I'm curious what those "7 additional causes of his heart disease" were.

These refer to the lipoprotein sorts of abnormalities we commonly uncover, e.g., small LDL, IDL, VLDL, deficient vit D, etc.

I am interested in learning what you prescribe for lessening plaque rupture. My score was 1229 and I also easily passed an echocaridogram. I am doing all
I can to correct the deficiencies from my lippo testing
but what I fear most is plaque rupture. Currently I am
taking 2000 mg omega3s and 10mg Mevacor as prevention. I was taking an ACE inhibitor but discontinued 2 weeks ago as my blood pressure has stabilized for the first time in 14 years.
Any thoughts you may add would be appreciated.
Regards
Gene Mc

Hi, Gene--

I'm afraid that our approach is too lengthy to cover in this blog.

I would invite you to participate in the conversation on the www.trackyourplaque.com website. The entire website is, in fact, devoted to answering your question.

I will stress to you that, given your current regimen, an increase in heart scan score is virtually guaranteed unless you take appropriate action.

I've taken prescription Niaspan for over an year and a half.  Several times I've had an unintended "untoward" reaction, more than a blush, more than a flush... more like a niacin storm!  Each time I've learned something new, however.  Yes, hydration is very important.  There are certain foods and drugs which apparently dam up the same metabolic pathway as niacin, and can cause a pretty nasty reaction.  Among these, at least for me, are certain long acting antibiotics (Zithromax), spicy chai tea, pepperoni (not supposed to go there anyway!) and very spicy foods, if taken near the time of Niaspan dosing.  I was advised by my Dr. that Benadryl syrup would help to shorten the duration of the "storm".  Mostly it's a case of dietary management and timing of dosage.  The good done by niacin certainly still outweighs the occasional bad side effects!

Another comment about niacin from this long-time niacin user, maybe folks will find it useful...
Dr. Davis's advice to hydrate heavily to prevent/reduce flushing is, alas, not completely effective. One can easily prove this for oneself. The next time you experience a big flush, consume as much water as you are able, and see if the flush quickly resides..does it?  No. Hydration is certainly great advice, I'm not knocking it, but as a flush reduction strategy, it isn't enough. One commentor here mentioned quercetin.  It seems some recent research on certain flavonoids (quercetin, luteolin) have produced good results,better than aspirin, which was mentioned in this thread.  One needs to experiment and see if supplements such as these do help, taken maybe 30-45 minutes before the niacin dose. I have some other comments on niacin strategies I've hardly seen mentioned anywhere, but I'll wait until (1) I see my posts are approved (I'm new here), and (2) that people are interested. Let's see if there is any feedback. Regards, Jim

I've been taking niacin  2 times daily for 6 months and dropped my cholestral from 240 to 162.  Can I go back to once daily?

I have seen some research papers that report that NIACIN, Nicotinamide and/or SAMe ( maybe also other methyl donors such as TMG ) can cause Parkinson's disease. I wonder if niacin can be converted to Nicotinamide in the body. Please see their abstracts and URLs below. Thank you.



Niacin Metabolism and Parkinson’s Disease

Tetsuhito FUKUSHIMA1)
1) Department of Hygiene & Preventive Medicine, Fukushima Medical University School of Medicine
Abstract
Epidemiological surveys suggest an important role for niacin in the causes of Parkinson’s disease, in that niacin deficiency, the nutritional condition that causes pellagra, appears to protect against Parkinson’s disease. Absorbed niacin is used in the synthesis of nicotinamide adenine dinucleotide (NAD) in the body, and in the metabolic process NAD releases nicotinamide by poly(ADP-ribosyl)ation, the activation of which has been reported to mediate 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson’s disease. Recently nicotinamide N-methyltransferase (EC2.1.1.1) activity has been discovered in the human brain, and the released nicotinamide may be methylated to 1-methylnicotinamide (MNA), via this enzyme, in the brain. A deficiency in mitochondrial NADH:ubiquinone oxidoreductase (complex I) activity is believed to be a critical factor in the development of Parkinson’s disease. MNA has been found to destroy several subunits of cerebral complex I, leading to the suggestion that MNA is concerned in the pathogenesis of Parkinson’s disease. Based on these findings, it is hypothesized that niacin is a causal substance in the development of Parkinson’s disease through the following processes: NAD produced from niacin releases nicotinamide via poly(ADP-ribosyl)ation, activated by the hydroxyl radical. Released excess nicotinamide is methylated to MNA in the cytoplasm, and superoxides formed by MNA via complex I destroy complex I subunits directly, or indirectly via mitochondrial DNA damage. Hereditary or environmental factors may cause acceleration of this cycle, resulting in neuronal death.

Key words:
nicotinamide N-methyltransferase, 1-methylnicotinamide, poly(ADP-ribosyl)ation, mitochondria, complex I

Pasted from http://www.jstage.jst.go.jp/article/ehpm/10/1/10_3/_article


Parkinson's disease: the first common neurological disease due to auto-intoxication?
A.C. Williams1, L.S. Cartwright2 and D.B. Ramsden2
From the Divisions of 1Neurosciences and 2Medical Sciences, University of Birmingham, Birmingham, UK
 
Parkinson's disease may be a disease of autointoxication. N-methylated pyridines (e.g. MPP+) are well-established dopaminergic toxins, and the xenobiotic enzyme nicotinamide N-methyltransferase (NNMT) can convert pyridines such as 4-phenylpyridine into MPP+, using S-adenosyl methionine (SAM) as the methyl donor. NNMT has recently been shown to be present in the human brain, a necessity for neurotoxicity, because charged compounds cannot cross the blood-brain barrier. Moreover, it is present in increased concentration in parkinsonian brain. This increase may be part genetic predisposition, and part induction, by excessive exposure to its substrates (particularly nicotinamide) or stress. Elevated enzymic activity would increase MPP+-like compounds such as N-methyl nicotinamide at the same time as decreasing intraneuronal nicotinamide, a neuroprotectant at several levels, creating multiple hits, because Complex 1 would be poisoned and be starved of its major substrate NADH. Developing xenobiotic enzyme inhibitors of NNMT for individuals, or dietary modification for the whole population, could be an important change in thinking on primary and secondary prevention.


Pasted from http://qjmed.oxfordjournals.org/cgi/content/full/98/3/215

see also
http://www.springerlink.com/content/d5wurtwylvpcy04q/


But,on the contrary,the paper below seems to suggest that niacin protects from Parkinson's.

Title: Does diet protect against Parkinson's disease? Part 4 – vitamins and minerals
Author(s): Isabella Brown
Journal: Nutrition & Food Science
ISSN: 0034-6659
Year: 2004 Volume: 34 Issue: 5 Page: 198 - 203
DOI: 10.1108/00346650410560343
Publisher: Emerald Group Publishing Limited
Abstract: This paper is the fourth in a series on Parkinson's disease and diet and investigates the role which antioxidant vitamins A and C, niacin and selenium may have on the incidence of the disease. Oxidative stress is believed to be a key factor in the development of PD and all of these have a role in preventing oxidative stress mediated cell damage. Dietary information was obtained via questionnaires. Vitamin C was found to reduce the risk of PD by 40 per cent in one study, although this was not supported by other studies. Niacin was associated with an at least 70 per cent reduced risk of PD incidence in a number of studies. No evidence was found to support a role for vitamin A or selenium. There is a need for further research to support or disprove the roles of these antioxidant vitamins within the aetiology of PD.
Keywords: Diet, Diseases, Lifestyles, Vitamins
Article Type: Research paper
Article URL: http://www.emeraldinsight.com/10.1108/00346650410560343

One of the ways to deal with coronary heart disease is by eating healthy there is no magical pill in this case, it's just as simple as that.

Have a serious discussion and press for confident answers if you find your doctor reflexively telling you that the wart on your thumb should be blamed on niacin.

The proper diet is essential for diabetic treatment. It helps magically in patients suffering from diabetes. It provides relief from symptoms and various complications in diabetics. Many diabetic patients can control their blood glucose by losing weight and that is possible only be proper diet.

Regards
Alexa

It is absolutely ridiculous that doctors don't understand how to cure diabetes with a low-carb diet.

This is just really basic biochem 101, carbs release insulin, and prolonged excess insulin causes insulin resistance, then diabetes.

This seems so simple that almost anyone with any small knowledge of biology should understand it, yet the main diabetes experts in the world don't.

I sometimes wonder if the "experts" don't want to give out simple solutions, since then half of them will eventually be unemployed and they won't be experts anymore. Kind of like how the oil companies obviously don't want us to invent renewable energy sources.

Dr. Davis, just to nitpick for clarity,

I'm assuming in the second paragraph "reductions in weight loss and HbA1c" is really meant to read "reductions in weight and HbA1c".

Sadly, what the studies show is that when these low carb weight
loss studies are continued past six months, invariably the weight loss stops dead for most participants.

This is true even in studies where the researchers tested for ketones in urine to ensure that people were eating what they said they were eating. The six month prolonged (and often permanent) stall is a repeatable low carb diet phenomenon.

My own polls among the low carb community verify this finding. Most people with diabetes will report they easily drop 15-20% of starting weight on a low carb diet but after that weight loss often comes to a complete halt even in my sample population which was made up of people with diabetes who had continued to maintain A1cs in the 5% range.

There are some lucky people for whom this won't be true, but they are a minority and tend to be male.

Since they are enthusiastic and vocal you tend to run into them online. The people whose experience is more typical tend to blame themselves and keep quiet.  

The real benefit of low carb dieting is in how it controls blood sugar. That effect will persist.

But long term diets of all types, including the low carb diet, downregulate the metabolism in ways that make it progressively harder to lose weight.

The big problem with posts like this one is that they raise false expectations--if you do well the first six months, a year later wow! That kind of false expectations eventually lead to frustration, feelings of failure, self-blame and almost inevitably diet failure and regain.

I can't tell you how many people I've seen posting on online support groups who did well for those first six months but ended up crashing off their diets a year later because they couldn't lose any more weight.

So after 13 years of observing people dieting with the low carb diet, I'm convinced that it's best to start the diet because of the blood sugar benefits--not with the dream of reaching what is all too often an unrealistic weight goal.

Figure that you'll lose 15-20% of your starting weight (you'll lose more if you are very heavy). Maybe you will be one of the small number of lucky people who do much better, in which case it will be a lovely surprise.

That way, you won't end up blowing off the diet once weight loss stops at a level where you still are much heavier than you had hoped to be.

There's also Long term effects of ketogenic diet in obese subjects with high cholesterol level by Dashti et al. Serum TGs & Glucose dropped like a stone in the Met Syn group.

The economics are not right for doctors to cure diseases. Healthy people do not come back until the next disease. Such is life. Doctor should only be paid for cures, when one exists.

We need to take charge of our own health and stop eating sugar, grains, manufactured oils and eatable products. Get a bit of exercise most days, and live a bit.

but what do I know

My perception:  I live in the "Deep South", home of the most obese people in the world.  The frustration for many health care professionals is in the unwillingness of patients to significantly change their diet.  It seems culturally mandated for many people to eat a certain way.  I fear that most obese people in the south would rather take medications than adhere to a diet such as this.  We can hardly blame the health care industry for this.

But what about the normal weight relatively young (41) type two diabetic?  (BMI 24)  Could I lose 20 pounds to be model slim?  Yeah. And I do eat low carb, although not 10 gram low carb.  And I have gotten my Hba1c to 5.4.  But, my insulin is crazy high, I hit 90 at my last glucose challenge.  I think it would be a big help if we acknowledged that diabetes is a SYMPTOM of a variety of related but not identical diseases.  Not everyone ate their way to diabetes, and while diet can totally help control symptoms, for me neither maintaining a proper weight nor controlling my carbs has solved the underlying problem, which seems to be a severe insulin resistance.

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.

edit my previous text to read  "... cross-bred from migration ...." instead of inter-bred.

Just personal experience here, but I'm a postmenopausal female and have lost 35% of my starting weight by doing low-carb. I've maintained that loss for four years. My BMI is 21.0.

For me, the key to reaching goal was the realization that eventually calories start to count. Low-carb has a natural appetite-limiting effect, but it is not a perfect tool. For people like me who have rather robust appetites, it becomes necessary to keep track of carbs for health and calories for weight loss and weight maintenance.

I wish low-carb weight loss were as quick and easy as Dr. Atkins made it out to be, but it's not. Prescription drugs, thyroid issues and exercise all factor into the equation, but after a certain amount of weight has been lost on low-carb, the sad fact has to be faced: calories count.

I just read the article on the front page of the American Diabetic Association website where they compared the benefits of a low carb vs. low fat diet for diabetics, and they said the big advantage of the low carb diet was you can reduce or eliminate insulin.  It seems like this idea is getting more and more respect from mainstream medicine.

I agree with Jenny that it's cruel to promise people that their diabetes will be "cured" by ANY treatment, including drugs, diet, exercise, or a combination of the above.

It sets up unrealistic goals and is equivalent to the nurse who tells obese people that if they'd just lose 10 pounds their diabetes would "go away."

It's simply not true. Type 2 diabetes is caused by faulty insulin-producing beta cells as well as insulin resistance, and that is often genetic.

Some people in very early stages of diabetes, when they're still producing a lot of insulin, can return to near-normal blood sugar levels with various regimens. Low carbing is one.

But if those people resume eating carbs, their blood sugars will go into diabetic ranges. They're not cured. They're just well controlled.

I have type 2 and I'm on a LC diet to control blood sugar, but I also take metformin and inject a basal insulin once a day or my blood sugars will be higher (I'm not comfortable with fasting or premeal numbers over 100, which they can be without the insulin).

I was diagnosed in late stage of type 2, and nothing we know about today will bring my beta cells back.

Please don't promise people false cures.

Anon posted "But what about the normal weight relatively young (41) type two diabetic? (BMI 24) Could I lose 20 pounds to be model slim? Yeah. And I do eat low carb, although not 10 gram low carb. And I have gotten my Hba1c to 5.4. But, my insulin is crazy high, I hit 90 at my last glucose challenge."

Just sounds like insulin resistance to me.  Some causes are transient fat in blood stream from high fat meals (In my experience in my body, saturated fat is more of a culprit than unsaturated by a very large measure), excess body fat and lack of muscle (lots of people are what I call "skinny fat").  Low carb diet, in one sense bypasses the problem since w/ low carb you don't produce much blood sugar load at once so the insulin resistance makes little difference.

I had fairly high postprandial readings (175-180's at one hour) and rising A1c.  Low carb per Bernstein made me feel terrible and worse the longer I did it though it did lower my sugar readings dramatically.  Now I eat a very high carb diet and about 30% fat (from whole, raw, seeds and nuts) but all the carbs are in high fiber veg and fruits and beans (with their resistant starch component)(occasional starchy veg and rarely whole grains NOT flour) and my one hour postprandials are in low 120's to teens and my most recent A1c was 4.7

My mother is a type 2, overweight diabetic. She's been helped tremendously by Dr. Davis's advice to eat low-carb and avoid wheat. But even on a VLC diet, her fasting blood sugar is typically in the 120s. Her diabetes was uncontrolled for 20 years, and her blood sugar was wonky for probably most of her adult life. She's never going to be back to normal.

Excerpt, ' Experiments described in the medical literature have tested the effects of high-fat diets on insulin intolerance. In one study, healthy young medical students were fed a very high fat diet containing egg yolks, heavy cream, and butter, and within two days all of the students had blood sugar levels high enough to be labeled diabetic.1 Complex carbohydrates have been shown to have the opposite effect.

Again I am not saying that low fat diet will work for everyone, but I think it worth trying, expecially if low car dose not work.

Sorry my previous post was not posted so do it again,
I think what people dont understand, that fat reduces insulin sensitivity and effectiveness, so when glucose and fat present inthe blood stream need much more insulin to maintain glucose homeostasis, and in many people even hyperinsulinaemia cannot compensate. Listen a few interviews with Dr. Delgado, dr. McDougle they explain it more clearly. When you keep your fat intake under 10%, the insulin is much more sensitive , sure you need to eat whole grain, proper carbs, and not junk cereals, breatds etc.
However, low carb diet works when people restict carbs, so they are able to maintai low blood glucose,  but once they consume more carbs,  blood sugar goes sky high.

Moreover, in some studies, has been shown, that when people eat fat diet, even pure sugar does not cause glucose spikes, as it is immediately regulated by insulin. , here i do not advocate eating sugar.
Another study Hollenbeck C, Doner CC, Williams RA, Reaven GM. The effects of variations in percent of naturally occurring complex and simple carbohydrates on plasma glucose and insulin response in individuals with non-insulin dependent diabetes mellitus. Diabetes 1985; 34:151.

http://www.joe-cannon.com/home/wp/can-type-ii-diabetes-be-cured/comment-page-1/#comment-1394

"I make the bold statement that type II diabetes can be cured because I care and I desperately want people to know the facts about type II diabetes that few people appear to have ever been told. I want people to know:

"1. Type II diabetes will go away -and stay away – in most people who take care of their health.

"2. Most people don’t have to get type II diabetes. Most type II diabetes is environmental  (eating too much and exercising too little).

"3. Losing a little weight and getting some exercise every day – even 20 minutes a day – can make profound changes not only on type II diabetes, but how long that diabetic lives."

Apparently Joe Cannon, personal trainer, whom I quote, believes most type 2s can be cured. Through 12 years of diabetes, type 2, I have exercised by ass off. I went from the typical ADA advice which didn't work for several years, to following Protein Power which brought management, to Dr. Berstein, which brought more and better management but didn't cure it. Found Dr. Davis's web site about 2 years ago and have been reading every post, becoming increasing radical in my approach. Dropped the steel cuts oats, added niacin, fish oil, you name it, I did it. Just ordered Dr. Ron Rosedale Diet because he says  diabetes can be cured in most cases. Okay, which radical approach is going to cure diabetes? I am one of your readers that is taking your words in your blog as a personal challenge. And I'm taking the personal trainer to task as well. I expect to be cured in six months (and am devoting six months to do that!) I expect you to continue to give fabuous advice, and as your experiment of one, I expect this to happen. I now have adopted the theme: "Diabetes is the Terminator"--it canot be reasoned with, doesn't show pity, and absolutely will not stop until you are dead!" Sorry if I sound desperate, but some of us are taking your words to heart!

Type 2 diabetes will rise and rise until people stop overeating. I see it around me everyday. Obese friends/relatives. For the last 20 years I'v watched them live an unhealthy lifestyle. Now it is catching up on them. One relative, age 48 type 2 diabetic, and one friend diagnosed last year. Age 52. Both have not changed their diet since diagnosis. Each carries an average of 60 extra pounds.
They were given nutritional guidance from a dietician, and I gave them websites to check out. Neither is interested in changing their lifestyle.

They refuse to change. Period. I'm sure there are thousands more like them out there......

Fat is not all the same or always acting as we think. An unusual poly-petptide in the intestine is upregulated by fat; and it follows a diurnal rhythm (inactive at night).

After "fasting" in response to
the first meal the body synthesizes bile acids for digestion of fat intake. When their litocholic and chono-de-oxy-cholic acids hit the small intestine they
interact with bile's Farnesoid X Receptor. This  upregulates Fibroblast Growth Factor 19 (FGF 19) in the intestines.

FGF 19 cycle is at maximum 1.5 to 2 hours after the post-prandial bile production kicked off; and bile synthesis had largely came on and abated. If the breakfast had no fat content then FGF 19's "on" trigger of specific bile acids can be low.

FGF 19 for it's part acts somewhat like a hormone; it integrates into a feed back loop. Humans have at least 22 different types of FGF with distinct action.

FGF 19 acts in turn to upregulate the anti-diabetic protein Insulin-like Growth Factor BP2. So there is less insulin resistance and blood glucose levels drop.

FGF 19 accelerates adaptive thermogenesis by  upregulating Uncoupling Protein 1 (UCP 1); the mitochondria energy gets "spilled" as heat. This makes the metabolic rate go higher and fatty acids are oxidized for energy.

Weight gain from fat is, in this scenario, less; but mostly from less liver cell fat. There is increased fatty acid oxidation burning for useful energy, since the mitochondria energy supply shifted from ATP delivery.

"Carbohydrates cause diabetes; elimination of carbohydrates cures diabetes."

"Type 2 diabetes will rise and rise until people stop overeating."

Stupid slogans like the above just confuse what is already a complex issue. To reiterate what has been said so many time, we have plenty of evidence of societies where carbs make up 65% or more of daily calories, but those societies show little obesity, diabetes, or heart disease, and they show long-life expectancy. The Japanese are a fine example of a developed society which eats a carb-based diet, and refined carbs at that, but doesn't have a diabetes epidemic. Clearly, carbs is NOT the problem.

And just as clearly, plenty of fat type II diabetics want to lose weight, but they can't. It is perfectly realistic to ask people to suffer hunger for a few months while getting down to normal weight. What is not realistic is asking them to suffer for the rest of their lives. So the real question is, why is causing people to have such huge appetites? And that is not an easy question to answer.

I grew up in the 1960's and everyone then was eating plenty of refined wheat, sugar and partially-hydrogenated vegetable oils, but people weren't fat like they are nowadays. Perhaps the manufacturers of processed foods have simply gotten much better at arranging fat, sugar and salt so as to make food irresistible. Perhaps it is a cultural thing: the same media brainwashing that has everyone wanting to supersize their house (McMansions) and car (SUV's) has them wanting to supersize their bodies as well. Perhaps the tendency towards obesity started after WWII, when food finally became cheap, and it simply took several generations for people to get accustomed to the idea of eating as much as they want, instead of treating food like something valuable not to be wasted. (Ever heard the expression "puts meat on the table?" Yes, there really was a time when an hour of labor at minimum wage didn't buy that much meat.)

If there is a magic bullet to the diabetes epidemic, it will have to do with appetite suppression. My impression, based on my own experiences and observations of people around me, is that low-fat/high-carb is more effective in the long-run at curbing appetite than low-carb/high-fat, at least for most people. In other words, the convention wisdom is right.

Japan obesity (BMI > 30 kg/m2) in 1990 - 1994  was nationally 3%. Japan statistic then for the overweight (BMI = 25 - 29 kg/m2) was 24% of men and 20% of women.

Adults were over weight 4 times more than they were in 1960 statistics; and mostly in the rural population. The 1994 school children (age 6 to 14) had 5 - 11 % obesity.

Data is from my notes (source was a Japanese translation) and I haven't looked up current statistics. Those 1994 obese school kids are all adults now
of course.

A recent analysis suggests that the lowest rate of death in East Asians (Japan, China, Korea) is for those with BMI of 22.6 to 27.5. This is similar to the European Prospective Studies Collaboration data of BMI = 23 - 27 as having least death risk in Caucasians.  

In obese East Asians with BMI >35the risk of death was 1.5 times greater. However, those with a BMI of 15, or less, saw their risk factor go up by 2.8 times. In those with super low BMI the theory is underlying co-morbidity is involved, like respiratory disease.

Coconut (like Doc's header image) has a  long 12:0 chain of lauric acid in it's fat that contributes to food satiety. It upregulates Glucagon-like Peptide 1 (GLP 1) release in the intestines.

GLP1 is secreted in the endocrino-cyte "L" cells and is one of the hormone group called incretins; some GLP is also active in the brain. GLP 1 inhibits gastric secretion, gastric emptying and digestive secretion from the pancreas.

It does enhance the release of insulin, which in this scenario
(GLP 1 activated) occurs in the context of slowed digestion; so blood sugar drops in real time. GLP 1 also stymies the release of glycogen (stored liver glucose) and the body is driven to burn something else.

GLP 1 does not provoke hypo-glycemia; the body burns it's fatty acids to run on. In fact if the individual does NOT graze between meals the satiation potential of coconut oil can work for up to 1.5 days worth of meals.

It seems coconut's lauric acid fat works on GLP 1 with a timed phase that also kicks in +/- 3 hours after a meal. This has the affect of getting some insulin out to sweep away the blood glucose and force the body to burn fatty acids.

Coconut's effect was greater than that of other fats; like milk fat, linoleic acid,stearic acid and oleic acid. Palm oil is more similarly satiating to coconut oil than other those other fats.

I detail this as a suggestion how dieters can keep the weight they lost off. Read Doc's old posts and you will see his objection to "grazing" food between meals; it supplants the GLP 1 surge benefits.

Here is a closing observation to amplify what others have infered. When western packaged foods switched out of palm and coconut oil shoppers lost the strongest activators of GLP1. Obesity from over eating got worse as we snacked up calories that sneak up on the waistline.

It is normal for people to overeat when food is readily available. That is a biological characteristic that has aided survival. We live in a time of excess. We need to learn to live normal in a abnormal world.

I try to do that by avoiding sugar, grain, manufactured oils and other eatable products.

but what do I know

Might-o'chondri-AL, thanks for that mini-treatise on coconut oil. Lately I have been eating two tablespoons of coconut oil for breakfast as part of my weight maintenance program. I have noticed that the coconut oil is able to produce satiety as well as lower my blood sugar, but I had no idea why it worked.

Some folks are very sensitive.  Control is probably a better word than cure, but the message is the same.  Low carb helps many folks with their blood sugar which is what seems to be so damaging.  It almost seems as though some cannot see beyond their own world views ("it isn't anyone's fault other than some medical-industrial complex", paraphrasing) when presented with evidence that INDIVIDUALS can help themselves, though some choose not to.

"Cure" implies that you no longer have diabetes, that you can eat whatever whenever and maintain normal blood sugars.  For almost everyone diagnosed as diabetic, that's not ever going to happen.  

Diabetes -> High blood sugar -> complications

You cannot change condition one - if you're diabetic, you're diabetic.  You can't really do much with link two - high blood sugar is going to cause complications in everyone who isn't killed by something else first.  But many type 2 diabetics can break link 1 and maintain normal blood sugars by limiting (or effectively eliminating) the amount of carbohydrate in their diets.

But "cure" is definitely the wrong word to use.

Diabetic Cookery 1917 Rebecca Oppenheimer
Trouble is we forget what we once knew.

This is an interesting discussion.  Like "Anonymous" who is a young diabetic with a BMI of 24, I didn't eat my way into diabetes, and if I could eat my way out of it, I would have by now.  

To M-Al and proponents of both low-carb and low-fat approaches, my experience tells me that type II diabetes is definitely NOT one disease, and (I'm getting to be a broken record on this forum I'm afraid) therefore the best regimen for control won't be the same for each person.  I do believe that many diabetics benefit from low-carb, and some from low-fat.  I suspect you will find refugees from one diet in the forums of the other - e.g., people for whom one alternative didn't work.

One thing you probably can't do as a diabetic is eat both fats and carbs. And diabetes is so complex - a research article I read said that many diabetics seem to have disturbed lipid *and* carbohydrate metabolisms.  So where do you go from there?  Plus, you just dump sugar from your liver for no good reason, regardless.  This is why many diabetics (most?) will need to add medications to their diet and exercise routines.

To commenters saying things like, "I know why there's diabetes - everyone's eating too much":

Look at all of us: we're on a health blog.  We all have in common an unusual interest in health matters.  The fact that some people not reading this blog do not want to change their habits doesn't make it okay to blame diabetics for their disease.   Easy for you to say if it hasn't happened to you.

What people do not take into consideration is that blood glucose is not dependant solely on dietary intake.  The liver dumps glucose into the blood stream in response to catecholamines.  Beta cells do not respond to endogenously produced glucose.  Glucose not utilized by the brain and the skeletal muscles will circulate for long periods of time.

Hi Helen,
Me, for my part, am just trying to examine the science of what Doc says works. It intrigues me, as do your comments.

Whatever the causes of insulin resistance it starts unnoticed. The pancreas cells that should respond to circulating glucose go awry.

Beta cells don't polarize their
mitochondria membranes in the "normal" response to blood sugar (for many reasons, as you say).The Potassium ( K+) Channel is ruled by ATP and is unable to perform it's K+ channel function; it closes up for those people. (Mitochondria in other tissue can still be functioning normally.)

So that Beta cell's mitochondrial
Calcium ( Ca++) Channel gets a disorganized electrical charge. The Ca++ can't reach the triggering level the islet
cell needs to put out insulin.

A rhythmic swinging of Ca++ between the cell's mitochondria and that cell's cytoplasm (interior) is what sustains "normal" insulin activity. Why this happens, when and to whom is as you say  variable.

First comes that pancreatic
islet Beta cell mal-function, which instigates body's
insulin resistance and then that
individual shows symptom of hyper-glycemia (high blood sugar). If that kind of Beta cells' mitochondria mis-step (detailed above)is happening when someone's body tries
to respond to blood glucose Doc's carbohydrate restriction is logical (to me).

Insulin resistance apparently starts for adults long before blood glucose tests indicate
even "pre-diabetes"; by age 60 +/-  1 in 5 will become Type II diabetic in the U.S.A. It seems with age our Beta cell mitochondria get out of whack and what we got away with in youth is not going to last forever.

Genetic, epi-genetic and age are part of the disease progression; diabetes is a process, not a static condition over time. Abnormal Beta cell workings can lead to improper protein structure of the insulin molecule itself.

This afflicts the Endoplasmic Reticulum (ER)where proteins are supposed to be appropriately folded. The erroneous protein configurations trigger the cell to "opt" for pre-programmed death (apoptosis, kind of like cell "suicide").

That apoptosis is what eventually
causes the diminished number of Beta cells in Type II diabetes.
Early on Type II diabetics are not neccessarily suffering from dying Beta cells, or even always shrunken (atrophied) ones.

Once the Type II diabetic's Beta cells die, then they suffer irreversable insulin insufficiency. That person has no response to hyper-glycemia and again Doc's regimen makes sense (and,I think he alluded to
adding prescription diabetes drugs in certain individual cases).

Anon about typo: Thanks for catching that. Now fixed.

Hi, Jenny--

Thanks, as always, for your insights.

However, I am witnessing something different. I see 30, 40, 70, 80, 100 lbs of weight loss, followed by profound reversals of diabetes and all its associated measures.

I suspect that many of the people you are talking to are not really following the diet that has the potential, in most diabetics but not in all as you well know, to completely reverse diabetes. It is a matter of the intensity of diet, the long-term commitment, and knowing what feedback tools to monitor.

Just doing--

Well said!

Gretchen--

Same response as that to Jenny.

I was diabetic 20 years ago. No longer. I have a long list of former diabetics. It ain't that tough.

There are indeed people who are physiologically incapable of reversing or ending diabetes. Jenny's LADA, for instance, can only be minimized, not completely reversed.

But, as much as I respect the opinions of both of you very sophisticated ladies, I disagree with you on this issue. In fact, I would crudely estimate that 70-80% of all current diabetics, with the proper insight and information, can completely rid themselves of diabetes. This is no false hope.

Revelo--

You are venturing very close to my Zero Tolerance Policy for rude behavior. Nonetheless, you often have insightful comments, so I'll let this one pass.

Having done this in many patients, I can tell you it works in many, perhaps most, thought not all. There are too many paths to this place called diabetes, variable residual beta cell function, variable leptin status, variable adiponectin status, varying apo E status, etc. to allow 100% generalizations.

The important lesson here is that MANY people, me included, who can kiss diabetes goodbye.

Incidentally, I made myself diabetic 20 years ago eating low-fat, high- carb while jogging 5 miles a day.

Another typo? About the paper you link to, is about a "small experience" or a "small experiment"?

Just to be argumentative

Dr. Davis, if you are no longer diabetic, how could you start with a blood sugar of 84 mg/dl, eat 4 ounces of whole wheat bread, and then have a blood sugar of 167 mg/dl one hour later?

In search of wheat: Einkorn and blood sugar

I'm not a physician, but a postprandial blood sugar of 167 might indicate that your diabetes has not been cured.

after losing 70 lbs, even at 6:2 225 lbs, I was still in the Obese category.  I am not a bigbfan of one size fits all number ranges.  

btw:  funny how it is the last ten lbs as if the number is the same. most low crabbers lie about their REAL carb intake.. We forget how quickly they add up.  


Calories do NOT count.

better the last ten is harder than the first fifty.

GRAND control but no cure.

'I see 30, 40, 70, 80, 100 lbs of weight loss, followed by profound reversals of diabetes and all its associated measures."

Dr Davis, with all due respect, if I lost 100 pounds, I'd weigh 20 pounds, which doesn't sound very appealing to me.

As I noted, *people who are diagnosed in early stages of diabetes when they're still producing a lot of insulin* can go into remission with any kind of weight loss diet. These are the patients you're seeing.

But they're not CURED. If they regain the weight, they'll have the same problems again.

And people who aren't grossly overweight when diagnosed can't even go into remission by reducing carbs and giving up wheat. There are many many reports of this on the discussion boards and the anger the patients feel because medical people promised them something that didn't happen. They lose faith in doctors and try all kinds of alternative treatments, some of which could be dangerous.

I think it's fine to tell patients that they MAY find that the weight loss puts them into remission. But to tell them that any diet will cure their diabetes is cruel, IMHO.

If you had diabetes 20 years ago, then you still have it. Nondiabetics can be grossly overweight and maintain normal blood sugar levels. Some very obese people aren't even very insulin resistant.

Human physiology is complex, and simplistic slogans (it used to be "fat makes you fat") are misleading.

(BTW, Jenny is MODY, not LADA).

I thought of an analogy: Someone is alcoholic. He gets counseling and gives up alcohol. Is he no longer alcoholic?

I don't think so. Nonalcoholics can have one or two drinks and stop. He can't. He's controlled, but not cured.

A lot of this controversy involves definitions. If you define "diabetes" as an A1c in the 4s, which is found in truly healthy young people, then if you get your A1c down that low with diet, you're not diabetic.

But if you define diabetes as an inability to eat a lot of carbohydrate without going over 120 mg/dL, then you could have a low A1c on a low-carb diet and still be diabetic.

Here are some quotes from lists from people who tested nondiabetic relatives:

"My non-diabetic husband has never tested above 4.7 (85) and I've tested him a few times 1 and 2 hrs after amazing carb loads - 200g plus in 1 meal. Once after a Christmas dinner with 2 desserts (one dessert was sugar pie) and once after a pasta+white bread+dessert meal. After gigantic amounts of pancakes and gobs of maple syrup. He stays pretty much rock-steady."

"I took my glucometer down for Thanksgiving and tested everyone an hour and two hours after the big meal with potatoes and pies etc. My brother in law's BG was only 82!"  and "I did the same thing with my siblings...including a sister who is close to 400 pounds. She was 84, my other sis who is about 220 lb was 75 and my brother who is thin was 100."

It's not just weight.

I don't like to argue about this, because I think you're doing a lot of good by urging people to cut carbs. But I think we need to face facts. Weight is an important factor, but not the primary cause of diabetes.

I think that Grtchen's comment sums it up well. Dr Davis is a cardiologist. He also has a strong interest in nutrition and its impact on cardiovascular health. He is not an endocrinologist. And this shows in many of his comments regarding diabetes.

Stargazey,

  I'm not diabetic, neither my wife, both of use can get 170 mg/dl after a vegetable sandwich with white bread. So, from my perspective your comment does not make much sense.

Seems to me that low carb with elimination of grains and fructose would be a necessity for anybody with impaired glucose tolerance or diabetes.  Depending on how bad your insulin sensitivity is, you may have to switch from saturated fat to mono-unsaturated as well.  Add an hour a day of physical activity and I expect a significant percentage of diabetics/prediabetics will be off their meds.  The others will hopefully at least stabilize and not get worse.  Are they "cured"?  Not exactly...they still can't eat all that sugary stuff we all like to eat.
But here's how I look at it.  Maybe they were never "sick" to begin with.  Maybe they were just poisoning themselves with foods they were never adapted to eat. After prolonged and sustained exposure to these poisons they got sick. Remove the poison and they no longer have the "disease" of diabetes.  I wonder what percentage of diabetics this definition of "disease" might apply to?

@GeoffreyLevens
I would be interested in how much exercise you do along with your diet to keep your bloodsuger (and A1C) that low.

exercise has little positive effect on blood sugar in the short term, in fact, in early efforts to control my numbers without meds, exercise would increase BS numbers after excerise. But in the long term, as a means to repair the body, it is very positive with diet.

I find that exercise is a significant way to control blood sugar level. For me, a 30-min brisk walk (breathing hard at end) will reduce a 150+ blood sugar to under 125 mg/dL.
I have found that the time of day for exercise is important. Physiologically we release glucose from liver glycogen prior to and on wake-up, preping our metabolism for activity so to speak. With increasing insulin resistance blood sugar will rise from the released glucose. Blood sugar is controlled by the insulin release in nondiabetics. Diabetics and the insulin resistant, can verify this with a series of fasting morning sugar checks, say on rising every 20 mins for an hour. By the way, this is known as the "dawn effect". For diabetics, the effect seems to be compounded with rigorous morning exercise. Exercise later in the day does not seem cause a problem. I had to go low carb (reducing stored hepatic glycogen) to reduce this natural response.
This is my experience, and I am a DMT2. Be curious to hear about impact of exercise from you non-diabetic types.

semsons.group: You may not consider yourself a "diabetic" but hitting a one-hour postprandial blood sugar of 170 after eating a sandwich is not healthy. Increased postprandial blood sugar levels is a sign of possible insulin resistance and a prediabetic condition.
Continuous glucose monitoring studies show that for healthy individuals blood sugar rarely rises over 130 mg/dL and then only briefly during a 24-hour period. It is generally beleieved that blood sugar levels over 140 mg/dL are harmful.

I use the term "cure" loosely. "Latent" would be a better term.

Personally, I run HbA1cs of around 4.7%, fasting glucose below 90 mg/dl, and postprandial glucoses of less than 100 mg/dl. In other words, no diabetes.

However, if I have whole grain bread, cookies, and pretzels, I will be fully diabetic in short order, especially if I gain weight.

I've seen this played out many, many times.

Thanks, Dr. Davis. I suspected that might be the case.

On a related topic, semsons.group and his wife may wish to avoid vegetable sandwiches with white bread.

Dr Davis, thanks for clarifying your terminology. The reason I'm so adamant about avoiding the word "cure" is the following.

I knew a man who was Dx'd with type 2. He did all the right things and got his BGs into normal ranges. So he thought he was cured and stopped testing. Nondiabetics don't test, and he was cured and nondiabetic, right?

Then he had a piece of cake for his birthday. It was pretty good. Soon he was having cake every Sunday. Then every day. Then he forgot about the diet altogether. He was cured, right?

One day he noticed he was thirsty all the time and decided to test. His BG was in the 400s or 500s. He wasn't worried. He knew what to do and went back to the diet that "cured" him before.

Only this time it didn't work. He'd burned out his beta cells with high glucose. And he had to start injecting insulin.

If instead of being told he was cured, he'd been told he was in remission but still had to be careful, he might have tested and discovered the problems before they were irreversible.

This also illustrates the benefit of early diagnosis. If you wait too long, the condition may become irreversible no matter how strict your diet.

A difference between Dr. Davis's patients and typical low-carb dieters is that the patients may be taking more supplements of the right kind. There's a whole school of thought that overweight is caused by lack of nutrients, especially minerals. I believe that whacking out the empty, carby calories is important, but I also believe you need vitamins and minerals to metabolize fat--including your own fat. It's often forgotten that Dr. Atkins recommended supplements, and even wrote a book on the subject.

In some studies I've seen, low-carb dieters were allowed, over time, to go back to eating more and more carb. (I'm sure this happens sometimes in real life, too.) Naturally, they stopped losing weight.

Has anyone used supplements like lipoic acid ? (The R version is supposedly superior). It is used in Germany as a treatment in diabetes.

Revelo: No, my comments are not stupid. I have yet to see a Type 2 diabetic within their normal weight range, AND eating healthy. I am surrounded by fat relatives/co-workers who live on highly processed boxed packaged foods, morning, day, and night at home and work place.  

Myself and only 2 others bring our lunch to work from home, the rest on a daily basis eat out at Taco bell, Burger King, Pizza Hut, MsDonalds, etc. Now imagine doing this again for dinner??

How much more can your body take of this diet before you become a DIABETIC?? I see it day in and day out before my eyes people eating themselves into Type II Diabetes.

Interesting: when Jenny points out that a theory applied doesn't actually work, the response isn't, "hm, perhaps the theory isn't right..." it's, "Well, then you have to be doing it wrong."  So, if I go on a rigorously-applied low-carb diet (no grains of any kind, no vegetable starches, limited fruits, no juices, fats being animal and EVOO only, and I STILL don't lose even a single pound despite cycling 20+ miles per day, Dr. Davis will unblushingly inform me that it's my fault, it's not that there's something wrong with the theory.  This is the case, by the way -- been doing this as a test since January. FWIW, my blood sugar, which before January, was typically 80 or so in the morning is now 120+, as often as not.  I'm not impressed with the results of this "health" approach, which hasn't changed even one of my health issues for the better, and appears to have worsened several rather significantly.

Meg:  Not a single pound?   Then something is very unusual.  Many of us know Jenny and her work and are familiar with her POVs. But not a single pound and claims of worse health leaves many of us speechless, What in the world would one expect to hear on an internet forum?  


Annom-  I have used R  acid large doses twice a day. I cannot say that it worked by itself. I stopped when money got tight and didn't start again. It was a part of many things I was doing at a time when I was having my best results away from using any meds. I am thinking of going back to it and a few other things.

As for exercise, only heavy lifting, strength training had any effect on my BS numbers on the short term. Walks and aerobics increased the numbers.  Type II is different for all of us. My best numbers are when I wake up and at night. go figure.

To Anonymous, who said:

"Revelo: No, my comments are not stupid. I have yet to see a Type 2 diabetic within their normal weight range, AND eating healthy. I am surrounded by fat relatives/co-workers who live on highly processed boxed packaged foods, morning, day, and night at home and work place."

Well, then you have yet to meet me.  And my father-in-law.  Your tone is very judgmental and your comments uninformed.  About 1/4 of type II diabetics are not overweight.  I have always eaten healthfully - people are always commenting on it, and now they say, "Diabetes - you?"

On the other hand, most obese people do not have diabetes, even though they may have other health problems.  Diabetes can be triggered by a poor diet and overweight, which lead to insulin resistance, but you have to have other, usually genetic, risk factors to develop diabetes.

Anonymous, I once gave a talk to a local diabetes group. What really impressed me was that there were very few obese people in the audience. One man with a "beer belly," but most were post middle age women, not skinny, but not fat. Some were thin.

I find it sad when people blame the victims. I think it's a form of self-protection. "Well, I don't do those things, so I'll never get disease X."

I know a lot of people with diabetes who eat healthy diets, but I live in a rural area where most of us have vegetable gardens and some raise animals for meat as I used to.

When you work in an urban area where everyone else in the office goes to fast food places for meals (I once noticed there was nothing but fast food available in the Harvard Medical School area and I wondered if they were trying to drum up business), it's difficult to be different, especially if you're the only one. Lots of peer pressure. People hate "holier than thou" eaters.

I recently heard a talk on obesity by Jeffrey Friedman, who discovered leptin. He said many people think obesity is caused by gluttony and sloth, adding that "this view is mostly espoused by thin people." He thinks genetics has a very large role.

Anonymous, have some compassion and have the courage to use your real name.

Megeara, I have had a similar experience, although I did lose weight on low-carb.  It may be that this diet simply isn't compatible with your particular genetic profile and how you handle lipids and carbs.  Try some other approaches, keep checking your blood sugar, and see what works best for you.

By the way, I find that supplemental fish oil and also vitamin C drive my blood sugar up.  (Both of these personal experience were backed up by research, I discovered.)  Check out if any supplements you are taking might be driving your numbers up.

Megaera--just a thought--are you doing anything close to zero-carb? For some reason, in people over 50 a zero-carb diet can cause elevated blood sugar.

I tried a zero-carb diet a couple of years ago, thinking it would help me lose weight and stave off diabetes. Instead, I gained weight and my fasting blood sugars went above 100 mg/dl for the first time in my life. I surveyed a bunch of people at my blog and found that those over 50 had similar experiences. (Google: Stargazey Observations on Protein Intake, if you want to read about it.)

I tend to agree with what Stargazey is getting at here and Dr. Davis has since rephrased:  VLC is not a cure for diabetes.  VLC is clearly one way of managing one of the major symptoms implicated in health risks associated with diabetes (e.g. hyperglycemia -> glycation).  

However, eating VLC does not cure diabetes, which at its core is pancreatic beta cell dysfunction.  Indeed it seems it can exacerbate the dysfunction as illustrated by the anecdotal evidence (don't like it but we have no real studies on this that I am aware of) that long term low carbers become more and more sensitive to any carb in the diet = worsening glycemic control.  

A normal person can handle quite the glucose excursion and mounts an appropriate insulin response to handle it.  A diabetic cannot handle this, and neither can VLC'ers or the advice to carb up with 150g/day for several days in advance of an OGTT would not be circulating around the web.

Can diabetes be cured?  Well, apparently yes.  I'm not suggesting gastric bypass surgery, but the remission rate - as in cessation of meds and "passing" an OGTT - is remarkable in morbidly obese diabetics undergoing the procedure.  In the 80-85% range in a matter of days/weeks prior to significant weight loss.  

This tells me that our beta cells are remarkably more resilient than we give them credit for - we're talking some of the most deranged metabolisms snapping back to "normal" relatively quickly.

In the short run, especially in IR obese and with weight loss, low carb generally seems to be a more successful approach.  But long term, more moderate approaches with higher carb and lower fat intake seem to be better, especially once compliance is taken to account.  

(In Westman, after randomized assignments of 97 participants, 10 of those who drew the LCKD diet didn't show up to do the study, while only 3 of the LGID did.  So they started with 38 and 46 respectively.  Of these 5 KD's dropped out for refusal/dissatisfa41%ction with the diet while only 2 dropped out of GI diet.  17 total dropped from each group.  So from assignment to completion,  27/48 = 56% of screened recruits effectively dropped the LCKD while only 20/49 = 41% dropped out of LGID.  This can definitely impact results.  And the post-6 month rebound is common in longer term studies.)

The results in the 2 year Shai study for example:  http://carbsanity.blogspot.com/2010/09/shai-and-diabetes.html

Nuttal's group has achieved some excellent results absent weight loss with their LoBAG diets - high protein (30%) with 20,30 or 40% carb splitting the 70% baby with fat.  http://carbsanity.blogspot.com/2010/09/lobag-diets-for-treatment-of-type-ii.html

I think Dr. Davis is an example of what Dr. Dansinger (who treats diabetics with a relatively low carb but less extreme version than others) refers to as a "carb cripple".

I use the antioxidant R-lipoic acid as a supplement.
Daily:  3x 200mg R-Lipoic Acid
1x 1000 mg Evening Primrose Oil
1x 1000 mcg Biotin
As suggested by Richard Bernstein in his book, “Dr. Bernstein's Diabetes Solution: The Complete Guide to Achieving Normal Blood Sugars.” The Evening Primrose Oil provides gamma-linolenic acid (GLA) that is believed to increase the effectiveness of the lipoic acid effect. The biotin replaces the body’s supply consumed in the lipoic reaction.
The R-isomer is believed to be better utilized than the S-isomer.
In Germany, R-lipoic acid is used to relieve diabetic peripheral neuropathy, however, the supplement is given intravenously.

I can not say that it has improved my blood sugar control but I continue to use it more as a “universal antioxidant”, and because of Bernstein’s endorsement. R Bernstein, a type 1 diabetic, is an endocrinologist and one of the original proponents for the use of at-home meters for measuring blood sugar levels in diabetics. He is one of the very early supporters of low carbs for blood sugar control in diabetics. He is in his 70s.

I am a type 2 diabetic on metformin and low-carbs, maintaining HbA1cs at the low-end of 5%.

For supplements this is the most expensive one I take. I go back and forth between the Doctors Best and Life Extension products, whatever is cheaper on Amazon at the time.

Perhaps Jenny/Blood Sugar 101 can add a few more comments …

Very interesting to me here, thanks everyone. Beta cells, in human adults, have their individual life span; they are not replaced from stem cells.

A few at a time, of the already differentiated, Beta cells duplicate themselves. New ones form and in the absence of hyper-glycemia (high blood sugar) can become larger than their progenitors.

This might explain how Doc gets latency, CarbSane suggest a "snapping" back, and why standard carbohydrate intake does not always induce diabetes. Each Beta cell has more than one mitochondria in order to sustain it's insulin role.

Another commentator mentions that as some Type II diabetics age they (diabetics) do better off the low carbohydrate diet. Maybe the very slow time which Beta cells self-duplicate in has reached a good formation (in those individuals) and best to  "use it, or lose it".

A low carb period gives fresh Beta cells enough of a break from high blood sugar then they can become large. Then that co-hort of Beta cells can follow the "normal" response; which is to get larger in response to  insulin demand from blood sugar (ex: when middle age Type II diabetic does "better" off of a strict low carb diet).

What stops Beta cell self-duplication in Type I diabetes is the auto-immune T cell "attack". The immune system stymies regeneration.

In Type II diabetes the inability to prevent toxic exposure side effects can be what impedes Beta cell self-duplication. Distorted  down-stream signal pathways can affect the transcription of a "fledgeling" Beta cell's replication of it's actin cyto-skeleton .

Might-o'chondri-AL, if you don't mind my asking, where do you get all your information? Are you a graduate student, perhaps?

Hi Stargzy,
I'm "semi-retired" 60 year old who hopes to avoid degeneration as I age. I've been investigating how to live well for over 40 years. Doc's blog appeals to me because he has clinical cases to draw on and good input from his readers.

When I first began looking into things maintaining health the science was much different. I am just trying to organize my thoughts on contemporary research to preserve my mental capacity.

In the Westman study, it bears noting that the gender and racial make-up of the "completers" - which is all that counts for comparisons - varies considerably between the diet study groups:
LKCD:  67% female, 67% white, 24% African-American
LGID:  79% female, 45% white, 52% African-American

On the "carbohydrates cause diabetes" front, I remain unconvinced.  When one looks at populations who are most susceptible to developing the disease, what does they tell us?  The traditional Pima ate an 80% carb diet and had low diabesity.  Expose to SAD - rates soar.  Japanese in Japan eating traditional diet with lots of rice = low diabesity rates.  Expose to SAD = rates soar.  The SAD is lower in carb by % (generally comes in at 40-45% carb for "usual" diet in studies) than the traditional diets.  So how can we say that carbs cause diabetes?

I tried to post this before, but it got lost.  

A question for Dr. Davis:  When you got diabetic blood sugars on a "healthy, whole grain" diet, were you supplementing with niacin and fish oil, which you recommend on your site?  I'm curious, because both are associated with impaired glucose tolerance in type II diabetics, and I have seen the effects of fish oil on my own glucose control.  There's a theory I've read that, while niacin has cardiovascular benefits, which is why you recommend it, food fortification with niacin may be in part responsible for increased rates of diabetes.  

Is it possible that niacin is beneficial with low-carb, but deleterious with high-carb?

Sorry for that comment above.

Afghans (people of Afghanistan) eat a wheat based diet. In fact, wheat bread is almost the entire diet of many of them (and they suffer from iodine deficiency and other problems as a result). But they have little obesity, little diabetes, no problems with insulin-resistance:

http://maisonneuve.org/pressroom/article/2010/nov/15/the-diseases-affluence/

Things are more complicated than simply "carbs = bad".

Hi Helen,
Niacin induces vaso-dilation ("flush") from the action of prostaglandins on capillaries Prostaglandins are made from the lipids stashed in our membranes.

This is how fish oil DHA/EPA (n-3) and poly-unsaturated vegetable oil (n-6) are involved; these can form Arachidonic Acid (AA)for making prostaglandins. Aspirin (salicylic acid) works as an anti-inflammatory because it blocks the AA pathway engendering prostaglandins.

1876 salicylate was known to decrease diabetic's glucose in their urine. A modern study showed injected salicylate restored acute (ie: 1st) insulin response to glucose in
10 out of 12 Type II diabetics who were administered prostaglandin.

For the 2nd insulin phase, with a few gr. glucose challenge, 12 out of 12 Type II diabetics had a 4x increase in their 2nd insulin response (ie: with a
salicylate booster before glucose administered and having those prostaglandins they got to start the test.)Prostaglandins,
in Type II diabetics, interfere with insulin response; in the controls the prostaglandins did not blunt the 1st nor the 2nd insulin "pulse" put out.

Women (some) "flush" from effect of prostaglandins at lower concentrations (ie: less niacin)than men (some). This is believed to be related to estrogen levels; suggesting that
post-menopausal women should review their original pre-menopausal niacin dose.

Doc specificly stated no one should take more than 1,500 mg. niacin without medical supervision (ex: liver enzymes
that monitor inflammation
tests). Diabetics who see their blood sugar worsen and/or liver
tests worsen while taking niacin, might be able to find their individual dose that does not induce levels of prostaglandins interfering with insulin phases 1 and/or 2.
Aspirin, as a salicylate, could be an additional way to block AA (thus prostaglandins)and foster timely insulin secretion for glucose clearance.

Another latest study showed that carbs and fats do not mix well and results into high blood sugar. YOu need to read the full studyy, to see the whole picture. healthy subjects were given hig fat meal (only fat) in the morning and their glucose and insulin remained at the fasting level for the next 5 hours. Then they were given coffee or nothing and then did glucose challenge. Sugar shut sky high (10 mmol/l ~180sh). Coffein further increases glucose.

This study again demonstrates that fat even after many outs of eating got negative effect on glucose. If if you eat low carb diet thats ok, but like most peole eat 30-40% energy from fat that leads to disaster.
'An Oral Lipid Challenge and Acute Intake of Caffeinated Coffee Additively Decrease Glucose Tolerance in Healthy Men ' http://jn.nutrition.org/content/early/2011/02/23/jn.110.132761.abstract

THis give some explanation why low fat diet work on some ppl.
Also emaging what wouldve happen if this study was done with diabetics.

Hi L/C/Andy,
Is it more likely that caffeine's classic effect on the adrenals, causing the liver to naturally put glycogen (sugar storage molecule)into circulation, is the reason blood glucose "surged" after coffee? I admit to not having read the study, so this is speculation.

I'm getting to the end of the Taubes book.  Unfortunately any interview I've heard or seen hasn't come close to doing justice to this book!  I went from angry and frustrated to joyful as I read.  Angry because there is so much misinformation and so much excellent research that has been ignored and forgotten, but happy because I think Taubes book will reawaken the passion in the souls of skeptics to challenge the status quo and delve into researching things forgotten.

The first 100 or so pages are a little dry but so fascinating.  Stick with it, there are lessons on so many levels to be learned.

The most important one is to stop blaming people for being fat.  Rather blame what they eat because the underlying reason they eat, is because they are literally starving.

Loved the book, backs up just about everything Atkins ever said. One strange thing I read however is that he doesn't think excercise does any good towards weight loss { he says it just makes you hungrier ?}

As an authority in coronary plaque imaging (medically directing EBCT imaging centers in 4 cities) and now the chief medical officer of Atherotech, I am knowledgeable but admittedly biased in  the following views--

Although i am a big fan of Dr. Davis and his efforts in tracking plaque, i strongly believe that the VAP test gives far more useful and accurate information than the NMR test he continues to promote. We at Atherotech use Apo B for particle number and provide it at no extra cost--Apo B is far more credible and internationally respected than NMR spin particle number.  One definitely deserves a DIRECT LDL available on all VAP tests. Anything else misclassifies 50% of patients whose LDL should be <100.   Liposciences falls far short in providing information (it doesnt routinely include things like Lp(a) and cannot even measure cholesterol content with its technology.

We at atherotech believe patients and doctors deserve a lot more accuracy and information than is provided by NMR. Therefore, we provide the gold standard process for lipid analysis--ultracentrifugation. In fact, our test is accurate fasting or NON-FASTING...something liposciences cannot do. Consider doing a non-fasting VAP test 2-4 hours after a typical meal. The TG we report now is relevant and predictive of heart attacks.

James Ehrlich, MD
chief medical officer, Atherotech

dr jim:

As a EBT technologist I want to thank you for hanging in there and backing this technology.  Techs have to practice ALARA and I personally would  have issues with performing heart scans using conventional CT scanners. (although it's better to be scanned than not if the technology is not available).  Beyond  that, I was wondering if you could direct us to any sources that would provide us with more information about the VAP testing.  Have you found many physicians willing to deal with this data?

Thank you,

radtech

The only weak area in Taubes book is his view on exercise.  He cites low-level exercise and blue-collar vs white-collar workers.  There's no mention of the studies that show working at 90% of maximum heart rate causes dramatic weight loss without alterations in diet.  I agree, walking or jogging doesn't lead to weight loss because appetite is increased.

Hi Dr. Ehrlich,

Your participation in this conversation is greatly appreciated.

It's difficult for a lay person to sort through the characteristics of the three major lipoprotein tests (NMR, VAP, and Berkeley's) and reach a judgment about which is best.

It seems to me, however, that one thing is clear.  Your Atherotech Vap Test is without question the simplest of the three to make happen for people on these issues outside of a doctors care.

Liposcience does not now provide it's full report to such people (like me).  And it's not that they won't, it's that they can't.  And if you call them up and ask them to give you a list of doctors who will order the test for you locally, their response is to say, "sorry, we don't have such a list."

And you're absolutely right that Liposcience not providing an LP(a) number as part of it's standard lipoprotein report makes no sense and wastes their customers time.

Incredible when you think about it.

Meanwhile, the situation is not much different with the Berkeley Heart Lab Test.  A person like me can get the complete report but ONLY after I find a doctor who will order it.  There is no option at all to order the test without a local doctor's order.

Meanwhile, you folks at Atherotech offer your test through the Life Extention Foundation and that includes an LP(a) test.  I take that to mean that Atherotech shares in a vision of patient directed health care that Dr. Davis often writes about.

As news of the results of participation in Dr. Davis' Track Your Plaque program spreads, it seems to me that there are going to be hundreds and even thousands of more CAD patients who are going to want to take these tests.

At this point, it seems to me that only Atherotech has a lipoprotein report marketing and product distribution strategy to meet the needs of folks who want to move quickly.

Having said that, IMO, there is an important element in the NMR and Berkeley reports that is missing from the Vap Test report.  Both of those reports provide a graphic visualization of lipoprotein size distributions from the raw data in the report.  The Vap Test report doesn't provide such a graphic visualization.

I put it to you that for purposes of patients/customers understanding the meaning of the report such visualizations can be extremely useful.  IMO, Atherotech should think long and hard to improve it's report by adding an additional page to it with various graphically displays that make report data content easier and more quickly grasped.

I recommend to you the work of Edward Tufte who has written about the power of graphical displays of information in multiple books.

http://www.amazon.com/exec/obidos/
search-handle-url/104-2972233-4103153?%
5Fencoding=UTF8&search-type=ss&index=books
&field-author=Edward%20R.%20Tufte

Dr. Ehrlich,

I figured out what was bothering me about the current Vap Test format.  I'm not talking about the content.  I'm talking display of the content.

As I understand it, Edward Tufte is considered to be a preeminent expert on "Envisioning Information" in the US.  The New York Times called Mr. Tufte "the Leonardo da Vinci of Data".  His wikipedia entry is here:

http://en.wikipedia.org/wiki/Edward_Tufte

In a book called "Envisioning Information", Mr. Tufte has written a chapter entitled "Layering and Separation".  I put it to you that some data display issues with the current Vap Test report format become clear pretty quickly upon reading that chapter.

But that's not the only problem with the report format.

I'm looking at the example pdf version at http://www.thevaptest.com/files/5615-VAPDefin_LIN_FINALrev.pdf.

I see the following line about 2/3 of the way down the report.

"Consider 2 hr GTT, Hemoglobin A1c, fasting glucose test"

Now, I have no idea what that means and I'm relatively educated about these matters.  However, I know that is must be important because the font is red.  I guess someone thought that knowledge of the acronym "GTT" should be known by everyone.  It's not.  

Now maybe  the report designer believed there wasn't enough space on the report to spell out what GTT means.  But then why waste a large amount of space at the bottom of the report on the information below the text line that reads:

"For Lab Use Only: Subspecies Real LDL (Cholesterol concentrations in mg/dL)"

If it's for "Lab Use Only", then why is that information on the report going to doctors and patients?

Finally, one of the things I've learned recently from Dr. Davis is that the HDL-2 value is critical.  I think it's more than coincidence that I've got that great CABG scar on my chest and my HDL-2 score is abnormally and extremely low.  And yet, on the example Vap Test at the link above, the HDL-2 value is 60% of the minimum desirable level and yet it receives no "in red" special highlighting text recommendation.

Meanwhile, the LDL-C number at the top of the page is lower than desirable (as is best) and yet, in the middle of the report, a recommendation about lowering LDL-C appears in red.

The Vap Test raw data may very well be the most accurate measure of CAD risk factors in patients.  But, for what it's worth, IMO, in the contest with Berkeley and Liposcience on the "data presentation intelligibility" the Vap Test report comes in 3rd.

The net of all this...

Dr. Ehrlich:  I'm not a doctor and have no formal training in science.  But I have been forced by my own experience to become educated about CAD and have become passionate the subject.

In the next several years, when more people in the US learn that there's this obscure doctor in Milwaukee with a website whose members are seeing empirically proven 10% to 61% reductions in plaque and associated risk, there's going to be an avalanche of requests for blood testing.  And the're not not going to want to have to go through some cumbersome process to get it done.

You're #1, IMO, in being the easiest blood test company to "get it done quickly and easily."

And with Liposcience being unable (that's right, not unwilling, it's actually UNABLE at present) to produce it's full report for patients directing their own destinies, you are positioned, it seems to me, for great things.

But your current report format is running a distant 3rd to the NMR and the Berkeley.

You need to get that fixed.

IMO, Atherotech should find some world-class "information presentation designer" to consult on a complete rethinking of the data presentation of it's Vap Test report so that the presentation is as world-class as is the data itself.

wccaguy--

As always, your insights are right on target. I agree that a graphic presentation and more clarification of the VAP report would be tremendously helpful. Atherotech has also been the most successful in providing access to the public without a doctor's order.

The late Dr. Atkins deservers an apology from many many doctors, to bad he didn't live long enough to be vindicated. There has NEVER been any proof that saturated fats are bad for you. I wonder how many doctors have CAUSED heart attacks by telling patients to stop eating saturated fats and/or eat more carbs. Shame on them for repeating this unfounded myth, and thanks to Gary Taubes for the most thoroughly researched book EVER on diet and health.

How could a Canadian get these blood tests done thru a lab in USA???

The best way I know of is to go to Web Resources on the www.trackyourplaque.com website. Ther e you will find listed the websites of the lipoprotein laboratories that can steer you in the right direction.

Thank you,

Seth Roberts has been posting a very interesting interview with Gary Taubes: Interview with Gary Taubes (directory)

I very much appreciate the wonderfully helpful input from fellow bloggers about the VAP test and the deficiencies in the graphic aspects. I share your opinion and it has been the subject of much discussion at headquarters. Frankly, although it is not at all ideal yet, our direct report from Birmingham is much better than the usual report a patient gets which comes from Quest or Labcorp. Their IT interface people have resisted our report format in favor of the text format you are getting.  Having said that, we believe we can  improve our direct reports and influence the labs to do the same.

My main difficulty with NMR is the fact that they don't give enough information and pretend that particle number is a strong predictor of risk. If one wants a strong predictor of risk, get a heartscan as Dr Davis advises. Use a lab test to figure out whether you should be on statins, combination therapy with niaspan, fibrates, omega 3s, etc.

Here is the analogy i use in looking at liposciences-- "If you had 1200 coins (= particle #) in your pocket...how much money do you have?"  Well, the VAP test tells you how many quarters (Lpa), dimes (VLDL, IDL), nickels (LDL), etc.

Even when debating the issue with physicians, Taubes' arguments shine through as a voice of reason, cutting through the flabby and tired arguments that have been proven misguided by the experience of those around us.