with that advice.

I found Walmart carries a Bayer at home A1c test kit that gives results in 5 minutes.  It came with two test cartridges so I was able to take one when I started lowcarb and another one 4 months later to see how much it came down.  (I came down from 8.3 to 5.2 in 4 months)

What is HbA1c for those long-lived okinawans with their rice-based diet, or those long-lived cretans with their wheat-based diet?

Wouldn't a lean healthy body (especially if there is occasional fasting) eventually clean up glycated and otherwise damaged proteins?

Glycation picks on the amino acid valine "wing" on the molecule of haemoglobin's B-chain portion. Aldehydes, both glucose aldehydes and non-glucose ones can become bound to that valine.

This can occur several ways. Glucose oxidation yields a byproduct, called gly-oxal; this is what most people monitor. In the glyco-lytic pathway called Embden-Meyerhof triose-phosphate drives gly-oxal into the molecule methyl-glyoxal (MG).

Type 1 diabetics have circulating methyl-glyoxal (MG) levels that are +/- 6 times greater normal. MG is a glycation end product.

Tyler's comment links to a discussion of fructosamine monitoring. This is from a non-enzyme driven reaction, called Amadori, where fructo-selysine and the fructos-amine 3 kinase cascade generates 3 De-oxy-glucos-ane (3DG); another glycation end product.

Enzymatic glycation occurs in pathological states. Macrophage activity spins off  the enzyme myelo-peroxidase; this generates hypo-chlorite. Hypo-chlorite pulls in the amino acid serine and then together they cause the formation of certain advanced glycation end-products; namely glyco-aldehyde and glycer-aldehyde.

Yet another non-enzyme chain of events can generate advanced glycation end products. This is when the molecule per-oxy-nitrite (ONOO-)gets stalled inside the cell and it induces the formation of gly-oxal/gluco-sone/aldehyde molecules that can contribute to glycation.

ONOO- normally is part of healthy cell signaling. When a metabolic processes is under sustained "stress" it (ONOO-) can't shift the cell function over to what it (the cell) needs to do (in order to adapt and cope). Instead of briefly signalling, signing off and going away ONOO-
lingers in the cell; a situation that may also be related to ageing.

I wonder if Dr. Davis can comment on situations where carb intake is reasonable and the patient has a decent HBA1c, yet still has higher than normal triglycerides and small LDL?

My own HBA1c has been in the 4.5-4.6 range, yet my trigs hover around 140-150, and I still have more small LDL than I'd like.

If restricting carbs doesn't work, D levels normalized, etc. what else could be the cause of higher than optimal triglycerides?

I know people with HBA1cs in the 5.4+ range, eat many more carbs than I do, yet still have lower trig numbers.

Hi Revelo,
Vitis vinifera leaf inhibits advanced glycation end product (AGE) formation. That is what many cultures, like Crete, eat wrapped around their cereal grain; we call it Grape Leaves in English (ex: stuffed grape leaves, a.k.a. Dolma in Greek).

Japan researchers (2009?) took 1 kilogram of dried grape leaves in 20 liters of water and stirred it for 3 hours at 80*Celcius. They administered the decoction in various dosages and found it can reduce the AGE of 3DG (3 de-oxy-gluco-sone) and also a marker of AGE in kidney disease, pentosidine, down to 1/5th the level from that study's AGE control levels.

The same study experimented with Anthemis nobilis using the same extraction technique detailed above. They propose the active ingredient responsible for the AGE inhibition is the compound called chamaemoliside.

Chamomile is the name of this plant in English; I suspect it is drunk as a tea in Crete. In the range of AGE inhibitors that they tested Chamomile was better acting than any other; grape leaves efficacy came in second.

Plants studied that inhibit AGE forming, in no particular order of effectiveness may interest you. These are: Crataegus oxyacantha (English = Hawthorn berry), Houttuynia cordata (English = Chameleon plant) and Astragalus membranaceous (English = Astragalus). Chameleon plant is a regular condiment used in Vietnamese and some south-east asian food; it smells kind of "fishy".

According to Steven Gundry MD, it is MEAT which is the primary cause of AGE's. (He doesn't cite any references for this in his "Diet Evolution" book.) He recommends Atkin's style low-carb/high-protein to lose weight, then low-fat (15% of calories from fat) as the maintenance diet. He is not too keen on grains, tubers or fruit, but rather emphasizes green vegetables.

Thanks for the nice explanations Might-o'chondri-AL

Diabetic nephro-pathy (ie: kidney complication), and kidney disease have elevated AGE. These are monitored as pento-sidine, gly-oxal, methyl-gly-oxal and 3 de-oxy-gluco-sane; which the body tries to excrete as carbonyly compounds.

Carbonyl compounds are hard to get through the kidney filters and cause an increase in uric uremia, which can be toxic. Too many carbonyls can cause, the so called, "carbonyl stress" of diabetic nephro-pathy.

Diabetic patients' kidneys eventually can't excrete enough sodium (Na); and that contributes to the high blood pressure (hyper-tension) diabetics tend to suffer from.

Ketones merit mentioning too. One of the markers for AGE in the kidneys is N-carb-oxy-ethl-lysine; which may (or may not) be a side effect of ketones. Type 1 diabetics do show elevated ketone levels incidently.

I am not able to offer any perspective on ketogenic diets and AGE however. However, vitamin C is known to decrease ketone bodies. (In the previous post, "Battery acid ...", more
diabetic responses to vitamin C appears among the comments.)

I've been eating low-carb (basically paleo) for the last 4-5 mo and just got my lipid panel results.  They sky-rocketed.

Cholesterol 300
  
Triglyceride 150  
    
HDL          33
    
LDL             237


Every number got worse.  The part that really sucks, is that the diet makes me feel great and nearly all my body fat is gone.  I'm 37, 5'11, 180 lbs and probably about 9% body fat.  Now I'm wondering what kind of trade-off I'm making.  Any thoughts, doc?

Testing different foods one hour after meals, it seems like a good rule of thumb for me is that each ounce of carbs raises my blood sugar about 10 mg,and that the kind of carb doesn't matter nearly as much as the quantity.

Paradoxical low carb yet relatively high HbA1c & higher carb but relatively lower HbA1c is reported by Annon. Doc assuredly deals with cases like these and has to resolve their enigma one by one.  

The gene HFE (human hemochromatosis protein, nicknamed High Fe  where iron = Fe)can have a variation (reference code = HFE rs1800562). This variation is seen in +/- 5% of Caucasians, but is not found in East Asian nor African genes.

More hemoglobin is in circulation for those having this HFE genetic variation. In this case, the same amount of blood sugar that can contribute to glycation of hemoglobin has more hemoglobin surfaces to glycate. Think of it as the glycation has to spread itself thin; the dilution of it's effect makes the % of Hb1Ac less (ie: lower Hb1Ac % measured in the blood sample).

On the other hand, genetic variation rs855791 of the gene TMPRSS6 (trans-membrane protease, serine 6)is implicated in anemia. In these individuals Hb1Ac readings range higher; there is less hemoglobin relative to the glycation potential in their blood stream. Think of it as the relatively low proportion of hemoglobin which has to bear all the glycation burden
(ie: Hb1Ac % is higher in their blood sample).

Anemic (hemolytic) tendency is also driven by variation of gene HK1 (hexo-kinase 1). This enzyme modulates how glucose inside the cell goes through  it's processing pathways.

This gene (HK1) codes for the unique iso-form of erythrocytes; erythrocyte configuration can figure in to low hemoglobin. In other words it is also a factor in high Hb1Ac readings; glycation potential in the blood over burdens the limited amount of hemoglobin around.

In response to several questions about the potential disconnect between small LDL/triglycerides and HbA1c: Yes, there are people in which one measure is more resistant. It varies based on the mix of underlying genetic predispositions, so it's hard to generalize.


Might-o'-chondri-AL--

Great discussion. Thanks, as always. You bring an incredibly sophisticated perspective!

Jonathan--

Spectacular! And within an unusually brief timeline for HbA1c.


Revelo--

Might-o'chondri-AL is referring to endogenous glycation. You are citing a discussion about exogenous glycation, two separate phenomena.

Might Jenny's observation and Nigel's study reference be reconciled somewhat ? I'll tag on my disclaimer of being unqualified to judge low carb or specific diets; since I've never struggled with weight or diabetes, and am not a doctor.

The study Nigel linked was done with all Kuwaiti subjects. In that country co-sanguinity in marriage is practised by +/- 54.3 % of Kuwaitis. And 1 in 5 are reported to be diabetic.

The data is very admirable; my suggestion is that the data trend may not exactly transfer to a modern Caucasian population; which is essentially interbred from migration and war (rape). This may be why Jenny sees a +/- 6 month plateau among her respondents and the co-sanguine Kuwaitis saw changes continue for a year +.

Genetic poly-morphisms influence fasting glucose (GCK, G6PC2 and MTNR1B), are implicated in Hb1Ac, triglyceride levels, HDL levels & so on. That said, I personally would try the low carb approach if I was diabetic.

oops posted this in wrong thread

Re: Anonymous with Cholesterol 300,  Triglycerides 150,  HDL 33 ...

Suggest you try a technique many dieabetics find helpful to understand food consumption influence on their blood sugar profile,"eating to your meter".
For a few days, record your blood sugar level immediately before eating a "normal" meal, and then after the meal get 1-hour and 2-hour post-meal blood sugar readings. Separate meals by at least 4 hours. Concentrate on monitoring your main meals and ignore snacking for the first go around. Better however, if you can actually avoid all snaking during period of the testing. Also you will want to add to your journal the foods, ammount consumed, and time it was consumed. If post-meal blood sugar values are high, then to determine a pattern folllowing a meal do a series of hourly post-meal readings until you reach 85 mg/dL or so. As a graph, these results should be helpful to you. Expect that the results will be revealing to you with unexpected high blood sugar values even after following a paleo diet. And if so, it does mean that paleo is not for you, only that you need to more discriminating in what and how much you actually consume.

I would be interested in hearing about your findings. By the way, you did not mention the blood glucose or HbA1c results of your recent lab tests.

My regards and good luck ... spo

BTW: practice good technique with the finger sticks. Do a quick but good hand wash using soap and a warm water rinse prior to a stick. Dry hands well. Dont squeeze hard at the site to encourage blood flow. The original stick should be sufficent to raise a drop of blood for the test strip. Using alcohol swabs and changing out lancets is not necessry when only working on youtself. Keep the test strip vial tightly closed other then when removing the current test strip. If you encounter an "extreme" value, retest for confirmation but clean hands again prior to the retest. My experiences regarding unexpected readings seems to usually invovle hand and finger contamination of some form.

Finally, on Amazon.com I am able to purchase unexpired test strips in 50 strip lots for my old AcuCheK Confort Curve meter for less than $0.16 or so a strip and often with free shipping. You just have to broswe around a bit.

@ Anonymous with 300 TC
I would say it could possibly be your liver cleaning itself out (it could have been getting fatty).  The higher Trig might be a sign you are getting too many carbs from somewhere (at least till your sugar stores empty some and insulin sensitivity goes back up) but it could be the liver cleaning out as well.  I think HyperLipid posted something about this once.