CIS: Carbohydrate intolerance syndrome 28. enero 2009 William Davis (28) Carbohydrate intolerance comes in many shades and colors, shapes and sizes. I call all of its varieties the Carbohydrate Intolerance Syndrome, or CIS. (Not to be confused with CSI, or Crime Scene Investigation . . . though, come to think of it, perhaps there are some interesting parallels!)At its extreme, it is called type II diabetes, in which any carbohydrate generates an extravant increase in blood sugar, followed by the domino effect of increased triglycerides, reduction in HDL, creation of small LDL, heightened inflammation, etc. and eventually to kidney disease, coronary atherosclerosis, neuropathies, etc. An intermediate form of carbohydrate intolerance is called metabolic syndrome, or pre-diabetes. These people, for the most part, look and act like diabetics, though their reaction to carbohydrate intake is not as bad. Blood sugar, for instance, might be 125 mg/dl fasting, 160 mg/dl after eating. The semi-arbitrary definition of metabolic syndrome includes at least three of the following: HDL <40 mg/dl in men, <50 mg/dl in women; triglycerides 150 mg/dl or greater; BP 135/80 or greater; waist circumference >40 inches in men, >35 inches in women; fasting glucose >100 mg/dl. This is where the conventional definitions stop: Either you are diabetic or have metabolic syndrome, or you have nothing at all. Unfortunately, this means that the millions of people with patterns not severe enough to match the standard definition of metabolic syndrome are often neglected.How about Kevin? Kevin, a 56 year old financial planner, is 5 ft 7 inches, 180 lbs (BMI 28.2). His basic measures:HDL 36 mg/dlTriglycerides 333 mg/dlBP 132/78Waist circumference 34 inchesBlood sugar 98 mg/dlKevin meets the criteria for metabolic syndrome on only two of the five criteria and therefore does not "qualify" for the diagnosis. Kevin's basic lipids showed LDL 170 mg/dl, HDL 36 mg/dl, triglycerides 333 mg/dl.But take a look at his underlying lipoprotein patterns (NMR):LDL particle number 2231 nmol/L (equivalent to a "true" LDL of 223 mg/dl)Small LDL 1811 nmol/l Large HDL 0.0 mg/dlIn other words, small LDL constitutes 81% of all LDL particles (1811/2231), a severe pattern. Large HDL is the healthy, protective fraction and Kevin has none. These are high-risk patterns for heart disease. These, too, are patterns of carbohydrate intolerance.Foods that trigger small LDL and reduction in healthy, large HDL include sugars, wheat, and cornstarch. Kevin is carbohydrate-intolerant, although he lacks the (fasting) blood sugar aspect of carbohydrate intolerance. But he shows all the underlying lipoprotein and other metabolic phenomena associated with carbohydrate intolerance. We could also cast all three conditions under the umbrella of "insulin resistance." But I prefer Carbohydrate Intolerance Syndrome, or CIS, since it immediately suggests the basic underlying cause: eating carbohydrates, especially those that trigger rapid and substantial surges in blood sugar. CIS is the Disease of the Century, judging by the figures (both numbers and humans) we are seeing. It will dominate healthcare in its various forms for many years to come. The first treatment for the Carbohydrate Intolerance Syndrome? Some would say the TZD class of drugs like Avandia. Others would say a DASH or TLC (American Heart Association) diet. How about liposuction, twice-daily Byetta injections, or even the emerging class of drugs to manipulate leptin and adiponectin? How do "heart healthy" foods like Cheerios and Cocoa Puffs fit into this? (Don't believe me? The American Heart Association says they're heart healthy!)The first treatment for the Carbohydrate Intolerance Syndrome is elimination of carbohydrates, except those that come from raw nuts and seeds, vegetables, occasional real fruit (not those green fake grapes), wine, and dark chocolates.
Making sense out of lipid changes 27. enero 2009 William Davis (9) Maggie had been doing well on her program, enjoying favorable lipids near our 60-60-60 targets (HDL 60 mg/dl or greater, LDL 60 mg/dl or less, triglycerides 60 mg/dl or less). Last fall, her last set of values were:Total cholesterol: 149 mg/dlLDL cholesterol: 67 mg/dlHDL cholesterol: 73 mg/dlTriglycerides: 43 mg/dl The holidays, as with most people, involved a frenzy of indulgent eating: Christmas cookies, cakes, pies, stuffing, potatoes, candies, etc.Maggie returned to the office 6 pounds heavier with these values: Total cholesterol: 210 mg/dlLDL cholesterol: 124 mg/dlHDL cholesterol: 57 mg/dlTriglycerides: 144 mg/dl In other words, holiday indulgences caused an increase in LDL cholesterol, a reduction in HDL, an increase in triglycerides, an increase in total cholesterol. What happened? At first glance, many of my colleagues would interpret this as fat indulgence and/or a "need" for statin drug therapy. Having done thousands of lipoprotein panels, I can tell you that, beneath the surface, the following has occurred:--Overindulgence in carbohydrates from the goodies triggered triglyceride (actually VLDL) formation in the liver, released into the blood. --Increased triglycerides and VLDL triggered a boom in conversion of large LDL to small LDL (since triglycerides are required to form small LDL particles) via cholesteryl-ester transfer protein (CETP) activity.--Increased triglycerides and VLDL interacted with HDL particles, causing "remodeling" of HDL particles to the less desirable, less protective small particles, which do not persist as long in the blood, resulting in a reduction of HDL. The critical factor is carbohydrate intake. This triggered a domino effect that is often misintepreted as excessive fat intake or a genetic predisposition. It is nothing of the kind. I discussed this phenomenon with Maggie. She now knows to not overindulge in the holiday snacks in future and will revert promptly back to her 60-60-60 values.
How to Give Yourself Hashimoto's Thyroiditis: 101 25. enero 2009 William Davis (18) I borrowed this from the enormously clever Dr. BG at The Animal Pharm Blog. How to Give Yourself Hashimoto's Thyroiditis: 101--lack of sunlight/vitamin D/indoor habitation--mental stress--more mental stress--sleep deprivation... (excessive mochas/lattes at Berkeley cafes)--excessive 'social' calendar--inherent family history of autoimmune disorders (who doesn't??)--wheat, wheat, and more wheat ingestion ('comfort foods' craved in times of high cortisol/stress, right? how did I know the carbs were killing me?)--lack of nutritious food containing EPA DHA, vitamin A, sat fats, minerals, iodine, etc--lack of play, exercise, movement (or ?overtraining perhaps for Oprah's case)--weight gain -- which begins an endless self-perpetuating vicous cycle of all the above (Is it stressful to balloon out for no apparent reason? YES)If you haven't done so already, take a look at Animal Pharm you will get a real kick out of Dr. BG's quick-witted take on things. We are systematically looking for low thyroid (hypothyroidism) in everyone and findings oodles of it, far more than I ever expected. Much of the low thyroid phenomena is due to active or previous Hashimoto's thyroiditis, the inflammatory process that exerts destructive effects on the delicate thyroid gland. It is presently unclear how much is due to iodine deficiency in this area, though iodine supplementation by itself (i.e., without thyroid hormone replacement) has not been yielding improved thyroid measures.I find this bothersome: Is low thyroid function the consequence of direct thyroid toxins (flame retardants like polybrominated diphenyl ethers, pesticide residues in vegetables and fruits, bisphenol A from polycarbonate plastics) or indirect toxins such as wheat via an autoimmune process (similar to that seen in celiac disease)? I don't know, but we've got to deal with the thyroid-destructive aftermath: Look for thyroid dysfunction, even in those without symptoms, and correct it. This has become a basic tenet of the Track Your Plaque approach for intensive reduction of coronary risk.
Framing 24. enero 2009 William Davis (0) Heart health without a 12" incisionHeart health for less than $44,483 (Cost of a coronary stent according to the American Heart Association 2008 Update)Track Your Plaque: A drug-free zone
Why an RDA for vitamin D? 24. enero 2009 William Davis (10) The Food and Nutrition Board (FNB) of the Institute of Medicine is charged with setting the values for the Recommended Daily Allowances of various essential nutrients. However, when it comes to vitamin D, the FNB decided that "evidence is insufficient to develop an RDA and [an Adequate Intake, AI] is set at a level assumed to ensure nutritional adequacy."The National Institutes of Health Office of Dietary Supplements lists the AI's for various groups of people:14-18 years Male 200 IUFemale 200 IU 19-50 years Male 200 IUFemale 200 IU 51-70 years Male 400 IUFemale 400 IU 71+ years Male 600 IUFemale 600 IU A reconsideration is apparently being planned in near-future that will (hopefully) incorporate the newest clinical data on vitamin D. My question: Who cares what the FNB decides? Let me explain. I monitor blood levels of 25-hydroxy vitamin D to assess the 1) starting level of vitamin D without supplementation, and 2) levels while on supplementation, preferably every 6 months (during sunny weather, during cold weather). I have done for the past 3 years in over 1000 people. The requirement for vitamin D dose in adults, in my experience, ranges from as low as 1000 units per day to as high as 20,000 units per day, rarely more. The vast majority of women require 5000 units per day, males 6000 units per day to maintain a blood level in the desirable range. (I aim for 60-70 ng/ml.) A graph of the distribution of vitamin D needs in my area (Milwaukee, Wisconsin) is a bell curve, a curve more heavily weighted towards the upper vitamin D dose range. Need for vitamin D to achieve the same blood level is influenced by age, sex, body size, race, presence or absence of a gallbladder, as well as other factors. But needs vary, even among similar people. For instance, a 50-year old woman weighing 140 lbs might need 4000 units per day to achieve a blood level of 25-hydroxy vitamin D of 65 ng/ml. Another 50-year old woman weighing 140 lbs might need 8000 units to achieve the same level, and 4000 units might increase her level to only 38 ng/ml. Two similar women, very different vitamin D needs. The differences can be striking. Being a hormone--not a vitamin, as it was incorrectly labeled--vitamin D needs to be tightly regulated. We should have neither too little nor too much. I would liken it to thyroid hormones, which need to be tightly regulated for ideal health. Now the FNB, in light of new data, wants to set new AI's, or even RDA's, for vitamin D for the U.S. This is an impossible--impossible--task. There is no way a broad policy can be crafted that serves everyone. It is impossible to state that all men or women, categorized by age, require X units vitamin D. This is pure folly and it is misleading. The only rational answer for the FNB to provide is to declare that:It is not possible to establish the precise need for vitamin D in a specific individual because of the multiplicity of factors, only some of which are known, that determine vitamin D needs. Individual need can only be determined by assessing the blood level of 25-hydroxy vitamin D prior to initiation of replacement and periodically following replacement to assess the adequacy of replacement dose. Continuing reassessment is recommended (e.g., every 6-12 months), as needs change with weight, lifestyle, and age. Sure, it adds around $100-150 per year per person for lab testing to assess vitamin D levels. But the health gains made--reduced fractures, reduced incidence of diabetes, reduced colon, breast, and prostate cancer, less depression, reduced heart attack and heart procedures--will more than compensate.
Bargains for Armour Thyroid 23. enero 2009 William Davis (10) We use Armour thyroid almost exclusively. I take it myself. I am thoroughly convinced that, for at least 70% of people requiring thyroid replacement, the added T3 component makes a world of difference compared to isolated T4: More energy, greater alertness, better mental clarity, better weight loss, larger effects on lipoprotein(a). However, there are substantial price disparities in different pharmacies. For instance, in Milwaukee, a one month supply of 1 grain (60 mg) tablets costs:Walgreen's: $36.00Walmart: $9.54That's a considerable price difference of nearly 400%. It therefore always pays to do a little bit of shopping.
Heart scan mis-information on WebMD 22. enero 2009 William Davis (3) If you want information on how prescription drugs fit into your life, then go to WebMD. But, if you are looking for information that cuts through the bullcrap, is untainted by the heavy-handed tactics of the drug industry, or doesn't support the "a heart catheterization for everyone" mentality, then don't go there. A Heart Scan Blog reader turned up this gem on the WebMD site:Should I have a coronary calcium scan to check for heart disease?In their report, they list some reasons why a heart scan should not be obtained: Most of the time, a physical exam and other tests can give your doctor enough information about your risk for heart disease.You've got to be kidding me. What tests are they talking about? EKG? An EKG is a crude test that tells us virtually nothing about the coronary arteries or risk for heart attack. It is helpful for heart rhythm disorders and other abnormalities, but virtually useless for coronary disease unless a heart attack is underway or has already occurred. Cholesterol? What level of cholesterol tells you whether you have heart disease? Tim Russert, for instance, had the same cholesterol values 5 years before his death as on the day of his death. How would cholesterol have told his doctor that heart disease was present? Does an LDL cholesterol of 180 mg/dl tell you that someone has heart disease, while a value of 130 mg/dl does not?Stress test? You mean like the normal stress test Bill Clinton had 3 months before his near-fatal collapse? Stress tests are a gauge of coronary flow, not of coronary atherosclerosis. Huge amounts of coronary plaque can be present while a stress test--flow--remains normal.No, a physical exam does not uncover hidden heart disease. The annual physical is, in fact, a miserable failure for detection of hidden heart disease. You already know that your risk for heart disease is low or high. The test works best in people who are at medium risk but have no symptoms. This bit of fiction comes from a compromise statement in the American College of Cardiology and American Heart Association "consensus" document detailing the role of heart scans in heart disease detection. Because conventional thinkers don't like the idea of very early detection in seemingly "low risk" people, nor do they like the idea of diabetics and smokers getting a heart scan because it's "obvious" that they are already at high risk, the middle ground was taken: Scan only people at "intermediate risk." What the heck is "intermediate risk"? Are you intermediate risk? In real life, using standard criteria (e.g., Framingham scoring) to decide who is low-, intermediate-, or high-risk fails to identify over 1/3 of people with heart disease, while subjecting many without heart disease (plaque) to needless treatment (meaning statins, since that's the only real preventive treatment on most doc's armamentarium).Another fact: Heart scans are quantitative, not just normal or abnormal. Your heart scan score could be 5, it could be 150, it could be 500, or 5000---it makes a world of difference. The risk of someone with a score of 5000 is at very different risk than someone with a score of 5. It also provides much greater precision in determining a specific individual's risk. The test could give a high score even if your arteries aren't blocked. This might lead to extra tests that you don't need.This is true--if you doctor has no idea what he's doing. This is like saying that you should never take your car to the repair shop because all mechanics are crooks. If you have an unscrupulous cardiologist who tells you that your heart scan score of 25 means you are a "walking time bomb" and heart catheterization is necessary to determine whether you "need" a stent . . . well, this is no different than the shady mechanic who advises you that your car's engine needs to be rebuilt for $3000, when all you really needed was a few new spark plugs. Coronary plaque is coronary plaque, and all coronary plaque has potential for rupture (heart attack)--even if it doesn't block flow. This is true at a score of 10, or 100, or 1000--all plaque is potentially rupture-prone, though the more plaque you have, the greater the likelihood. Not all blocked arteries have calcium. So you could get a low calcium score and still be at risk. They're missing the point: ANY calcium score carries risk, so a low score should not be interpreted as having no risk. But, just because a procedure like stenting or bypass surgery is not necessary to restore flow, it does not mean that risk for plaque rupture is not present--it is. Any heart scan score should be taken seriously, meaning sufficient reason to engage in a program of heart disease prevention. Although not perfect, coronary calcium scoring remains the easiest, most accessible, and least expensive means for identifying and quantifying coronary atherosclerosis--whether or not WebMD and drug industry money endorse them.
Heart disease prevention for the helpless, ignorant, or non-compliant 19. enero 2009 William Davis (9) The media outlets are gushing with the "research"/marketing spinoff of the JUPITER trial, an analysis conducted by Dr. Erica Spatz of Yale University, that suggests that statin use should be expanded to many millions more Americans. USA Today: Study: 11M more should get statinsMedPage: JUPITER Findings Could Boost Statin Use by 20%Health Day: Millions More Americans Might Be Placed on StatinsWebMD: More May Benefit From Cholesterol Drugs: Study Shows More Would Qualify for Statin Treatment if Levels of C-Reactive Protein Are ConsideredYou may recall that the JUPITER trial (discussed previously in a Heart Scan Blog post) studied the cardiovascular event risk in people with "normal" LDL cholesterols (calculated, of course, not measured) of 130 mg/dl or less, along with increased c-reactive protein, a crude inflammatory measure, of 2.0 mg/dl or greater. A 54% (relative) reduction in cardiovascular events occured in the group taking Crestor 20 mg per day.What I see is a confluence of events that have brought us to the "statin drugs are necessary for everybody" mentality: --The low-fat diet advice of the last 40 years has increased non-fat or low-fat foods that increase LDL, since removing fat from the diet provokes small LDL particle production and increases the inflammatory measure, c-reactive protein (CRP). --The proliferation of "healthy whole grains" in the diet have also caused an enormous boom in small LDL particles, which is interpreted to the uninformed as "high cholesterol." It has also provoked CRP substantially. --The advice to reduce salt intake has brought a broad re-emergence of iodine deficiency. When thyroid hormone production flags due to lack of iodine, LDL cholesterol (both large and small) increase. --Our lives, which are increasingly conducted indoors, have worsened the already substantial vitamin D deficiency. While deficiency of vitamin D primarily reduces HDL cholesterol and increases triglycerides, it can also cause an increase in small LDL and a large increase in CRP. In other words, a collection of events have converged to provide the appearance of high LDL cholesterol and high CRP. This creates the appearance of a "need" for statin drugs. The JUPITER trial now exploits both the LDL-reducing and CRP-decreasing effects of statins.I view the foisting of Crestor via the JUPITER argument on the public as taking full advantage of the helpless situation many Americans find themselves in: Reduce fat intake, eat more healthy whole grains and . . . cholesterol and CRP skyrocket! "You need Crestor! See, I told you it was genetic," says the doctor after attending the nice AstraZeneca-sponsored drug dinner. The notion of using a drug like Crestor to suppress inflammatory patterns is absurd. There are far better, easier, cheaper ways to achieve this goal, along with dramatic reduction in cardiovascular risk. But, to the ignorant, the helpless, or non-compliant with real change in diet and lifestyle, then Crestor does serve a purpose. I can only hope that the excessive pushing of statin drugs on the public will sooner or later trigger a revolt.
Dangerous mis-information on vitamin D 16. enero 2009 William Davis (12) Please be aware of the ignorant propagating information they have no business talking about. This is one such example, a newsletter from pop exercise guru, Denise Austin. Although I'm sure she means well, I have a problem with people who have little to no experience acting as experts, often simply repeating something they heard or read somewhere else. This has become particular problem with the internet, in which bad information can get repeated thousands of times, gaining a veil of "truth" through its repetition. I don't mean to pick specifically on Ms. Austin, since she joins a growing rank of pseudo-experts on vitamin D and other topics, but she provides a good example of how far wrong mainstream information can be. Simple StepsDo Your D!Calcium often gets all the glory when it comes to bone health. But calcium wouldn't benefit your bones much without its partner, vitamin D!Why? Vitamin D helps your body absorb calcium and keeps your bones strong; without enough vitamin D, the bones become weak and brittle, a condition called rickets in children, and osteomalacia in adults. Adults from 19 to 50 need 200 IU (international units) per day, while those from 51 to 70 need 400 IU daily. Those over 70 need 600 IU per day.Unfortunately, not too many foods contain vitamin D naturally. (Tuna and sardines canned in oil are exceptions.) The good news is that many foods are now regularly fortified with vitamin D, including milk, some yogurts, margarines, and cereals. You can check the Nutrition Facts panel on packages and containers to see which products contain vitamin D. It should be listed after vitamins A and C, along with the percentage of the Daily Value that a serving of the food contains. The Daily Value (a standardized amount) for vitamin D is 400 IU, so if your milk has 25 percent of the Daily Value, it provides 100 IU per serving.Your skin can also make vitamin D using sunlight — you need about a half hour of exposure to the midday sun twice a week to make enough. However, because of the increasing incidence of skin cancer in recent years, many experts are wary about recommending sun exposure.So take a closer look at milk, yogurt, cereal, and margarine selections when you're doing your weekly shopping, and stock up on brands that are fortified with vitamin D. Challenge yourself to consume one source of vitamin D at least three days in the coming week! If you cannot eat or do not like any foods that contain vitamin D or are fortified with it, talk with your health care provider ASAP about taking a supplement. Your bones will thank you for it!Let me list the mistakes in this piece: Adults from 19 to 50 need 200 IU (international units) per day, while those from 51 to 70 need 400 IU daily. Those over 70 need 600 IU per day.This is the same non-information that was the advi Cureality | Real People Seeking Real Cures Toggle navigation Home Blog Home Archive Join Now Log in You just THINK you're low-carb 27. February 2010 William Davis (72) Systematically checking postprandial (after-eating) blood sugars is providing some great insights into crafting a better diet for many people. I last discussed the concept of postprandial glucose checks in To get low-carb right, you need to check blood sugars.Here are some important lessons that many people--NON-diabetic people, most with normal blood glucoses or just mildly increased--are learning:Oatmeal yields high blood sugars. Even if your fasting blood sugar is 90 mg/dl, a bowl of oatmeal with skim milk, walnuts, and some berries will yield blood sugars of 150-200 mg/dl in many people. Cheerios yields shocking blood sugars. 200+ mg/dl is not uncommon in non-diabetics. (Diabetics have 250-350 mg/dl.) Fruits like apples and bananas increase blood sugar to 130 mg/dl or higher. Odd symptoms, such as mental "fog," fatigue, and a fullness in the head, are often attributable to high blood sugars. A subset of people with lipoprotein(a) can have wildly increased blood sugars despite their slender build and high aerobic exercise habits. Once you identify the high blood sugar problem, you can do something about it. The best place to start is to reduce or eliminate the sugar-provoking food. The LDL-Fructose Disconnect 26. February 2010 William Davis (8) I believe that we can all agree that the commonly obtained Friedewald LDL cholesterol (what I call "fictitious" LDL cholesterol) is wildly inaccurate. 100%--yes, 100% inaccuracy--is not at all uncommon.This flagrant inaccuracy, unacceptable in virtually every other discipline (imagine your airplane flight to New York lands in Pittsburgh--close enough, isn't it?), is highlighted in the University of California study by Stanhope et al I discussed previously.32 participants consumed either a diet enriched with either fructose or glucose. Compared to the effect of glucose, after 10 weeks fructose:Increased LDL cholesterol (calculated) by 7.6%Increased Apoprotein B (a measure of the number of LDL particles) by 24%Increased small dense LDL by 41%Increased oxidized LDL by 12.6% In other words, conventional calculated LDL substantially underestimates the undesirable effects of fructose. The divergence between calculated LDL and small LDL is especially dramatic. (By the way, this same divergence applies to the studies suggesting that calculated LDL cholesterol is reduced by low fat diets--While calculated LDL may indeed be reduced, small LDL goes way up, a striking divergence.) This is yet another reason to not rely on this "fictitious" LDL cholesterol value that, inaccuracies notwithstanding, serves as the foundation for a $27 billion per year industry. I told you bread was bad 26. February 2010 William Davis (10) "I dream about bread" 25. February 2010 William Davis (14) Marion sat in my office, sobbing. It had been 4 weeks since the last piece of bread, bagel, or bun had passed her lips. "I can't do it! I just can't do it! I've tried to eliminate wheat, but it's making me crazy. I'm having dreams about bread!"Yes, Timmy, such dark corners of human behavior are truly unveiled by removing wheat from the diet. (See the previous Heart Scan Blog post, Wheat withdrawal.)This is a real phenomenon: Wheat is the crack cocaine of the masses. Maybe you don't exchange $100 bills in dark corners of an inner city crack house, but I'll bet you paid $3.99 for your latest fix of French bread. Just in the last 2 weeks, people in my office who have eliminated wheat have experienced:14 lbs weight loss in 14 daysIncreased mental clarity, reduced moodiness, deeper sleep70% reductions in small LDL More than 300 mg/dl reductions in triglyceridesRelief from chronic scalp rashI could go on. All the while, the USDA, the American Heart Association, the American Diabetes Association, the American Dietetic Association, the Surgeon General's Office all advise you to eat more "healthy whole grains." 70% of people (NOT 100%, but the majority) will experience unexpected health benefits by eliminating this corrupt, unphysiologic product called wheat from their diet. You won't know until you try. Prototypical Lipoprotein(a) 25. February 2010 William Davis (23) Here's the prototypical male with lipoprotein(a):Several features stand out in the majority of men with lipoprotein(a), Lp(a):Slender--Sometimes absurdly so: BMIs of 21-23 are not uncommon. These are the people who claim they can't gain weight. Intelligent--Above average to way above average intelligence is the rule. Gravitate to technical work--Plenty of engineers, scientists, accountants, and other people who work with numbers and/or technical details are more likely to have Lp(a). Enjoy high levels of aerobic performance--I tell my Lp(a) patients that, if they want to see a bunch of other people with Lp(a), go to a marathon or triathlon. They'll see plenty of people with the pattern among the aerobically-elite. Are rabid fans of Star Trek. Okay, I made the last one up. But the rest are uncannilly true, shared by the majority (though not all) men with Lp(a). Why? I can only speculate that the gene(s) for Lp(a) are closely linked to gene(s) for intelligence of a quantitative kind and some factor that enhances aerobic performance or yields a desirable emotional state with exercise. Oddly, the same patterns tend not to occur in women in Lp(a). I have yet to discern a personality or body configuration phenotype among the ladies. Gastric emptying: When slower is better 20. February 2010 William Davis (18) When it comes to the Internet and Nascar, speed is good: The faster the better. But when it comes to gastric emptying (the rate at which food passes from the stomach and into the duodenum and small intestine), slower can be better. Slower transit time for foods passing through the stomach leads to lower blood sugar, lower blood glucose area under-the-curve (AUC), i.e., reduced blood glucose levels over time. Lower postprandial (after-eating) blood sugars can reduce cardiovascular risk. It can lead to a reduction in net calorie intake and weight loss. Strategies that can slow gastric emptying include:--Minimizing fluids during a meal--Drinking a lot of fluids, e.g., water, accelerates gastric emptying by approximately 20%. --Cinnamon--While the full reason to explain Cassia cinnamon's blood glucose-reducing effect has not been completely worked out, part of the effect is likely to due slowed gastric emptying. Thus, a 1/4-2 teaspoons of cinnamon per day can reduce postprandial blood sugar peaks by 10-25 mg/dl. --Vinegar--Two teaspoons of vinegar in its various forms slows gastric emptying. The effect is likely due to acetic acid, the compound shared by apple cider vinegar, white vinegar, red wine vinegar, Balsamic vinegar, and other varieties. --Increased fat content--Fat is digested more slowly and slows gastric emptying time, compared to the rapid transit of carbohydrates. Not everybody should slow gastric emptying. Diabetics with a condition called diabetic gastroparesis should not use these methods, as they can further slow the abnormal gastric emptying that develops as part of their disease, making a bad situation worse. However, in the rest of us with normal gastric emptying time, a delay in gastric emptying can reduce blood sugar and induce satiety, effects that can work in your favor in reducing cardiovascular risk. Genetic vs. lifestyle small LDL 19. February 2010 William Davis (59) Let me explain what I mean by "genetic small LDL." I think it helps to illustrate with two common examples. Ollie is 50 years old, 5 ft 10 inches tall, and weighs 253 lbs. BMI = 36.4 (obese). Starting lipoproteins (NMR):LDL particle number 2310 nmol/LSmall LDL: 1893 nmol/L (1893/2310 = 81.9% of total, a severe small LDL pattern)Stan is 50 years old, also, 5 ft 10 inches tall, and weighs 148 lbs. BMI = 21.3. Starting lipoproteins:LDL particle number 1424 nmol/LSmall LDL 1288 nmol/L (1288/1424 = 90.4% of total, also severe)Both Ollie and Stan go on the New Track Your Plaque diet and eliminate wheat, cornstarch, and sugars, while increasing oils, meats and fish, unlimited raw nuts, and vegetables. They add fish oil and vitamin D and achieve perfect levels of both. Six months later, Ollie has lost 55 lbs, Stan has lost 4 lbs. A second round of lipoproteins:Ollie:LDL particle number 1810 nmol/LSmall LDL: 193 nmol/L (193/1810 = 10.6% of total)Stan:LDL particle number 1113 nmol/LSmall LDL 729 nmool/L (729/1113 = 65.4% of total)Ollie has reduced, nearly eliminated, small LDL through elimination of wheat, cornstarch, and sugars, along with weight loss, fish oil, and vitamin D. Stan, beginning at a much more favorable weight, reduced both total and small LDL with the same efforts, but retains a substantial proportion (65.4%) of small LDL. Stan's pattern is what I call "genetic small LDL." Of course, this is a presumptive designation, since we've not identified the specific gene(s) that allow this (e.g., gene for variants of cholesteryl ester transfer protein, hepatic lipase, lipoprotein lipase, and others). But it is such a sharp distinction that I am convinced that people like Stan have this persistent pattern as a genetically-determined trait. Carbohydrate sins of the past 17. February 2010 William Davis (15) Fifty years ago, diabetes was a relatively uncommon disease. Today, the latest estimates are that 50% of Americans are now diabetic or pre-diabetic. There are some obvious explanations: excess weight, inactivity, the proliferation of fructose in our diets. It is also my firm belief that the diets advocated by official agencies, like the USDA, the American Heart Association, the American Dietetic Association, and the American Diabetes Association, have also contributed with their advice to eat more “healthy whole grains.” When I was a kid, I ate Lucky Charms® or Cocoa Puffs® for breakfast, carried Hoho’s® and Scooter Pies® in my lunchbox, along with a peanut butter sandwich on white bread. We ate TV dinners, biscuits, instant mashed potatoes for dinner. Back then, it was a matter of novelty, convenience, and, yes, taste. What did we do to our pancreases eating such insulin-stimulating foods through childhood, teenage years, and into early adulthood? Did our eating habits as children and young adults create diabetes many years later? Could sugary breakfast cereals, snacks, and candy in virtually unlimited quantities have impaired our pancreas’ ability to produce insulin, leading to pre-diabetes and diabetes many years later? A phenomenon called glucose toxicity underlies the development of diabetes and pre-diabetes. Glucose toxicity refers to the damaging effect that high blood sugars (glucose) have on the delicate beta cells of the pancreas, the cells that produce insulin. This damage isirreversible: once it occurs, it cannot be undone, and the beta cells stop producing insulin and die. The destructive effect of high glucose levels on pancreatic beta cells likely occurs through oxidative damage, with injury from toxic oxidative compounds like superoxide anion and peroxide. The pancreas is uniquely ill-equipped to resist oxidative injury, lacking little more than rudimentary anti-oxidative protection mechanisms. Glucose toxicity that occurs over many years eventually leaves you with a pancreas that retains only 50% or less of its original insulin producing capacity. That’s when diabetes develops, when impaired pancreatic insulin production can no longer keep up with the demands put on it. (Interesting but unanswered question: If oxidative injury leads to beta cell dysfunction and destruction, can antioxidants prevent such injury? Studies in cell preparations and animals suggest that anti-oxidative agents, such as astaxanthin and acetylcysteine, may block beta cell oxidative injury. However, no human studies have yet been performed. This may prove to be a fascinating area for future.)Now that 50% of American have diabetes or pre-diabetes, how much should we blame on eating habits when we were younger? I would wager that eating habits of youth play a large part in determining potential for diabetes or pre-diabetes as an adult. The lesson: Don’t allow children to repeat our mistakes. Letting them indulge in a lifestyle of soft drinks, candy, pretzels, and other processed junk carbohydrates has the potential to cause diabetes 20 or 30 years later, shortening their life by 10 years. Kids are not impervious to the effects of high sugar, including the cumulative damaging effects of glucose toxicity. Saturated fat and large LDL 16. February 2010 William Davis (44) Here's a half-truth I often encounter in low-carb discussions:Saturated fat increases large LDL particlesFor those of you unfamiliar with the argument, I advocate a low-carbohydrate approach, specifically elimination of all wheat, cornstarch, and sugars, to reduce expression of the small LDL pattern (not to mention reduction of triglycerides, relief from acid reflux and irritable bowel, weight loss, various rashes, diabetes, etc). Small LDL particles have become the most common cause for heart disease in the U.S., exploding on the scene ever since agencies like the USDA and American Heart Association have been advising the public to increase consumption of "healthy whole grains." This has led some to make the pronouncement that saturated fat increases large LDL, thereby representing a benign effect. Is this true? It is true, but only partly. Let me explain. There are two general categories of factors causing small LDL particles: lifestyle (overweight, excess carbohydrates) and genetics (e.g., variants of the gene coding for cholesteryl-ester transfer protein, or CETP). If small LDL is purely driven by excess carbohydrates, then adding saturated fat will reduce small LDL and increase large LDL. If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles. So to say that saturated fat increases large LDL is an oversimplification, one that can have dire consequences in the wrong situation. Is glycemic index irrelevant? 14. February 2010 William Davis (20) University of Toronto nutrition scientist, Dr. David Jenkins, was the first to quantify the phenomenon of "glycemic index," describing how much blood sugar increased over 90 minutes compared to glucose. The graph is from their 1981 study, The glycemic index of foods: a physiologic basis for carbohydrate exchange. The research originated with an effort to characterize carbohydrates for diabetics to gain better control over blood sugar.Since Dr. Jenkins’ original work, thousands of clinical studies have been performed by others exploring this concept. The food industry has also devoted plenty of effort exploiting it (e.g., low-glycemic index noodles, low-glycemic index cereals, etc.). Most Americans are now familiar with the concept of glycemic index. You likely know that table sugar has a high glycemic index (60), increasing blood sugar to a similar degree as white bread (glycemic index 71). Oatmeal (slow-cooked) has a lower glycemic index (48), since it increases blood sugar less than white bread. A number of studies have shown that when low glycemic index foods replace high glycemic index foods (e.g., whole wheat bread in place of cupcakes), people are healthier: less diabetes, less heart attack, less high blood pressure. Books have been written about glycemic index, touting its benefits for health and weight control. Health-conscious people will try to substitute low-glycemic index foods for high-glycemic index foods. So what’s not to like here? There are several fundamental flaws with the notion that low-glycemic index foods are good for you:1) Check your blood sugar after a low-glycemic index food like oatmeal. Most non-diabetic adults will show blood sugars in the 140 to 200 mg/dl range. The more central (visceral) fat you have, the higher the value will be. In other words, an apparently “healthy” whole grain food like oatmeal can generate extravagantly high blood sugars. Repeated high blood sugars of 125 mg/dl or greater after eating increase heart disease risk by 50%. 2) Foods like whole wheat pasta have a low glycemic index because the blood sugar effect over the usual 90 minutes is increased to a lesser degree. The problem is that it remains increased for an extended period of up to several hours. In other words, the blood sugar-increasing effect of pasta, even whole grain, is long and sustained. 3) Low-glycemic index foods trigger other abnormalities, such as small LDL particles, triglycerides, and c-reactive protein (a measure of inflammation). While they are not as bad as high-glycemic index foods, they are still quite potent triggers. Low-glycemic index foods trigger the very same responses as high-glycemic index foods—they’re just less bad. But less bad does not equate to good. Low-glycemic index foods cause weight gain, trigger appetite, increase blood pressure, and lead to the patterns that cause heart disease. High-glycemic index foods are bad for you. This includes foods made with white flour (bagels, white bread, pretzels). Low-glycemic foods (whole grain bread, whole wheat crackers, whole wheat pasta) are less bad for you—but they are not necessarily good. Don’t be falsely reassured by foods because they are billed as “low-glycemic index.” View low-glycemic index foods as indulgences, something you might have once in a while, since a slice of whole grain bread is really not that different from a icing-covered cupcake. << Older posts Newer posts >> Newer posts12...282930313233343536...123124Older posts
You just THINK you're low-carb 27. February 2010 William Davis (72) Systematically checking postprandial (after-eating) blood sugars is providing some great insights into crafting a better diet for many people. I last discussed the concept of postprandial glucose checks in To get low-carb right, you need to check blood sugars.Here are some important lessons that many people--NON-diabetic people, most with normal blood glucoses or just mildly increased--are learning:Oatmeal yields high blood sugars. Even if your fasting blood sugar is 90 mg/dl, a bowl of oatmeal with skim milk, walnuts, and some berries will yield blood sugars of 150-200 mg/dl in many people. Cheerios yields shocking blood sugars. 200+ mg/dl is not uncommon in non-diabetics. (Diabetics have 250-350 mg/dl.) Fruits like apples and bananas increase blood sugar to 130 mg/dl or higher. Odd symptoms, such as mental "fog," fatigue, and a fullness in the head, are often attributable to high blood sugars. A subset of people with lipoprotein(a) can have wildly increased blood sugars despite their slender build and high aerobic exercise habits. Once you identify the high blood sugar problem, you can do something about it. The best place to start is to reduce or eliminate the sugar-provoking food.
The LDL-Fructose Disconnect 26. February 2010 William Davis (8) I believe that we can all agree that the commonly obtained Friedewald LDL cholesterol (what I call "fictitious" LDL cholesterol) is wildly inaccurate. 100%--yes, 100% inaccuracy--is not at all uncommon.This flagrant inaccuracy, unacceptable in virtually every other discipline (imagine your airplane flight to New York lands in Pittsburgh--close enough, isn't it?), is highlighted in the University of California study by Stanhope et al I discussed previously.32 participants consumed either a diet enriched with either fructose or glucose. Compared to the effect of glucose, after 10 weeks fructose:Increased LDL cholesterol (calculated) by 7.6%Increased Apoprotein B (a measure of the number of LDL particles) by 24%Increased small dense LDL by 41%Increased oxidized LDL by 12.6% In other words, conventional calculated LDL substantially underestimates the undesirable effects of fructose. The divergence between calculated LDL and small LDL is especially dramatic. (By the way, this same divergence applies to the studies suggesting that calculated LDL cholesterol is reduced by low fat diets--While calculated LDL may indeed be reduced, small LDL goes way up, a striking divergence.) This is yet another reason to not rely on this "fictitious" LDL cholesterol value that, inaccuracies notwithstanding, serves as the foundation for a $27 billion per year industry.
"I dream about bread" 25. February 2010 William Davis (14) Marion sat in my office, sobbing. It had been 4 weeks since the last piece of bread, bagel, or bun had passed her lips. "I can't do it! I just can't do it! I've tried to eliminate wheat, but it's making me crazy. I'm having dreams about bread!"Yes, Timmy, such dark corners of human behavior are truly unveiled by removing wheat from the diet. (See the previous Heart Scan Blog post, Wheat withdrawal.)This is a real phenomenon: Wheat is the crack cocaine of the masses. Maybe you don't exchange $100 bills in dark corners of an inner city crack house, but I'll bet you paid $3.99 for your latest fix of French bread. Just in the last 2 weeks, people in my office who have eliminated wheat have experienced:14 lbs weight loss in 14 daysIncreased mental clarity, reduced moodiness, deeper sleep70% reductions in small LDL More than 300 mg/dl reductions in triglyceridesRelief from chronic scalp rashI could go on. All the while, the USDA, the American Heart Association, the American Diabetes Association, the American Dietetic Association, the Surgeon General's Office all advise you to eat more "healthy whole grains." 70% of people (NOT 100%, but the majority) will experience unexpected health benefits by eliminating this corrupt, unphysiologic product called wheat from their diet. You won't know until you try.
Prototypical Lipoprotein(a) 25. February 2010 William Davis (23) Here's the prototypical male with lipoprotein(a):Several features stand out in the majority of men with lipoprotein(a), Lp(a):Slender--Sometimes absurdly so: BMIs of 21-23 are not uncommon. These are the people who claim they can't gain weight. Intelligent--Above average to way above average intelligence is the rule. Gravitate to technical work--Plenty of engineers, scientists, accountants, and other people who work with numbers and/or technical details are more likely to have Lp(a). Enjoy high levels of aerobic performance--I tell my Lp(a) patients that, if they want to see a bunch of other people with Lp(a), go to a marathon or triathlon. They'll see plenty of people with the pattern among the aerobically-elite. Are rabid fans of Star Trek. Okay, I made the last one up. But the rest are uncannilly true, shared by the majority (though not all) men with Lp(a). Why? I can only speculate that the gene(s) for Lp(a) are closely linked to gene(s) for intelligence of a quantitative kind and some factor that enhances aerobic performance or yields a desirable emotional state with exercise. Oddly, the same patterns tend not to occur in women in Lp(a). I have yet to discern a personality or body configuration phenotype among the ladies.
Gastric emptying: When slower is better 20. February 2010 William Davis (18) When it comes to the Internet and Nascar, speed is good: The faster the better. But when it comes to gastric emptying (the rate at which food passes from the stomach and into the duodenum and small intestine), slower can be better. Slower transit time for foods passing through the stomach leads to lower blood sugar, lower blood glucose area under-the-curve (AUC), i.e., reduced blood glucose levels over time. Lower postprandial (after-eating) blood sugars can reduce cardiovascular risk. It can lead to a reduction in net calorie intake and weight loss. Strategies that can slow gastric emptying include:--Minimizing fluids during a meal--Drinking a lot of fluids, e.g., water, accelerates gastric emptying by approximately 20%. --Cinnamon--While the full reason to explain Cassia cinnamon's blood glucose-reducing effect has not been completely worked out, part of the effect is likely to due slowed gastric emptying. Thus, a 1/4-2 teaspoons of cinnamon per day can reduce postprandial blood sugar peaks by 10-25 mg/dl. --Vinegar--Two teaspoons of vinegar in its various forms slows gastric emptying. The effect is likely due to acetic acid, the compound shared by apple cider vinegar, white vinegar, red wine vinegar, Balsamic vinegar, and other varieties. --Increased fat content--Fat is digested more slowly and slows gastric emptying time, compared to the rapid transit of carbohydrates. Not everybody should slow gastric emptying. Diabetics with a condition called diabetic gastroparesis should not use these methods, as they can further slow the abnormal gastric emptying that develops as part of their disease, making a bad situation worse. However, in the rest of us with normal gastric emptying time, a delay in gastric emptying can reduce blood sugar and induce satiety, effects that can work in your favor in reducing cardiovascular risk.
Genetic vs. lifestyle small LDL 19. February 2010 William Davis (59) Let me explain what I mean by "genetic small LDL." I think it helps to illustrate with two common examples. Ollie is 50 years old, 5 ft 10 inches tall, and weighs 253 lbs. BMI = 36.4 (obese). Starting lipoproteins (NMR):LDL particle number 2310 nmol/LSmall LDL: 1893 nmol/L (1893/2310 = 81.9% of total, a severe small LDL pattern)Stan is 50 years old, also, 5 ft 10 inches tall, and weighs 148 lbs. BMI = 21.3. Starting lipoproteins:LDL particle number 1424 nmol/LSmall LDL 1288 nmol/L (1288/1424 = 90.4% of total, also severe)Both Ollie and Stan go on the New Track Your Plaque diet and eliminate wheat, cornstarch, and sugars, while increasing oils, meats and fish, unlimited raw nuts, and vegetables. They add fish oil and vitamin D and achieve perfect levels of both. Six months later, Ollie has lost 55 lbs, Stan has lost 4 lbs. A second round of lipoproteins:Ollie:LDL particle number 1810 nmol/LSmall LDL: 193 nmol/L (193/1810 = 10.6% of total)Stan:LDL particle number 1113 nmol/LSmall LDL 729 nmool/L (729/1113 = 65.4% of total)Ollie has reduced, nearly eliminated, small LDL through elimination of wheat, cornstarch, and sugars, along with weight loss, fish oil, and vitamin D. Stan, beginning at a much more favorable weight, reduced both total and small LDL with the same efforts, but retains a substantial proportion (65.4%) of small LDL. Stan's pattern is what I call "genetic small LDL." Of course, this is a presumptive designation, since we've not identified the specific gene(s) that allow this (e.g., gene for variants of cholesteryl ester transfer protein, hepatic lipase, lipoprotein lipase, and others). But it is such a sharp distinction that I am convinced that people like Stan have this persistent pattern as a genetically-determined trait.
Carbohydrate sins of the past 17. February 2010 William Davis (15) Fifty years ago, diabetes was a relatively uncommon disease. Today, the latest estimates are that 50% of Americans are now diabetic or pre-diabetic. There are some obvious explanations: excess weight, inactivity, the proliferation of fructose in our diets. It is also my firm belief that the diets advocated by official agencies, like the USDA, the American Heart Association, the American Dietetic Association, and the American Diabetes Association, have also contributed with their advice to eat more “healthy whole grains.” When I was a kid, I ate Lucky Charms® or Cocoa Puffs® for breakfast, carried Hoho’s® and Scooter Pies® in my lunchbox, along with a peanut butter sandwich on white bread. We ate TV dinners, biscuits, instant mashed potatoes for dinner. Back then, it was a matter of novelty, convenience, and, yes, taste. What did we do to our pancreases eating such insulin-stimulating foods through childhood, teenage years, and into early adulthood? Did our eating habits as children and young adults create diabetes many years later? Could sugary breakfast cereals, snacks, and candy in virtually unlimited quantities have impaired our pancreas’ ability to produce insulin, leading to pre-diabetes and diabetes many years later? A phenomenon called glucose toxicity underlies the development of diabetes and pre-diabetes. Glucose toxicity refers to the damaging effect that high blood sugars (glucose) have on the delicate beta cells of the pancreas, the cells that produce insulin. This damage isirreversible: once it occurs, it cannot be undone, and the beta cells stop producing insulin and die. The destructive effect of high glucose levels on pancreatic beta cells likely occurs through oxidative damage, with injury from toxic oxidative compounds like superoxide anion and peroxide. The pancreas is uniquely ill-equipped to resist oxidative injury, lacking little more than rudimentary anti-oxidative protection mechanisms. Glucose toxicity that occurs over many years eventually leaves you with a pancreas that retains only 50% or less of its original insulin producing capacity. That’s when diabetes develops, when impaired pancreatic insulin production can no longer keep up with the demands put on it. (Interesting but unanswered question: If oxidative injury leads to beta cell dysfunction and destruction, can antioxidants prevent such injury? Studies in cell preparations and animals suggest that anti-oxidative agents, such as astaxanthin and acetylcysteine, may block beta cell oxidative injury. However, no human studies have yet been performed. This may prove to be a fascinating area for future.)Now that 50% of American have diabetes or pre-diabetes, how much should we blame on eating habits when we were younger? I would wager that eating habits of youth play a large part in determining potential for diabetes or pre-diabetes as an adult. The lesson: Don’t allow children to repeat our mistakes. Letting them indulge in a lifestyle of soft drinks, candy, pretzels, and other processed junk carbohydrates has the potential to cause diabetes 20 or 30 years later, shortening their life by 10 years. Kids are not impervious to the effects of high sugar, including the cumulative damaging effects of glucose toxicity.
Saturated fat and large LDL 16. February 2010 William Davis (44) Here's a half-truth I often encounter in low-carb discussions:Saturated fat increases large LDL particlesFor those of you unfamiliar with the argument, I advocate a low-carbohydrate approach, specifically elimination of all wheat, cornstarch, and sugars, to reduce expression of the small LDL pattern (not to mention reduction of triglycerides, relief from acid reflux and irritable bowel, weight loss, various rashes, diabetes, etc). Small LDL particles have become the most common cause for heart disease in the U.S., exploding on the scene ever since agencies like the USDA and American Heart Association have been advising the public to increase consumption of "healthy whole grains." This has led some to make the pronouncement that saturated fat increases large LDL, thereby representing a benign effect. Is this true? It is true, but only partly. Let me explain. There are two general categories of factors causing small LDL particles: lifestyle (overweight, excess carbohydrates) and genetics (e.g., variants of the gene coding for cholesteryl-ester transfer protein, or CETP). If small LDL is purely driven by excess carbohydrates, then adding saturated fat will reduce small LDL and increase large LDL. If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles. So to say that saturated fat increases large LDL is an oversimplification, one that can have dire consequences in the wrong situation.
Is glycemic index irrelevant? 14. February 2010 William Davis (20) University of Toronto nutrition scientist, Dr. David Jenkins, was the first to quantify the phenomenon of "glycemic index," describing how much blood sugar increased over 90 minutes compared to glucose. The graph is from their 1981 study, The glycemic index of foods: a physiologic basis for carbohydrate exchange. The research originated with an effort to characterize carbohydrates for diabetics to gain better control over blood sugar.Since Dr. Jenkins’ original work, thousands of clinical studies have been performed by others exploring this concept. The food industry has also devoted plenty of effort exploiting it (e.g., low-glycemic index noodles, low-glycemic index cereals, etc.). Most Americans are now familiar with the concept of glycemic index. You likely know that table sugar has a high glycemic index (60), increasing blood sugar to a similar degree as white bread (glycemic index 71). Oatmeal (slow-cooked) has a lower glycemic index (48), since it increases blood sugar less than white bread. A number of studies have shown that when low glycemic index foods replace high glycemic index foods (e.g., whole wheat bread in place of cupcakes), people are healthier: less diabetes, less heart attack, less high blood pressure. Books have been written about glycemic index, touting its benefits for health and weight control. Health-conscious people will try to substitute low-glycemic index foods for high-glycemic index foods. So what’s not to like here? There are several fundamental flaws with the notion that low-glycemic index foods are good for you:1) Check your blood sugar after a low-glycemic index food like oatmeal. Most non-diabetic adults will show blood sugars in the 140 to 200 mg/dl range. The more central (visceral) fat you have, the higher the value will be. In other words, an apparently “healthy” whole grain food like oatmeal can generate extravagantly high blood sugars. Repeated high blood sugars of 125 mg/dl or greater after eating increase heart disease risk by 50%. 2) Foods like whole wheat pasta have a low glycemic index because the blood sugar effect over the usual 90 minutes is increased to a lesser degree. The problem is that it remains increased for an extended period of up to several hours. In other words, the blood sugar-increasing effect of pasta, even whole grain, is long and sustained. 3) Low-glycemic index foods trigger other abnormalities, such as small LDL particles, triglycerides, and c-reactive protein (a measure of inflammation). While they are not as bad as high-glycemic index foods, they are still quite potent triggers. Low-glycemic index foods trigger the very same responses as high-glycemic index foods—they’re just less bad. But less bad does not equate to good. Low-glycemic index foods cause weight gain, trigger appetite, increase blood pressure, and lead to the patterns that cause heart disease. High-glycemic index foods are bad for you. This includes foods made with white flour (bagels, white bread, pretzels). Low-glycemic foods (whole grain bread, whole wheat crackers, whole wheat pasta) are less bad for you—but they are not necessarily good. Don’t be falsely reassured by foods because they are billed as “low-glycemic index.” View low-glycemic index foods as indulgences, something you might have once in a while, since a slice of whole grain bread is really not that different from a icing-covered cupcake.