The Westman Diet

Dr. Eric Westman has been a vocal proponent of carbohydrate restriction to gain control over diabetes, as have Drs. Richard Bernstein, Mary Vernon, Richard Feinman, and Jeff Volek.

Several studies over the years have demonstrated that reductions in carbohydrate content of the diet yield reductions in weight and HbA1c (glycated hemoglobin, a reflection of average blood glucose over the preceding 60-90 days).

Among the more important recent clinical studies is a small experience from Duke University's Dr. Eric Westman. In this study, obese type 2 diabetics reduced carbohydrate intake to 20 grams per day or less: no wheat, oats, cornstarch, or sugars. Participants ate nuts, cheese, meats, eggs, and non-starchy vegetables.

After 6 months, average weight loss was 24.4 lbs, BMI was reduced from 37.8 to 34.4. At the end of the study, 95% of participants on this severe carbohydrate restriction reduced or eliminated their diabetes medications.

That was only after 6 months. Note that the ending BMI was still quite well into the obese range. Imagine what another 6-12 months would do, or achieving BMI somewhere closer to ideal.

Curiously, this idea of severe low-carbohydrate restriction to cure or minimize diabetes is not new. Sir William Osler, one of the founders of Johns Hopkins Hospital and author of the longstanding authoritative text, Principles and Practice of Medicine, advocated an diet identical to Dr. Westman's diet. So did Dr. Frederick Banting, discoverer of the pancreatic extract, insulin, to treat childhood diabetics. Before insulin, Banting and his colleagues at the University of Toronto used carbohydrate elimination (less than 10 g per day) to prolong the lives of children with diabetes.

This lesson was also learned many times during war time, when staples like bread were unavailable. The Siege of Paris in 1870 yielded cures for diabetes in many (or at least they stopped passing urine that tasted--yes, tasted--sweet and attracted flies), only to have it recur after the siege was over.

These are lessons we will have to relearn. As long as the American Diabetes Association and most physicians continue to advocate a diet of reduced fat, increased carbohydrate that includes plenty of "healthy whole grains," diabetics will continue to be diabetics, taking their insulin and multiple medications while developing neuropathy (nervous system degeneration), nephropathy (kidney disease and failure), atherosclerosis and heart attack, cataracts, and die 8 to 10 years earlier than non-diabetics.

All the while, we've had the combined wisdom from antiquity onwards: Carbohydrates cause diabetes; elimination of carbohydrates cures diabetes.

(This applies, of course, only to adult overweight type 2 diabetics, not type 1 or some of the other variants.)

Comments (71) -

  • Kris @ Health Blog

    3/26/2011 7:20:19 PM |

    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.

  • Anonymous

    3/26/2011 7:47:36 PM |

    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".

  • Jenny

    3/26/2011 8:31:26 PM |

    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.

  • justdoinglife

    3/26/2011 10:47:22 PM |

    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

  • Susan

    3/27/2011 12:14:55 AM |

    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.

  • Anonymous

    3/27/2011 1:12:07 AM |

    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-o'chondri-AL

    3/27/2011 1:38:24 AM |

    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.

  • Might-o'chondri-AL

    3/27/2011 1:47:27 AM |

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

  • Stargazey

    3/27/2011 4:38:41 AM |

    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.

  • Peter

    3/27/2011 1:27:27 PM |

    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.

  • Gretchen

    3/27/2011 3:33:59 PM |

    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.

  • Geoffrey Levens

    3/27/2011 4:05:14 PM |

    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.

  • Geoffrey Levens

    3/27/2011 4:10:26 PM |

    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

  • Lori Miller

    3/27/2011 4:49:39 PM |

    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.

  • LifeCoachAndy

    3/27/2011 6:05:26 PM |

    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.

  • LifeCoachAndy

    3/27/2011 6:11:06 PM |

    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.

  • Darrell D.

    3/27/2011 8:48:06 PM |

    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!

  • Anonymous

    3/27/2011 10:49:45 PM |

    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......

  • Might-o'chondri-AL

    3/28/2011 3:51:02 AM |

    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.

  • revelo

    3/28/2011 4:05:23 AM |

    "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.

  • Might-o'chondri-AL

    3/28/2011 5:37:28 AM |

    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.

  • Might-o'chondri-AL

    3/28/2011 6:26:37 AM |

    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.

  • justdoinglife

    3/28/2011 7:43:52 AM |

    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

  • Stargazey

    3/28/2011 2:07:25 PM |

    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.

  • Anonymous

    3/28/2011 2:39:14 PM |

    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.

  • Lyford

    3/28/2011 3:40:49 PM |

    "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.

  • Helen

    3/28/2011 9:39:20 PM |

    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.

  • Gabriella Kadar

    3/28/2011 11:07:45 PM |

    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.

  • Might-o'chondri-AL

    3/29/2011 12:34:52 AM |

    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).

  • Dr. William Davis

    3/29/2011 1:29:59 AM |

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

  • Dr. William Davis

    3/29/2011 1:33:27 AM |

    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.

  • Dr. William Davis

    3/29/2011 1:33:49 AM |

    Just doing--

    Well said!

  • Dr. William Davis

    3/29/2011 1:36:24 AM |

    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.

  • Dr. William Davis

    3/29/2011 1:42:12 AM |

    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.

  • Rick

    3/29/2011 1:54:54 AM |

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

  • Stargazey

    3/29/2011 2:40:14 AM |

    Just to be argumentative Smile

    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.

  • PJNOIR

    3/29/2011 7:27:14 AM |

    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.

  • PJNOIR

    3/29/2011 7:35:36 AM |

    GRAND control but no cure.

  • Gretchen

    3/29/2011 1:29:19 PM |

    '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).

  • Gretchen

    3/29/2011 3:06:24 PM |

    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.

  • Anonymous

    3/29/2011 3:45:45 PM |

    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.

  • semsons.group

    3/29/2011 5:11:37 PM |

    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.

  • Alex

    3/29/2011 6:23:02 PM |

    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?

  • rhc

    3/29/2011 6:53:47 PM |

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

  • PJNOIR

    3/29/2011 8:28:06 PM |

    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.

  • Anonymous

    3/29/2011 9:17:43 PM |

    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.

  • Dr. William Davis

    3/29/2011 10:19:17 PM |

    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.

  • Stargazey

    3/29/2011 11:26:16 PM |

    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.

  • Gretchen

    3/30/2011 1:01:46 AM |

    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.

  • Lori Miller

    3/30/2011 1:59:12 AM |

    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.

  • Anonymous

    3/30/2011 2:39:32 AM |

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

  • Anonymous

    3/30/2011 4:19:26 AM |

    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.

  • Megaera

    3/30/2011 4:37:09 AM |

    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.

  • PJNOIR

    3/30/2011 12:15:09 PM |

    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.

  • Helen

    3/30/2011 1:15:56 PM |

    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.

  • Gretchen

    3/30/2011 1:16:01 PM |

    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.

  • Helen

    3/30/2011 1:17:05 PM |

    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.

  • Stargazey

    3/30/2011 1:41:24 PM |

    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.)

  • CarbSane

    3/30/2011 3:28:04 PM |

    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".

  • Anonymous

    3/30/2011 3:46:40 PM |

    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 …

  • Might-o'chondri-AL

    3/30/2011 6:48:26 PM |

    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 .

  • Stargazey

    3/30/2011 8:51:34 PM |

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

  • Might-o'chondri-AL

    3/30/2011 10:29:42 PM |

    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.

  • CarbSane

    3/31/2011 12:43:28 PM |

    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?

  • Helen

    3/31/2011 3:53:49 PM |

    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?

  • revelo

    3/31/2011 5:29:51 PM |

    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".

  • Might-o'chondri-AL

    3/31/2011 11:03:59 PM |

    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.

  • LifeCoachAndy

    4/2/2011 9:04:52 AM |

    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.

  • Might-o'chondri-AL

    4/2/2011 4:28:38 PM |

    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.

Loading

Why do the Japanese have less heart disease?

We should look to the Japanese to teach us a few lessons about preventing heart disease. A Japanese male has only 65% of the risk of an American male (despite 40% of Japanese men being smokers), while a Japanese woman has 80% less risk than an American woman. While the U.S. is near the top of the list of nations with highest cardiovascular risk, Japan is the lowest.

What are they doing right?

There is no one explanation, but several. Genetics probably does not play a substantial role, by the way, as demonstrated by observations of Japanese people who emigrate to Western cultures. People of Japanese heritage living in Hawaii, for instance, develop the same cardiovascular risk as non-Japanese living in Hawaii. They also develop obesity and diabetes.

Among the factors that likely contribute to reduced risk in Japanese people:

--A style of eating that does not include a lot of sweet foods. No breakfast cereal or donuts for breakfast, for instance, but miso soup with tofu, fish, green onions, and daikon (as takuan, or pickled radish).
--Seaweed--It's probably a combination of the green phytonutrients and iodine. Typical daily iodine intake is in the neighborhood of 5000 mcg per day from nori, kombu, wakame, and other seaweed forms. (The average American obtains 125 mcg per day of iodine from diet.)
--Seafood--Fish in many forms not seen in the U.S. are popular.
--Green tea--Consumption of green tea has been confidently linked to reduced cardiovascular risk, probably via visceral fat-reducing, anti-oxidative, and anti-inflammatory effects. Although tea in Japan is often the less flavonoid-rich oolong tea, softer benefits from this form are likely.
--Soy--Tofu, miso, and soy sauce are staples. It's not clear to me whether soy is intrinsically beneficial or whether it is beneficial because it serves to replace unhealthy alternatives. (Genetic modification may change this effect.)
--Reduced exposure to cooked animal products (except seafood). This is not a saturated fat issue, but probably an advanced glycation end-product/lipoxidation issue that result from cooking.
--The lack of a "eat more healthy whole grain" mentality, the advice that has plunged the entire U.S. into the depths of a diabetes and obesity crisis (along with high-fructose corn syrup and sugar). Noodles like udon and ramen do have a place in their diet, as do some dessert foods. But the overall wheat exposure is less--no bagels, sandwiches, and breakfast cereals.
--Less overweight and obesity--The above eating style leads to less weight gain.

Japanese foods have a unique taste, consistency, and mouth-feel that go well with saltiness, thus the downside of their diet: salt consumption. On a broad scale, high salt consumption has been associated with hypertension and gastric cancer. But the tradeoff has, on the whole, been a favorable one.


One study trying to find some answers:

Dietary patterns and cardiovascular disease mortality in Japan: a prospective cohort study.

Shimazu T, Kuriyama S, Hozawa A et al.
Division of Epidemiology, Department of Public Health and Forensic Medicine, Tohoku University Graduate School of Medicine, Japan.


We prospectively assessed the association between dietary patterns among the Japanese and CVD mortality. Dietary information was collected from 40 547 Japanese men and women aged 40-79 years without a history of diabetes, stroke, myocardial infarction or cancer at the baseline in 1994.
During 7 years of follow-up, 801 participants died of CVD.

Factor analysis (principal component) based on a validated food frequency questionnaire identified three dietary patterns: (i) a Japanese dietary pattern highly correlated with soybean products, fish, seaweeds, vegetables, fruits and green tea, (ii) an 'animal food' dietary pattern and (iii) a high-dairy, high-fruit-and-vegetable, low-alcohol (DFA) dietary pattern. The Japanese dietary pattern was related to high sodium intake and high prevalence of hypertension. After adjustment for potential confounders, the Japanese dietary pattern score was associated with a lower risk of CVD mortality (hazard ratio of the highest quartile vs the lowest, 0.73; 95% confidence interval: 0.59-0.90; P for trend = 0.003). The 'animal food' dietary pattern was associated with an increased risk of CVD, but the DFA dietary pattern was not.

The Japanese dietary pattern was associated with a decreased risk of CVD mortality, despite its relation to sodium intake and hypertension.

Niacin: What forms are safe?

Niacin, or vitamin B3, remains a confusing issue for many people. It shouldn't be.

It doesn't help that most physicians and many pharmacists also do not understand the basic issues surrounding niacin. The only reason why there is any level of prevailing knowledge about niacin is that Kos Pharmaceuticals managed to "pharmaceuticalize" a niacin preparation, prescription Niaspan, that provided the revenue to fund professional "education."

Niacin can be helpful to increase HDL, reduce small LDL particles and shift them towards the more benign large particles, reduce triglycerides, and reduce lipoprotein(a).

So here's a brief description of the various forms that you will find niacin:

Immediate-release niacin--Also called crystalline niacin or just niacin. This is the original niacin that releases within minutes of ingestion. Because it releases rapidly, it triggers the most intense "hot flush." While this form of niacin works wonderfully well, is the safest, and is dirt cheap, the majority of people are simply unable to tolerate the intense flush. It also works best taken twice a day, generating two intolerable flushes per day.

Slow-release niacin--These preparations were popular in the 1980s, since the slow 12 to 24 hour pattern of release minimized the annoying hot flush. But, with prolonged use, it also became apparent that an unnaceptable frequency of liver toxicity developed. Unfortunately, this means that any niacin preparation that trickles niacin out over an extended period, including many of the slow-release preparations now sold in health food stores and pharmacies, have potential for liver toxicity. These preparations should be avoided.

6-hour release niacin--Releasing niacin more slowly than immediate-release niacin but more rapidly than slow-release niacin, 6-hour release (or what the Niaspan people call "extended-release" niacin) is nearly as effective as immediate-release niacin with approximately the same low potential for liver toxicity. It is far less liver toxic than slow-release niacin. 6-hour release niacin therefore offers the best balance between effectiveness and safety. Preparations that show this pattern of release include Niaspan ($180 per month), the poorly-named Sloniacin (about $8 per month), and Enduracin (about $7 per month) for 1000 mg per day. (Some Track Your Plaque Members have also determined that several other over-the-counter preparations have been demonstrated to share a similar pattern of release.)

Then there are the scam products that have no useful effect at all:

Flush-free or no-flush niacin--Inositol hexaniacinate, or 6 niacin molecules bound to the sugar, inositol, has no effect in humans, at least not with the dozen or so preparations that I've seen used. Nor are there any data to document the effectiveness of flush-free niacin. It's also more expensive.

Nicotinamide--This niacin derivative likewise has no effect on the usual targets for niacin treatment.

While I used to prescribe Niaspan, the ridiculous pricing and aggressive marketing really turned me off. I now advise my patients and our online followers to use only Sloniacin or Enduracin, unless you can tolerate immediate-release niacin.

Introduction to the New Track Your Plaque book, version 2.0


Out with the old,
in with the new  



“I believe that you are suffering from what is called a fatty degeneration of the heart.”

Dr. Tertius Lydgate to Mr. Casaubon on making a diagnosis with the new medical device, the stethoscope.

George Elliot
Middlemarch, 1871





Old notions in medicine have a peculiar way of lingering.

In 1882, Dr. Robert Koch discovered the tubercle bacillus in tissues of people with “consumption.” By connecting a bacterium with the disease, he usurped the long held notion that tuberculosis was a degenerative disease caused by lack of fresh air. But, for decades after Dr. Koch’s revelation, the “bad air” belief persisted. Surgical collapse of the lung, a painful and barbaric treatment for tuberculosis, persisted well into the 1960s, years after effective antibiotics were discovered in 1947.

The medical community of the 19th century viewed mental illness as the hereditary end-product of ancestral nervousness, alcoholism, prostitution and criminal behavior, a bias that remained widespread well into the mid-20th century. Nazi physicians invoked the theory of heritable “mental degeneration” to justify wholesale extermination of schizophrenics. Electro-convulsive therapy (ECT, or “electroshock therapy”) was widely applied to treat schizophrenia, depression, homosexuality, and criminal behavior for over 30 years, gradually abandoned (at least in its original form) after years of abusive application to subdue patients, demonized in the 1975 movie, “One Flew Over the Cuckoo’s Nest,” depicting the author’s real-life experience with ECT.

Long after a theory or practice has been discredited, it can persist, refusing to die. The new and improved may not be adopted into mainstream practice for years, even decades.

Back to the 21st century: What if you realized that, by quirks of human nature and the uneven adoption of health information, your doctor practiced medicine appropriate for 1985? 1975?

While digital information nowadays is transmitted at the speed of light, disseminating as fast as it takes the next juicy tidbit to be “virally” reproduced via social networking websites, it’s the human factor that still operates with the inertia of human behavior. Habits and attitudes slow the adoption of new information in time measured not in seconds, but in years or decades.

A century ago, 20 years were required for the new technology of blood pressure measurement to be adopted after its introduction in the U.S. in 1910, since physicians were long comfortable with the practice of “pulse palpation” (feeling the pulse). (The arcane language of pulse palpation persists to this day, terms like “pulsus parvus et tardus,” the slow rising pulse of a stiff aortic valve; and the "water-hammer" pulse of a leaking aortic valve.)

The discovery of new, health-changing information today in the 21st century disseminates through the ranks of modern healthcare providers at much the same pace as measuring blood pressure did in the early 20th century.

It’s also tempting to paint American medicine as a fiefdom intent on maintaining exclusive rein over health information. Look back over the hierarchical relationship of medicine over nursing in the past century: When blood pressure measurement was adopted on a broad scale in the 1930s, it was practiced only by physicians, since nurses were deemed incapable. (Modern-day nurses should surely have a hearty laugh over this.) Stethoscopes, around even longer than blood pressure cuffs, weren’t permitted to fall into the hands of nurses until the 1960s, since the medical community feared that nurses might command too much control over patient care. Even after nurses were permitted to have their own stethoscopes, great pains were taken to be certain the nurses’ version was readily distinguishable from the “real” tool wielded by physicians; nurses’ stethoscopes were therefore labeled “nurse-o-scopes,” or “assistoscopes,” and were required to be smaller and flimsier.

Old and ineffective doesn’t always give way to new and better at once; it is slowed by habit as well as an unwillingness to relinquish control.

Somehow technology marches on. But it does so unevenly, sweeping some along in its first wave, others in its wake, some never at all.

Just as effective antibiotics to cure tuberculosis were available for 20 years while surgeons continued to remove patients’ lungs, so better solutions to heart disease are already available but not yet employed by your neighborhood physician. The primary care physician may have heard about some of the newest means to prevent heart disease, but is too overwhelmed with the day-to-day of sore throats, diarrhea, and rashes. Cardiologists, intent on inserting the next best stent or defibrillator, have little but passing interest in strategies that might halt or reverse the heart disease that can be “managed,” no matter how imperfectly, with procedural solutions like angioplasty and bypass surgery. We should bear these flawed human tendencies in mind as we explore the world of heart disease prevention.

We need look no farther than the front page of the newspaper to find evidence of the failure of present-day heart disease detection and management. Over the past several years, headlines have carried the likes of Tim Russert, Bill Clinton, Larry King, Dick Cheney, David Letterman, Tommy Lasorda, Ed Bradley, Mike Ditka, Walter Cronkite, Alberto Salazar, all heart disease sufferers. Some, like talk show host David Letterman, survived their brush with heart catastrophe and underwent successful bypass surgery. Others, like marathoners Fixx and Salazar, raised none of the conventional red flags for heart disease. All received standard, “modern” medical care . . . all the way up to their heart attack, bypass surgery, or untimely death.

Like the sphygnomanometer (blood pressure) cuffs of 1910, Track Your Plaque represents an example of the new. But, unlike the simple practice of taking blood pressure in the early 20th century, Track Your Plaque represents an entirely new way to look at coronary heart disease: a new way to measure it, a new way to identify its causes, and a new way to seize control over it, often to the point of achieving reversal of the process. It also puts control over much of this process into your hands and away from hospitals, cardiologists, and heart procedures. 

I could speak of revealing “secrets,” but that’s not true. In Track Your Plaque, I simply convey information about heart disease that you were likely unaware existed, strategies that doctors fail to discuss. I assemble them into a “package” that, together, create an enormously empowering unique approach to prevent heart disease and heart attack.

Track Your Plaque also challenges the high-tech status quo, practices that occupy exalted places in the enormous cardiovascular healthcare machine that has dominated American healthcare for the past 40 years. I propose that high-tech hospital procedures should join the practice of ECT for homosexuality and insanity¾and become yet another relic of the past.

What are "normal" triglycerides?

Among the most neglected yet enormously helpful values on any standard cholesterol panel is the triglyceride value.

Triglycerides traverse the bloodstream by hitching a ride on water (serum)-soluble lipoproteins, or lipid-carrying proteins. We measure triglycerides as an indirect index of triglyceride-containing lipoproteins.

Triglycerides are a basic currency of energy. While the average American ingests around 300 mg of cholesterol per day, he or she also ingests 60,000-120,000 mg (60-120 grams) of triglycerides, i.e., 200 to 400 times greater amounts, from fat intake. Zero triglycerides in the diet or in the bloodstream is not an option.

But what represents too much triglycerides in the bloodstream? There are several observations to help us make this determination:

1) When fasting triglycerides are 133 mg/dl or greater, 80% of people will show show at least some degree of small LDL particles.

2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

3) When fasting triglycerides are 200 mg/dl or greater, small LDL particles will dominate and large LDL particles will be in the minority or be gone entirely.

4) When triglycerides are 88 mg/dl or greater after eating, then risk for heart attack is doubled. Non-fasting triglycerides in the 400+ mg/dl range are associated with 17-fold greater risk for heart attack.



From Austin et al 1990. "Phenotype A" means that large LDL particles dominate; "phenotype B" means that small LDL particles dominate.

Note that conventional "wisdom" (i.e., NCEP ATP-3 guidelines) is that triglycerides of up to 150 mg/dl are okay, a level that virtually guarantees expression of small LDL particles and increased cardiovascular risk.

Based on observations like these, in the Track Your Plaque program we aim for fasting triglycerides of no higher than 60 mg/dl and postprandial (after-meal) triglycerides of no more than 90 mg/dl.

Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role. That will be an issue for another day.

1985: The Year of Whole Grains

In 1985, the National Cholesterol Education Panel delivered its Adult Treatment Panel guidelines to Americans, advice to cut cholesterol intake, reduce saturated fat, and increase "healthy whole grains" to reduce the incidence of heart attack and other cardiovascular events.

Per capita wheat consumption increased accordingly. Wheat consumption today is 26 lbs per year greater than in 1970 and now totals 133 lbs per person per year. (Because infants and children are lumped together with adults, average adult consumption is likely greater than 200 lbs per year, or the equivalent of approximately 300 loaves of bread per year.) Another twist: The mid- and late-1980s also marks the widespread adoption of the genetically-altered dwarf variants of wheat to replace standard-height wheat.

In 1985, the Centers for Disease Control also began to track multiple health conditions, including diabetes. Here is the curve for diabetes:


Note that, from 1958 until 1985, the curve was climbing slowly. After 1985, the curve shifted sharply upward. (Not shown is the data point for 2010, an even steeper upward ascent.) Now diabetes is skyrocketing, projected to afflict 1 in 3 adults in the coming decades.

You think there's a relationship?

Have some more

Wheat, via exorphin effects, is an appetite stimulant. Eat a whole wheat bagel or bran muffin, you want another. You also want more of other foods. You also want something to eat every two hours due to widely-swinging insulin-glucose responses: blood sugar high followed by a sharp downturn that triggers a powerful impulse to eat (thus the cravings for a snack at 9 and 11 a.m. after a 7 a.m. breakfast).

If wheat is a stimulant of appetite, then removing it should yield reduced appetite and reduced calorie intake. That is precisely what happens.

When wheat products are removed from the diet--without calorie restriction, without counting fat or carbohydrate grams, no exercise program, no cleansing regimen, no skipping meals . . . nothing--calorie intake drops 350 to 400 calories per day. This calorie figure remains curiously consistent across multiple studies in which wheat was eliminated.

400 calories per day results in 21 lbs lost over 6 months, based just on calories. (3500 calories per pound lost.) That is what happens in wheat elimination diets: 21-26 lbs lost over 6 months.

Wheat is the processed food industry's nicotine, a means of ensuring repeat food purchases. It's also low-cost (subsidized by the U.S. government), high-yield, an ingredient that even has its very own withdrawal syndrome should you miss a "hit."

When MIGHT statins be helpful?

I spend a lot of my day bashing statin drugs and helping people get rid of them.

But are there instances in which statin drugs do indeed provide real advantage? If someone follows the diet I've articulated in these posts and in the Track Your Plaque program, supplements omega-3 fatty acids and vitamin D, normalizes thyroid measures, and identifies and corrects hidden genetic sources of cardiovascular risk (e.g., Lp(a)), then are there any people who obtain incremental benefit from use of a statin drug?

I believe there are some groups of people who do indeed do better with statin drugs. These include:

Apoprotein E4 homozygotes

Apoprotein E2 homozygotes

Familial combined hyperlipidemia (apoprotein B overproduction and/or defective degradation)

Cholesteryl ester transfer protein homozygotes (though occasionally manageable strictly with diet)

Familial heterozygous hypercholesterolemia, familial homozygous hypercholesterolemia

Other rare variants, e.g., apo B and C variants

The vast majority of people now taking statin drugs do NOT have the above genetic diagnoses. The majority either have increased LDL from the absurd "cut your fat, eat more healthy whole grains" diet that introduces grotesque distortions into metabolism (like skyrocketing apo B/VLDL and small LDL particles) or have misleading calculated LDL cholesterol values (since conventional LDL is calculated, not measured).

As time passes, we are witnessing more and more people slow, stop, or reverse coronary plaque using no statin drugs.

Like antibiotics and other drugs, there may be an appropriate time and situation in which they are helpful, but not for every sneeze, runny nose, or chill. Same with statin drugs: There may be an occasional person who, for genetically-determined reasons, is unable to, for example, clear postprandial (after-eating) lipoproteins from the bloodstream and thereby develops coronary atherosclerotic plaque and heart attack at age 40. But these people are the exception.

Advanced topics in nutrition

Nutrition in the modern world has become an increasingly problematic topic. From genetic modification to commercialized methods of mass production, we are having to navigate all manner of complex issues in food choices, particularly if ideal health, including maximal control over coronary plaque, is among our goals.

We will therefore be releasing a series of discussions on the Track Your Plaque website in the coming months, a series I call "Track Your Plaque Advanced Topics in Nutrition." These will be, as the series title suggests, discussions for anyone interested in more than the "eat a balanced diet" nonsense that issues from "official" sources. Among the topics to be covered:

1)Advanced Glycation End-products--both endogenous and exogenous, including peripheral issues like lipoxidation and acrylamides.

2)Dietary influences on LDL oxidation--including the concept of "glycoxidation." Protection from oxidative phenomena is not just about taking antioxidants.

3) Foods you MUST eat--We've talked a lot about foods that you shouldn't eat. How about foods you should eat?

The New Track Your Plaque Guide now available

The New Track Your Plaque Guide is now available!

The Track Your Plaque program has evolved over its 8 year history. While the original Track Your Plaque book reflected the program details that got the program started back in 2003-2004, plenty has changed.

This new version of the book, what I call the program Guide, represents version 2.0 of Track Your Plaque and includes:

--Updated lipoprotein treatment strategies--including new and expanded treatment choices for small LDL and lipoprotein(a).

--An entire chapter on vitamin D and its crucial role in cardiovascular health and plaque control.

--A new and expanded diet--All the reasons why the New Track Your Plaque Diet can achieve spectacular improvement in lipids/lipoproteins, reversal of insulin resistance/pre-diabetes/diabetes, weight loss, reduction in blood pressure, etc. are discussed in considerable detail. The diet is crafted to achieve maximum control over both metabolic responses and coronary plaque.

--An entire chapter on the role of omega-3 fatty acids is included.

--A detailed discussion on the role of iodine and thyroid health--One of the newest additions to the Track Your Plaque menu of strategies is to achieve and maintain ideal thyroid health. This tips the scales in your favor for improved control over lipids/lipoproteins, weight, blood sugar, and coronary plaque.


The new guide, as well as our new Member kits that include the new Track Your Plaque Recipe Book, At-Home Lab Test kits, and nutritional supplements, are all available in the Track Your Plaque Marketplace.

Don't wet yourself

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

Modern wheat, in particular, is capable of causing "celiac disease" without intestinal symptoms---no cramping or diarrhea--but instead shows itself as brain injury (ataxia, dementia), peripheral nervous system damage (peripheral neuropathy), joint and muscle inflammation (rheumatoid arthritis, polymyalgia rheumatica and others), and gastrointestinal cancers.

One neurological manifestation of wheat's effect on the human brain is a condition called cerebellar ataxia. This is a condition that can affect adults (average age 48 years) and children and consists of incoordination, falls, and incontinence.

Because brain tissue has limited capacity for healing and regeneration, symptoms of cerebellar ataxia usually improve slowly and modestly with meticulous elimination of wheat and other gluten sources.

Such observations are relevant even to people without celiac disease. Celiac disease sufferers are more susceptible to such extra-intestinal phenomena, but it can also happen in people without positive celiac antibodies.



Some references:

Neurological symptoms in patients with biopsy proven celiac disease

A total of 72 patients with biopsy proven celiac disease (CD) (mean age 51 +/- 15 years, mean disease duration 8 +/- 11 years) were recruited through advertisements. All participants adhered to a gluten-free diet. Patients were interviewed following a standard questionnaire and examined clinically for neurological symptoms. Medical history revealed neurological disorders such as migraine (28%), carpal tunnel syndrome (20%), vestibular dysfunction (8%), seizures (6%), and myelitis (3%). Interestingly, 35% of patients with CD reported of a history of psychiatric disease including depression, personality changes, or even psychosis. Physical examination yielded stance and gait problems in about one third of patients that could be attributed to afferent ataxia in 26%, vestibular dysfunction in 6%, and cerebellar ataxia in 6%. Other motor features such as basal ganglia symptoms, pyramidal tract signs, tics, and myoclonus were infrequent. 35% of patients with CD showed deep sensory loss and reduced ankle reflexes in 14%. Gait disturbances in CD do not only result from cerebellar ataxia but also from proprioceptive or vestibular impairment.



Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics

Two hundred and twenty-four patients with various causes of ataxia from North Trent (59 familial and/or positive testing for spinocerebellar ataxias 1, 2, 3, 6 and 7, and Friedreich's ataxia, 132 sporadic idiopathic and 33 clinically probable cerebellar variant of multiple system atrophy MSA-C) and 44 patients with sporadic idiopathic ataxia from The Institute of Neurology, London, were screened for the presence of antigliadin antibodies. A total of 1200 volunteers were screened as normal controls. The prevalence of antigliadin antibodies in the familial group was eight out of 59 (14%), 54 out of 132 (41%) in the sporadic idiopathic group, five out of 33 (15%) in the MSA-C group and 149 out of 1200 (12%) in the normal controls. The prevalence in the sporadic idiopathic group from London was 14 out of 44 (32%). The difference in prevalence between the idiopathic sporadic groups and the other groups was highly significant (P < 0.0001 and P < 0.003, respectively). The clinical characteristics of 68 patients with gluten ataxia were as follows: the mean age at onset of the ataxia was 48 years (range 14-81 years) with a mean duration of the ataxia of 9.7 years (range 1-40 years). Ocular signs were observed in 84% and dysarthria in 66%. Upper limb ataxia was evident in 75%, lower limb ataxia in 90% and gait ataxia in 100% of patients. Gastrointestinal symptoms were present in only 13%. MRI revealed atrophy of the cerebellum in 79% and white matter hyperintensities in 19%. Forty-five percent of patients had neurophysiological evidence of a sensorimotor axonal neuropathy. Gluten-sensitive enteropathy was found in 24%. HLA DQ2 was present in 72% of patients. Gluten ataxia is therefore the single most common cause of sporadic idiopathic ataxia.