Disgusting
I've got a big tolerance for stupidity. Even supersized-stupidity. Mostly this is because I am somewhat a bit of ding-dong myself. Luckily... my husband has not divorced me yet after realizing for the millionth time that I'm a complete retardo (and too late, the genes have been dispersed to our offspring *haa*). Recently I put my cellphone through the wash. Seriously.
So.
The stupidity over saturated fat nonsense and low cholesterol diets *sigh* are over the top lately indeed and require a rant. Some cardiologists appear to fear the 'large buoyant LDL' created by saturated fat. I don't get this. Don't our cells possess the biochem to burn our b*tt PHAT? Maybe scientists lack this gene??
Conventional docs aim at LDL which is clearly the wrong target. In the primal/ancestral/crossfit world, the aim is focused on dense LDL. Yes -- this is emphasized by Cordain. He was courageous to stop condemning saturated fat. Xfit nutri certs *big smile* reinforced hyperlipidemia.
Here, biochem tiger Peter deciphers the medical literature. The core of atherosclerotic plaque is made up of lipids, mainly glycolated ones and oxidized LDL (oxLDL).
OxLDL is Lp(a)...
* Lipoprotein (a) is oxLDL
* Statins raise oxLDL and Lp(a)
Mouth
Let me speak freely.
Saturated fat controls Lp(a). (HERE, HERE, Krauss and DELTA)
Low carb controls Lp(a). (HERE and Volek; insulin-Lp(a))
This translates to the control of atherosclerotic plaque and regression.
It doesn't matter what level of Lp(a) one has (remember, Hecht showed that disease is associated with levels of 2 to 200 mg/dl) -- Lp(a)/oxLDL is like a 'spark' when lit. What lights up Lp(a)??! OMG. Saturated Fat Deficiency and Insulin. Hyperlipidity fixes Lp(a) and regresses plaque -- let Big Pharma chew on that. Are they colluding to keep us 'low sat fat'? It's not difficult.
Again. The only quartile associated with regression in women in ERA was the high saturated fat quartile. Mozzafarian et al. This is what I observe as well in real life.
Niwamae et al analyzed biometrics in 203 patients with peripheral vascular disease using IVUS. Plaque morphology was also analyzed: soft, hard/calficifed and lipid cores.
Should you be scared of intimal flaps? Errr. Yeah. If I had plaque -- I'd prefer 4-digit calcifications with stable hard-cores, than 2-digit FLAPPY soft-core plaque. Plaque rupture has been highly associated with the presence of intimal flaps -- like a poorly treaded Firestone, they are ready to burst with collision with sticky highway rubbish or pounding speeds.
Intimal flaps were only associated with 3 things according to Niwamae (see Fig 3, above):
(1) insulin resistance (read: high carb)
(2) low HDL (read: REALLY dense LDL, low sat fat, high carb)
(3) high total cholesterol (read: denseLDL/apoB/TG, high carb)
What lights up insulin? Carbs.
Read. High carbs KILL.
Carbs cause cancer. Carbs cause cholesterol concerns. Carbs cause PLAQUE.
Butterscotch
I like butter. *aah* EAT MORE BUTTER.
Recall, Ai M et al (boy the Japanese scientists ARE SO D*MN SMART) demonstrated that carbs trigger insulin, NOT SATURATED FAT. Previous animal pharm: Insulin and Aging, How Paleo Works
Soft plaque known as fatty streaks even develop in young hearts (Peter has a picture) and don't calcify unless oxidation occurs. EBT studies show that 95% of diabetics have calcified plaque, the other 5% probably have soft plaque which are vulnerable to stenosis. Why? Individuals withi diabetes are damaged/oxidized from carbs and insulin. How do you prevent oxidation? Eat some saturated fat d*mn it (ghee, butter, animal PHAT, coconut products, lard, beef, seafood, organ meats, schmaltz, etc) and keep your insulin low with a carb-appropriate diet (minimal fruit, no grains, no oats, no legumes, no soy) and lifestyles that are aligned to your evolutionary genetics. Maintain an intake of very low n-6 oils. Anything > 2-4% of the diet is excessive because it is associated with raising insulin resistance, CAD, cancer rates and inflammation. Walter Willet at Harvard and certain heart programs advise 40% fat with only *gasp* 8% sat fat and 15+% n-6 oils. Heart stopping and insane, isn't it?
Get In Line
Well.
There are a lot ding-dongs out there. In academia, the USDA, the ADA, the AHA and conventional cardiac programs (Dean Ornish)... T. Colin Campbell *haa* GO PALEO KING 'the stupidest think I've read'.
Take It Off
One thing I hate about the radio is the overuse of auto-tuning, a software technology employed that takes normal voices and 'tunes' up to desired levels, usually 'pitch perfect'.
The imperfect sounds better to me -- texture, depth, emotions shine through.
Naked. It ROCKS. Naked is true. *HA HAA*
Blah Blah Blah
How many times do we hear about low saturated fat diets? Too often.
Do they work? Hardly. Heart disease is still #1 in killing Americans. Low fat isn't working. Americans are SICKER, FATTER, and MORE TIRED than before 'low saturated fat'.
This Love...
For low fat is pervasive. People feel guilty and 'not healthy' if they fail to follow this advice from their esteemed cardiologist or doctor... I nearly choke when I see HDLs as low as 30's or 40's and people tell me they cut out egg yolks and fat. This is reflected in a heart-deadening drop from HDL of fantastic 60's 70's earlier. Their LDL's are subsequently auto-tuned with a statin to TESTOSTERONE-NUMBING levels of 40's to 50's.
AAAAARRRRRGGGGHHHH.
Then they tell me they are using more canola oil, olive oil and wholeheartdisease grains and oatmeal, and I wanna CRINGE and puke out loud. No wonder their numbers S*CK. Initiation and promotion of atherosclerosis and other inflammatory conditions (cancer, autoimmune, migraines, etc) are indeed inevitable.
You're Freaking Me Out
No. Unlike the current management of CAD (coronary artery disease) and the 'tuning' of LDL-cholesterol where Big-Pharma-sponsored heart disease management guidelines (NCEPIII) advise LDL < 70-100 mg/dl for for those with CAD or heart disease equivalents (EBT calcifications, diabetes, aneurysm, peripheral vascular disease, etc)... or other programs that endorse LDL of 60 or below, in contrast, low carb high sat fat evolutionary diets WORK. Small dense LDL are obliterated to zero or near zero. These individuals have heart scans of zero calcifications and definitive regression over time. Show me zero dense LDL and I will show you reversal. Here to be redundant are those succeeding: My Paleo Peeps.
Pushing the LDL below natural, naked, endogenous baselines with Big Pharma drugs (statins, zetia, vytorin, etc) miserably fail from my extensive observations, EBT statin trials (10 out of 12 show progression w/statins) and new ones like ARBITER-6 (vitamin B3 beats the cr*p out of zetia). EBT calcifications continue at unacceptable rates (20-50+%), heart attacks and re-stenosis of stents and bypasses still occur, and disability from lower extremities, kidneys, and failed hearts flagrantly progress despite *cough cough* 'life-saving' statins.
D-I-N-O-S-A-U-R
Archaic guidelines need to go extinct. Now.
Animal
Kesha's one of my favorite animals right now... The grrrrl cracks me up: Rolling Stone interview. If there's auto-tune, I can't tell... She sounds perfectly IMPERFECT.
While You Were Sleeping
Stuff is happening. Pro-active work in the blogsphere, media outlets, movies like Fathead, books like BSS, Primal Blueprint, and 6-Week Cure and... how 'bout infomercials with some haaaawwt Paleo peeps? We need some. Cordain and Wolf are putting together continuing education for docs -- he said they need a pharmaco person... so might fill in and express my st*pidity *haa*.
Boots And Boys
Not only are Crossfit boys and grrrrls ridiculously super HAAWWT but also require no auto-tuning w/drugs as optimal health falls naturally into place. Avoiding neolithic toxins (legumes, graines, dairy, refined n-6 oils, statins/drugs glyphosate herbicides, etc), eating whole foods, and taking nutraceuticals maximize our evolutionary heritage (omega-3, digestive enzymes, probiotics, vitamin D, insulin sensitizers, etc). These endogenously 'auto-tune' employing our inherent software, e.g. DNA and nutrigenomics.
Ultimately, Crossfit + Paleo (Robb Wolf + Nicki Violetti) and our ancient/primal/Protein-Power blogosphere are where I find unprecedented reversal stories. Mr. Billy E did so with only diet (Evo/Paleo low carb, high sat fat) and vitamin D!
A Bad Girl's Lament
What I've noticed is that the athletic field often 'get it' before the medical. A great example is the use of omega-3 fish oil by Dara Torres and other athletes. Ultimately performance trumps lipid panels. To me, results are strikingly self-evident with low abdominal obesity, X-image '300' buff xfit-trained warriors, NBA stars, cycling and Tour de France competitors, and Olympic stars like Apolo Ohno. Slowly people will figure it out and stop listening to their low-fat, conventional, Big Pharma-bribed, Koolaid-drinking doctors.
--Apolo Ohno, 4X Olympic Speedskater (NYT: coconut oil, eggs, low carb, appears grain-free (except rice prior to events))
--Christian Vande Velde, Tour de France (MH: Winning Without Wheat)
--Runner's World, Aug 2004, Should You Be Eating Like A Caveman?
--Men's Health: How the Low Fat Craze is Making Us Fat
--Beijing Olympic gluten-free foraging, runner Amy Yoder Begley
& Steve Nash: http://www.mensjournal.com/living-sugar-free (but I suspect he's missing the lipidity piece ...)
ReplyDeleteDear Dr. B.G.,
ReplyDeleteas always you R*O*C*K!
Sometimes one really can think it´s just a concept behind all those stupid/wrong/halftruth explanations/studies.
One silly thought surrounds me at the moment; if someone loose weight and lives by his own high sat bodyfat do you think that affects vitamins A/D/K? If soaking up your fat reserves does those labs go up or down? Regards and springlike Greetings via Munich.
Being a music producer, I was surprised at the term "Auto-tuning" being used in a nutrition blog, but did not expect it to be used in the same context as the actual Anteres Auto Tune!
ReplyDeleteAnyway, fantastic blog! Every single entry has educated me invaluably. Started off at 35% bodyfat April 2009. Now at 12% bodyfat and counting. All I did was change to eating paleo low carb + short intense exercise 4 times a week.
Thank you so much for your inspiration and education!
>>> What I've noticed is that the athletic field often 'get it' before the medical. <<<
ReplyDeleteI tell people this all the time. Here's an example I've used for years: Do you ever see bodybuilders using gluten as a protein to build muscle?
Never!
And that's because through trial and experience they know it's a trash protein, basically worthless to the human body.
In fact, the paleo community knows it's even worse than worthless--it's flat-out unhealthy for numerous reasons.
Speaking of bodybuilding supplements, I've never seen a healthy pre-made shake or a healthy protein bar made for bodybuilders. Never. And I've looked hard, and often, and scoured the Net, too. They all contain unhealthy ingredients that compromise to some degree the benefit.
The vast majority of bodybuilders are not yet savvy enough to know this yet, and so these cheap-ingredient (versus, not-so-cheap, but healthy and more effective) products sale well.
If I had a blog and time I'd greatly elaborate on this.
Hi Dr. B.G.
ReplyDeleteYou may want to take a look at an interesting study (see post below) of various hormone levels (including adiponectin and tumor necrosis factor-alpha) after a high saturated fat meal. What makes this study interesting is that it is one of the first to look at the effect of dietary saturated fat on adiponectin; a health-promoting hormone secreted by body fat.
http://healthcorrelator.blogspot.com/2010/03/adiponectin-and-tumor-necrosis-factor.html
The conclusion contradicted the authors’ initial assumptions. Saturated fat had positive effects: an increase in adiponectin and decrease in tumor necrosis factor-alpha.
Interestingly, those effects were later messed up by three low fat meals rich in refined carbs and sugars, which were supposed to help the participants “recover” from the high fat meal.
Brent,
ReplyDeleteSteve Nash ROCKS.
Love the link -- didn't know he went sugar-free... he's still sweet!
Byron in Munich,
I have not read that otherwise the adipose-stored ADEK serum levels change. Perhaps evolution-wise that is meant to happen during fasting (whether intermittent or via seasonal) and that is completely expected and normal. Would depend what our adipose stores are, no? If they are depleted, no big serum increase!
-G
Scott!
ReplyDeleteIf you blogged... that's a curious concept that you're hitting in your thoughts their dude. I'd love to see you blog and what you'd great elaborate on coz I'd learn A LOT.
Athletes have a potential to abuse. Come ON. They all would abuse if they could get away with it, one survey showed that I sawy so I am not surprised at all that body-builders ignore the fact that protein supplements and 'energy' bars are full if sh*t. Body builders hit the 'T' before the rest of us. Unfortunately only the bioidentical naturally derived T is the best that fits the conformation of our testostonerone receptors, but they don't care. synthetic 'T' raises sdLDL, Lp(a) and lowers HDL.
Funny thing... I went into my OB prior to my synthetic hormone H*LL and complained the darn IUD was giving me libido and hair loss issues.
I walked out with a jar of bioidentical (I think) T cream. wtf. it worked when I needed it but hey.
Hormones. Are good things.
Make us young. At appropriate doses.
-G
Ned,
ReplyDeleteCurious article!
With about 13 grams extra palmitic acid C16:0 there is significant reduction in TNF-alpha. (or does that also reflect the adverse effect of extra 6000mg linoleic omega-6??!).
Perhaps this is why fat is analgesia and anti-depression...
Thanks for the link!
-G
PS regarding the adiponectin -- I don't get it and I don't have access to this PDF. it appears to me the adiponectin may have dropped in the high SFA group? am I reading the graph incorrectly?
Adam,
ReplyDeleteMusic producers are all welcome here :)
Man is autotuning ubiquitous like statins??! *haa* ok, don't answer. Every industry has its VICE.
OMG what wonderful results!! In only 9-10mos of evo eating and minimal HIIT. YOU ARE ROCKIN AND SMOKING HOT!!!
Keep up the strong work and I'd love to hear your future progress too! Watch those groupies might go after YOU.
-G
Oh hey Ned,
ReplyDeleteAdiponectin is a VERY GOOD thing. Probably the carbs were still too high for supposed young health male subjects, the adiponectin did not decrease with neither 54.4% (low) vs. 70.5% SFA (of a 59 gram breakfast load) (unless I read the graph wrong which is entirely possible).
In vitro (and I highly believe in vitro from observations like Weston Price) adiponectin blocks and suppresses the differentiation of regularly EPC (epithelial progenitor cells) into BONE/vascular calcifications, in other words osteoprogenitor cells.
http://www3.interscience.wiley.com/journal/112582085/abstract
The authors in the post, Niwamae et al, alluded to his that hyperinsulinemia and hyperglycemia are implicated in the conversion to osteoprogenitor cells inside PLAQUE.
We oxidize just like rubber bands in the elements and over time. High refined carbs, overdosing on LA (omega-6) and not enough palmitic acid!! BAD THINGS.
Thank you again for going over that article and the other illuminating posts -- love them all.
-G
http://www.springerlink.com/content/gm65322081016547/
ReplyDelete----------------------------------
Abstract Obesity rates have dramatically increased over the last few decades and, at the same time, major changes in the type of fatty acid intake have occurred. Linoleic acid, an n-6 polyunsaturated fatty acid, is an essential fatty acid occurring in high amounts in several western diets. A potential role of this fatty acid on obesity has been suggested. Controversial effects of linoleic acid on insulin sensitivity have also been reported. Thus, the aim of this study was to examine the direct effects of linoleic acid on leptin and adiponectin production, two adipokines known to influence weight gain and insulin sensitivity. Because insulin-stimulated glucose metabolism is an important regulator of leptin production, the effects of linoleic acid on adipocyte metabolism were also examined. For this purpose, isolated rat adipocytes were incubated with linoleic acid (1–200 μM) in the absence or presence of insulin. Linoleic acid (1–200 μM) significantly decreased insulin-stimulated leptin secretion and expression (P < 0.05), however, no changes in basal leptin production were observed. Linoleic acid also induced a significant decrease (~20%) in adiponectin secretion (P < 0.05), but only in the presence of insulin and at the highest concentration tested (200 μM). This fatty acid did not modify either glucose uptake or lactate production and the percentage of glucose metabolized to lactate was not changed either. Together, these results suggest that linoleic acid seems to interfere with other insulin signalling pathway different from those controlling glucose uptake and metabolism, but involved in the regulation of leptin and adiponectin production.
---------------------------
You can't tell, but I spat on the floor after I pasted that. Yuck.
A prudent diet high in carbs and polyunsaturates might not be a good idea. I don't think a ketogenic diet based on omega 6 is a great idea either, but since replacing tallow with corn oil increases carbohydrate appetite (tallow is a leptin mimic, maybe. Palmitic acid?), that might not come up much.
http://naivenutrition.blogspot.com/2010/03/is-saturated-fat-beef-tallow-leptin.html
I've been telling my friends and family for 2 years that a high fat, high protein, low carb lifestyle is the key. It's the key to losing weight, staying lean, and bringing hormones back to homeostasis. Not to mention that excessive processed carbs are the culprit in obesity (leading to excessive calories of course), NOT fats from sources such as animals, coconut, olives, etc. Mix in some intermittent fasting and smart exercise and it's a recipe for a healthy, symptom-free life.
ReplyDeleteHi Dr. B G, thanks.
ReplyDeleteAdiponectin levels do not really start at the same level for both groups, which makes the graph a bit unclear. Looking at the actual numbers I think that, to better interpret the graph, it may be a good idea to simply ignore the first (white) circle at the zero mark on the vertical axis.
What you pointed out about the omega 6 content is correct; definitely a possible factor. The positive results are either due to the high SFA, or the low omega 6 content (which was a whopping 7.2 g in the low SFA group), or a combination of both.
donny,
ReplyDeleteLinoleic acid *blech!!* Recently I was complaining to Seth about my carpal tunnel -- haven't had it in years but I am typing dramatically more this year (work, projects, etc). Stopped flaxseed and ate a bunch of pecans and almond butter (omega-6/LA). Halted my weight control -- like the article you posted. Worse -- I ahd carpal tunnel again. Flaxseed, more fish oil and stopping ALL omega-6 has done wonders and it's almost gone now.
Tallow and leptin... please let me know when YOU figure it all out!!
-G
Sterling,
ReplyDeleteUnbelievably easy, huh?
Great tips at ur blog! I don't have P90x yet but I think I'd will like it (coz I like the beach body series).
-G
Ned,
ReplyDeleteTHANKXXX!!
-G
off topic- posted this at paleohacks.com, but was wondering if you had any experience with this.
ReplyDelete-i just had a monster monster period after 6 months of progressively better ones. i did a few things differently this month like eat a little more cheese and take nyquil and aspirin for a cold, but i think, not sure, that what really did it was taking 1000mg of vitamin c for my cold. i read on the internet (i don't have the background to properly evaluate the source) that megadoses of vitamin c can increase estrogen. in the past when i've had heavier that my usual heavy periods (pre-paleo), it was because i took aspirin,, or maybe fish oil. has anyone else got a real heavy period after months of good ones? what do you think caused it?
Anonymous,
ReplyDeleteHormone imbalances affect our menses...
Read about thyroid and adrenals here:
http://www.westonaprice.org/Low-Metabolic-Energy-Therapies.html
Read about estrogen and perimenopause from books by Dr. Uzzi Reis and Colgan PhD (see the bks on the sidebar).
Since you are getting 'better' periods post-paleo and after the re-intro of dairy they reverted back to heavy, could it be the dairy?
Sometimes I find strict paleo healthier for the great majority (including me). Even a small amount of dairy (if allergic) affects us, esp women for some reason. Omega-6 affects me MORE than most guys I know too (yea wtf not fair). Did you skip omega-3? Did you skip workouts? Did you gain weight? Did you increase omega-6 polyunsats unknowingly? These are the obvious factors that affect the ovaries in a short-time frame.
Hope that helps! Try a month of dairy-free again... see if that is a contributing factor coz it usually is.
-G
Thanks again, you have been such a bootylicious supercomputer of nutrition information - again!
ReplyDeleteBy the way, do you happen to know any good general book/article on horrors of linoleic acid for semi-lay person ? I have some serious motivation to write about n-6 related problems in finnish for my new paleo blog, yet the information floating in internet has seemed a bit hard to decipher so far.
How about (for example) linoleic acid's possible effects on the nowadays insane use and need of NSAID's ? Dropping n-6 may lessen causes of inflammatory pain in various tissues ?
I know Vitamin D has some power to do that which seems painfully clear after reading this (FULL report rocks!) :
http://pain-topics.org/clinical_concepts/vitamind.php
On another topic, talking about fats and our beloved brains, I have long been interested in this intriguing book and hoped you would give it some reviewing when you have time:
http://www.amazon.com/Survival-Fattest-Human-Brain-Evolution/dp/9812561919
This book simply rocks, it provides physiological/evolutionary basework for our critical need of iron, zinc, magnesium, selenium and copper and of course n-3 pufas. Fat is more than good - again ! :-)
Just some random thoughts, keep on rockin' !
Lot of information in this post! Thanks!
ReplyDeleteYou wrote:
"Intimal flaps were associated with:
(1) insulin resistance
(2) low HDL
(3) high total cholesterol
What lights up insulin? Carbs."
It is a well known fact that insulin resistance causes HDL to sunk and add the number of tiny LDL but what causes insulin resistance?
Not carbs. Carbs (glucose,starch) won't do you good if you are IR but they are not a causative factor for making you insulin resistant in the first place. Neither does insulin.
hey westie,
ReplyDeleteReally? Do you want to clarify?
You are correct -- I believe there are other factors attributed to IR -- smoking (in this subpop ~86% were smokers), hormone imbalance, PCBs (like found in seafood and inferior fish oil products), sedentary lifestyle, etc.
Would love to hear you expand on why carbs don't cause IR!
-G
Hi Neo,
ReplyDeleteThank you -- ur a sweetie!! I've been thinking of brains for a while! I've ordered the book which looks so cool. Interesting how they might discuss minerals.
The pain info is very interesting!!
I've found the best n-6 info at Stephan's WholeHealthSource. Haven't read Sears latest 'Toxic Fat' bk but I imagine it is full of good references and insights just like the 'Omega Rx Zone' bk. (The diet is bunk imho b/c it's low sat fat and high carb, but the rest is good).
I think ur blog is wonderful though I can't read it *haa*!!
-G
HI there- I think I must be sounding like an alcholoic, another wine related question please; red or white? When you google them you get wildly different opinions on which has more carbs and impacts insulin more. Some say only red will do for low carbs, others say white is actually very low carb too.. what do you think on this?
ReplyDeleteRed is liable to give me black teeth and red shot eyes from the tanins. Although of course high in antioxidants etc
Thanks, Elizabeth
Re: insulin resistance; endotoxins?
ReplyDeletehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC108207/
"Lipoprotein(a) Inhibits Lipopolysaccharide-Induced Tumor Necrosis Factor Alpha Production by Human Mononuclear Cells"
Peter's gone into this a few times. According to wikipedia, drugs that block tnf-alpha can cause inactive tuberculosis to turn into an active disease state. Reducing tnf and lp(a) by making it less necessary-- stopping endotoxins at the source?, vitamin d, fish oil, besides being heavy in saturated fat, coconut oil is famous for being anti-microbial, maybe that would work-- is Richard still the HDL king of Paleo? Is it a coincidence that he's also king of dental plaque reversal?
Corn oil might kill some of the good bacteria, bacteria that are okay with corn oil would probably increase. Once you've got the wrong type of bacteria, glucose is no longer innocent.
Glycine- also makes life difficult for some bacteria. (Candida loves the stuff, some people have to be careful.)
Hdl itself can help mop up endotoxins-- but it tends to go up in scenarios where endotoxins should be less of a problem.
donny,
ReplyDeleteGreat points!!
Chronic bacteria exposure and chronic LPS definitely could affect IR. Any chronic inflammation can. Perhaps this is why celiacs (who have the most 'leaky' gut) have more cancer and heart disease?
Drugs that reduce TNF-a all the time reduce immunity. These drugs include the glucocorticoids (prednisone for example) and are associated with reduced defenses and immunosuppression against infections including flaring TB. Hence steroids are employed to reduce autoimmune disease, host-vs-graft disease and hepatitis.
If think coconut oil, sat fat, vit D, and omega-3 all improve IR by a variety of mechanisms as you bring up
--reduce gut permeablility (hence less bacteria crossing, less LPS exposure)
--improve immunity TH1 TH2
--in vitro I think all have some antimicrobial action
--neural -- don't know how but I think they all improve the gut-neural link
--PPAR agonism this improves all the above and also improves IR in peripheral tissues (liver, muscles)
Thanks!
-G
donny,
ReplyDeleteOh YEA -- Richard is Paleo king -- king of immunity and king of all sorts of dental plaque and otherwise reversals!
I believe he takes/uses pastured butter -- lots of K2 and stigamestrol (plant sterol) -- great stuff as well.
-G
Hey Elizabeth,
ReplyDeleteI was surprised how much carbs wine -- either red or white have. Obviously, it depends on the winery and the fermentation. I learned wine has carbs first at Crossfit when Robb mentioned it (although he wasn't so much low carb at the time).
If someone is really watching their carbs due to BG (blood glucose) fluctuations, then counting carbs from wine may make a big deal. On the other hand, wine has alcohol which lowers BG. Sake and other spirits even have nutrients in them that promote lower BP and vasodilation (beyond what alcohol dose).
Too much alcohol can cause insulin resistance though I don't know the mechanism (probably involving the liver). So moderation is key.
Tequila, norcal margaritas, vodka, sake -- no carbs at all.
Hope that helps!
"Would love to hear you expand on why carbs don't cause IR!"
ReplyDeleteI've beginning to think that there may be only one cause/mechanism for insulin resistance and that is increased fatty acid avaibility. Fatty acids blogs the mitochondrial oxidation of glucose. If you read or allready know how chronic inflammation or stress effects on our metabolic function you might understand what I'm thinking.
Let's take for example PPARg agonists which restores abnormalities related to blood glucose regulation. It does it by directing fatty acids towards storage (triglycerides) and increase the number of adipocytes resulting more smaller adipocytes.
PPARg agonism restores adipose tissue metabolic function and insulin sentivity etc. are seen as a result of that.
I've tried to find an insulin resistant state that is not accompanied by elevated FFA's.
I see visceral adiposity as a marker of problems in a adipose tissue function.
Starch or glucose does have positive effects on lipid storage and they provide lot of energy for healthy metabolism. When adipocyte function is disturped glucose is not oxidized in the apidocyte mitochondria like in healthy cell. Large size of the adipocytes is a bad sign because it will lead to "inflamed adipose tissue" since when adiposytes grow too big they will eventually die and dying cells activates macrophages to clean the mess.
Increased circulating FFA's will compromise liver function and eventually pancreatic cells will suffer and T2DM will become evident.
westie,
ReplyDeleteLove your deep thoughts...
Trigs are free fatty acids that go up with carbohydrate intake -- are these the fatty acids that you are speaking of that related to development of IR?
I think you are RIGHT ON about our adipose tissue being dysfunctional, which is not really the way I have ever approached it... but fat is an organ. It's an endocrine organ -- releasing leptin and adiponectin. I didn't realize the macrophages were there to mop up dead adipocytes... this explains the massive chronic inflammation associated in certain obese phenotypes, esp those involved with chronic pain or mind diseases (bipolar, schizophrenia).
IR at the liver level can be improved with MCTs and coconut oil. Long-chain omega-3s do as well clinical research shows. Why? PPAR agonism.
You discussed synthetic PPARg analogues -- these do improve adipose. Where they fail are when patients continue to eat high carb (e.g. diabetes patients on the cr*ppy SAD AHA ADA diets...).
PPARg drugs 'shift' visceral fat (good thing) to subcutaneous fat (ok thing). Not good in diabetics with concomitant high insulin, hyperglycemia. This raises the risk of death, MI and congestive heart failure -- which cancel out any marginal outcomes Avandia showed. DREAM was a nightmare -- Avandia killed double the patients (39 v. 22).
The heart whose preferred fuel is fatty acids (like all 'slow twitch' myocytes) and when both carbs and a synthetic PPARg activity 24/7 all day in heart adipose stores are going on frankly the heart cannot remodel.
NEJM talks more: 'Part I: Thiazolidinediones and Their Evolving Cardiovascular Implications'.
I'd like to hear more of your thoughts on the immunity aspects of the adipose. Fascinating!
Thank you,
Grace
http://www.jleukbio.org/cgi/content/full/83/4/804
ReplyDelete"Pre-B cell colony-enhancing factor (PBEF)/visfatin: a novel mediator of innate immunity"
If visceral fat is an immune organ, an increase in visceral fat makes sense as a reaction to infection. So our bodies aren't trying to kill us.
That study I posted above describes how visfatin, a hormone put out by visceral fat, recycles niacin. Which maybe puts some light on why niacin supplementation increases adiponectin (which decreases visceral fat.)
http://www.medicalnewstoday.com/articles/133504.php
Okay, a little weirdness.
"A biological tit for tat may hold clues to improving the success of islet cell transplants intended to cure type 1 diabetes, according to a Medical College of Georgia scientist.
In type 1, the immune system attacks insulin-producing cells causing high blood glucose levels that may temporarily reduce the attack, said Dr. Rafal Pacholczyk, an immunologist in the MCG Center for Biotechnology and Genomic Medicine.
..............
High blood glucose, or hyperglycemia, causes all sorts of dysregulation throughout the body. "It throws off metabolism, hormonal interplay and increases the risk of severe infections," Dr. Pacholczyk said. A shot of insulin or an islet cell transplant normalizes blood glucose levels, enabling, among other things, restoration of the usual balance between effector T cells which mount an immune or autoimmune response and regulatory T cells which suppress attacks."
Elevated glucose as an immune suppressor? I guess cancer loves that. Glucose levels in general as an immune modulator, maybe? Does physiological insulin resistance protect us from our own immune systems? Are type 2 diabetics more in need of this protection than the rest of us?
I think maybe I've defined atherosclerosis.
ReplyDeletehttp://naivenutrition.blogspot.com/2010/03/tumour-necrosis-factor-to-rescue-no.html
I need someone to tell me whether I'm crazy. :)
donny,
ReplyDeleteYOU are so bright. Redefining heart disease and all neolithic conditions is:
--insufficient saturated fat (thereby knocking out apo E)
--excessive neolithic carbohydrates, gluten, lectins (thereby causing insulin resistance like TNFa knockouts, at the cell level)
Celiacs (HLA DQ positive) are associated with increased granulation and keloid production (e.g. organ calcifications and intravascular PLAQUE).
Collagen gone CRAZY.
I think you deserve a Nobel...
-G
Concerning the cause of insulin resistance, I have also seen indications that fatty acid buildup in the cell is a factor. However, it would seem excess need to burn sugar is the main culprit. With high carb percentage in the diet, it would seem one would have to virtually avoid fatty acids and not eat so much fructose as to raise triglycerides. I have seen no evidence that a high-percentage fat diet with low sugar/starch lerads to insulin resistance.
ReplyDeleteMurray
How do you interpet this study: Posted: 4/4/2010 6:45:33 PM
ReplyDelete--------------------------------------------------------------------------------
"With each 5% increase in the percentage of energy from polyunsaturated fats, there was a 10% reduction in the risk of coronary heart disease"
" but the great majority of polyunsaturated fats in the diet, 90% to 95%, were omega-6 fatty acids."
Replacing saturated fat with polyunsaturated fats—not carbs—reduces CHD risk
March 23, 2010 | Michael O'Riordan
Boston, MA - Replacing dietary saturated fats with polyunsaturated fats significantly reduces the risk of coronary heart disease events, a new study has shown [1]. The findings, say investigators, highlight the importance of replacing saturated fat with healthy food choices, such as fish and vegetable oils, in order to get the heart-protective benefits of a low-saturated-fat diet.
"For 60 years we've been recommending reduced saturated-fat consumption without a focus on what should replace it in the diet," lead investigator Dr Dariush Mozaffarian (Harvard University, Boston, MA) told heartwire. "In practice, what's happened, if you look at trends over the past decade, saturated fat has been replaced by carbohydrates, largely refined carbohydrates. There have been several recent meta-analyses of observational studies showing that if you reduce saturated fat and don't pay attention to the replacement, there is no association with lower heart-disease events."
Mozaffarian pointed to a recent meta-analysis of prospective epidemiologic studies showing that there was no significant evidence that dietary saturated fat is associated with an increased risk of coronary heart disease or cardiovascular disease [2].
"This is pretty important on a policy level," said Mozaffarian. "It's naturally assumed that lowering saturated fat is good for the heart, but that's not what the evidence shows." Simply reducing saturated fat without regard to what is substituted for it might not derive any benefit, he said.
The results of the study are published online March 23, 2010 in PLoS Medicine.
The average weighted consumption of polyunsaturated fats was 14.9% of energy consumption in the intervention groups compared with 5.0% of energy from the controls. The risk of MI and/or cardiac death was reduced a significant 19% for those who consumed more polyunsaturated fats. With each 5% increase in the percentage of energy from polyunsaturated fats, there was a 10% reduction in the risk of coronary heart disease.
"We found that there was a significant overall benefit in using polyunsaturated fat as a replacement for saturated fat, and this benefit was about a 20% reduction in heart disease for the exchange the individuals made," said Mozaffarian. "Most of the trials used soybean oil or other vegetable oils that have a little bit of omega-3 fatty acids, but the great majority of polyunsaturated fats in the diet, 90% to 95%, were omega-6 fatty acids."
n
This new study really confuses me as I was just getting more comfortable consuming more saturated fat. Plus, I thought it was best to avoid N-6 fats because they are pro-imflammatory.
I hope you get back to me on this Dr. B.G.
It's going to get worse before it gets better.
ReplyDeletehttp://carbwars.blogspot.com/2010/05/so-close.html
Since then the ADA have aligned themselves with a bunch of other health "charities"
http://www.diabetes.org/about-us/coalitions-and-collaborations.html
so none of them can change their recommendatons unless they ALL do.
Meanwhile
http://carbwars.blogspot.com/2010/06/of-mice-and-men-and-usda.html
I'm surprised at Mozzafarian, always regarded him as competent, but since Frank Hu went over to the dark side with Ron Krauss maybe he was ordered to redress the "balance" at Harvard