Bosom buddies 9. October 2010 William Davis (22) Male breast reduction surgery is a booming business. While most industries are in a downward tailspin, breast reduction surgery in men is growing at double-digit rates.Other efforts, some legitimate, some not, are also cropping up, all intended to help men deal with this embarassing problem:Exercise programs to reduce male breast size. Liposuction--Not just for the belly!Plastic surgeryGynexin--a supplement that purportedly reduces male breast size. Conventional medical treatment also includes estrogen blocking drugs, the same ones used to treat breast cancer, drugs like tamoxifen. There's even clothing intended to make breasts less obvious.While male breast enlargement--"gynecomastia"--can occasionally occur due to rare endocrinologic problems, such as high prolactin hormone levels (hyperprolactinemia) or somewhat more commonly as failed testosterone production (hypogonadism), the vast majority of men who suffer with this problem simply have high estrogen levels.Makes sense: Women develop larger breasts during development mostly due to increased levels of estrogen. A parallel situation in men likewise stimulates breast tissue. So where does the excess estrogen come from? Visceral fat converts testosterone to estrogen. Men with excess visceral fat therefore develop low levels of testosterone and high levels of estrogen. Estrogen levels can, in fact, be substantially higher compared to slender males.So what foods cause the accumulation of visceral fat and, thereby, increased estrogen and decreased testosterone? Foods that increase blood glucose and insulin to the greatest degree are the foods that begin this cascade. The common foods that increase blood sugar the most? Here's a list, starting with most blood glucose-insulin provoke at the top, least at the bottom:Gluten-free foods (dried, pulverized cornstarch, rice starch, potato starch, tapioca starch)Whole wheat breadSucroseMilky Way barsSnickers barsSo the whole wheat sandwiches you've been eating increase blood sugar and insulin, leading to visceral fat. (And, yes, whole wheat bread increases blood sugar higher than Milky Way bars and Snickers bars.) The more visceral fat grows, the more resistant to the effects of insulin you become, further escalating blood sugar. Estrogen increases, testosterone drops, mammary gland tissue grows, normal male breasts grow to B- or C-cup size. Yet again, an entire industry is growing from the unintended consequence of conventional advice. In this instance, the advice to "eat more healthy whole grains" leads to this booming industry of male breast reduction efforts from surgery to medications to clothing. The REAL solution: Eliminate the foods that start the process in the first place.
Don't be a dipstick 3. October 2010 William Davis (32) If I want to know how much oil is in my car's engine, I check the dipstick. The dipstick provides a gauge of the amount of oil in my engine. If the dipstick registers "full" because there an oil mark at one inch, I understand that there's more than one inch of oil in my engine. The dipstick provides an indirect gauge of the amount of oil in my engine. That's what cholesterol was meant to provide: A gauge, a "dipstick," for the kind of lipoproteins (lipid-carrying proteins) in the bloodstream. Lipoproteins are a collection of particles that are larger than a single cholesterol molecule but much smaller than a red blood cell. Lipoproteins consist of many components: various proteins, phospholipids, lots of triglycerides, as well as cholesterol. In the 1960s, methods to characterize lipoproteins were not widely available, so the cholesterol in lipoproteins were used as a "dipstick" to assess low-density lipoproteins ("LDL cholesterol") and high-density lipoproteins ("HDL cholesterol"). (Actually, even "LDL cholesterol" was not measured, but was derived from "total cholesterol," the quantity of cholesterol in all lipoprotein fractions.) Some other component of lipoproteins could have been measured instead of cholesterol, such as apoprotein B, apoprotein C, or others, all meant to act as the "dipstick" for various lipoproteins. Relying on cholesterol to characterize lipoproteins provides a misleading picture. Imagine watching cars go by at high speed while standing on the side of the highway. You want to count how many people--not cars, but people--go by in a given amount of time. Because you cannot make out the detail of each and every car whizzing by, you count the number of cars and assume that each car carries two people. Whether it's rush hour, Sunday morning, late evening, rainy, sunny, or snowing, you make the same assumption: two people per car. That's what cholesterol does: It is assuming that each and every lipoprotein particle (car) carries the same amount of cholesterol (people). But that may, obviously, not be true. A bus goes by carrying 25 people. Plenty of cars may carry just the driver. People carpooling may be in cars carrying 3 or 4 people. Assuming just 2 people per car can send your estimates way off course. That is precisely what happens when your doctor tries to use conventional cholesterol values (total cholesterol, LDL cholesterol) to gauge the lipoproteins in your bloodstream. Measuring cholesterol can also provide the false impression that cholesterol is the cause of heart disease, even though it was originally meant to simply serve as a "dipstick."What we need to do is to characterize lipoproteins themselves. We can distinguish them by size, number, density, charge, and the type and form of proteins contained within. It provides greater insight into the composition of lipoproteins in the blood. It provides greater insight into the causes underlying coronary atherosclerotic plaque. It can also tell us what dietary changes trigger different particle patterns and how to correct them.Until you have a full lipoprotein analysis, you can never know for certain 1) if you will have heart disease in your future, or 2) how your heart disease was caused.Unfortunately, the vast majority of doctors are perfectly content to just count cars going by and assume two people per car, i.e., confine assessment of your heart disease risk using cholesterol . . . just as drug industry marketing has instructed them.It's not your job to educate your doctor. If he or she refuses to provide access to lipoprotein testing to better determine your heart disease risk, then consider going out on your own. Many of our Track Your Plaque program followers have obtained lipoprotein testing on their own through Direct Labs.
The ultimate insurance company cost savings 29. September 2010 William Davis (48) I had a very disturbing conversation with a physician who is employed by an insurance company last week. I admitted a patient in the hospital for very clear-cut reasons. She is one of my few non-compliant patients, doing none of the strategies I advocate--no fish oil, no vitamin D, no correction of her substantial lipoprotein abnormalities, not even medication. Much of this was because of difficult finances, some of it is because she is from the generation (she is in her late 70s) that tends to ignore preventive health, some of it is because she is a kind of happy-go-lucky personality. So her disease has been progressive and, now, life-threatening, including an abdominal aneurysm near-bursting in size (well above the 5.5 cm cutoff). The patient is also a sweet, cuddly grandmother. I have a hard time bullying nice little old ladies. While she was in the hospital, the social worker told me that her case was being reviewed by her insurer and would likely be denied. Their medical officer wanted to speak to me. So the medical officer called me and started asking pointed questions. "Why did you do that test? You know that she's not been compliant. Are you sure you want to do that? I don't think that's a good idea." In other words, this was not just a review of the case. This was an opportunity for the insurance company to intervene in the actual care of the patient. Then the kicker: "Have you considered not doing anything and . . . just letting nature take its course?" At first, I was stunned. "You mean let the patient die?" Expressed in such blatant terms, while he was trying to be diplomatic, made him back down. "Well, uh, no, but she is a high-risk patient." Anyway, this was the first instance I've encountered in which the insurance company is not just in the business of reviewing a case, but actually trying to intervene during the hospital stay, to the point of making the ultimate healthcare cost savings: Letting the patient die. Unfortunately, never having had an experience like this before, I did not think to record the conversation or take notes. I am wondering if this is an issue to be taken up by the Insurance Board . . . or is this a taste of things to come as the health insurers fall under increasing pressure with the legislative changes underway?
Salvation from halogenation 24. September 2010 William Davis (26) Iodine is a halogen. On the periodic table of elements (remember the big chart of the elements in science class?), the ingenious table that lays out all known atomic elements, elements with similar characteristics are listed in the same column. The elegant genius of the periodic table has even allowed prediction of new, undiscovered elements that conform to the "laws" of atomic behavior. Column 17 (also called "group VIIa") contains all the halogens, of which iodine is one member. Other halogens include fluorine, chlorine, and bromine.Odd phenomenon in biologic systems: One halogen can often not be distinguished from another. Thus, a chlorinated compound can cleverly disguise itself as an iodinated compound, a brominated compound can mimic an iodinated compound, etc.What this means in thyroid health is that, should sufficient iodine be lacking in the body, i.e., iodine deficiency, other halogens can gain entry into the thyroid gland. While a polychlorinated biphenyl (PCB) molecule may be recognized as an iodinated compound, it certainly doesn't act like an iodinated compound once it's in the thyroid's cells and can disrupt thyroid function (Porterfield 1998). Another group of chlorine-containing compounds, perchlorates, that contaminate groundwater and are found as pesticide residues in produce, are extremely potent thyroid-blockers (Greer 2002). Likewise, bromine-containing compounds, such as polybrominated diphenyl ethers (PBDEs), widely used as flame retardants, also disrupt thyroid function (Zhou 2001). Perfluorooctanoic acid (PFOA), found in Teflon non-stick cookware and stain-resistant products, has been associated with thyroid dysfunction (Melzer 2010). PFOA, incidentally, can disrupt thyroid dysfunction that will not show up in the TSH test used by primary care physicians and endocrinologists to screen for thyroid dysfunction. (In fact, the presumed champions of thyroid health, the endocrinology community, have proven a miserable failure in translating and implementing the findings from toxicological science findings to that of preserving or restoring thyroid health. They have largely chosen to ignore it.)We therefore navigate through a world teeming with halogenated thyroid blocking compounds. We should all therefore avoid such exposures as perchlorates in produce by rinsing thoroughly or purchasing organic, avoid non-stick cookware, avoid use or exposure to pesticides and herbicides. Another crucial means to block the entry of various halogenated compounds into your vulnerable thyroid: Be sure you are getting sufficient iodine. While it doesn't make your thyroid impervious to injury, iodine circulating in the blood in sufficient quantities and residing in sufficient stores in the thyroid gland provides at least partial protection from the halogenated impostors in your life.I make this point in the context of heart disease prevention, since even the most subtle degrees of thyroid dysfunction can easily double, triple, or quadruple heart disease risk. See related posts, Is normal TSH too high? and Thyroid perspective update.
Lipitor-ologist 22. September 2010 William Davis (30) One of the things I do in practice is consult in complex hyperlipidemias, the collection of lipoprotein disorders that usually, but not always, lead to atherosclerosis. First order of business: Make the diagnosis--familial combined hyperlipidemia, hypoalphalipoproteinemia, lipoprotein(a), familial heterozygous hypercholesterolemia, familial hypertriglyceridemia, hyperapoprotein B with metabolic syndrome, etc. These are the disorders that start with a genetic variant, e.g., a missing or dysfunctional enzyme or signal protein, such as lipoprotein lipase or apo C3. I then ask: What can be done that is easy and safe and preferably related to diet and lifestyle? By following an effective diet, many of these abnormalities can be dramatically corrected, sometimes completely. Familial hypertriglyceridemia, for instance, an inherited disorder of lipoprotein lipase in which triglyceride levels can exceed 1000 mg/dl, high enough to cause pancreatic damage, responds incredibly well to carbohydrate restriction and over-the-counter fish oil. I have a number of these people who enjoy triglyceride levels below 100 mg/dl--unheard of in conventionally treated people with this disorder.Then why is it that, time after time, I see these people in consult, often as second or third opinions from lipidologists (presumed lipid specialists) or cardiologists, when the only solutions offered are 1) Lipitor or other statin drug, and 2) a low-fat diet? Occasionally, an aggressive lipidologist might offer niacin, a fibrate drug (Tricor or fenofibrate), or Lovaza (prescription fish oil). Sadly,ref="http://www.cureality.com/blog/author/William-Davis.html">William Davis (0)
What's better than a heart scan? 13. August 2006 William Davis (0) Do you know what's better than a heart scan?Two heart scans. No other method can provide better feedback on the results of your program. Say you've made efforts to correct high LDL; lost weight to raise HDL and reduce small LDL; added soluble fibers, nuts, and dramatically reduced wheat products; take fish oil, vitamin D, and follow a flavonoid-rich diet. Has it worked? After a year or so of your program, that's when another heart scan can give you invaluable feedback on whether it's been successful. I tell my patients that it's relatively easy to correct lipid and lipoprotein abnormalities. The difficult part is to know when it's good enough. Is your LDL of 67 mg/dl and HDL of 50 mg/dl good enough? Another heart scan score is the best way I know of to find out. Variation in plaque growth differs hugely from one person to another, even at equivalent lipoprotein values. Why? Lots of reasons. Humans are inconsistent day to day. Lipoproteins, being a snapshot in time and not a cumulative value, change somewhat from day to day. There's also the possibility of unmeasured, unrecognized factors that influence coronary plaque growth. We may not be smart enough to identify these hidden factors yet. But your heart scan score will incorporate the effects of these hidden factors.Ideally, we aim for zero growth in plaque (no change in score) or a reduction. But, particularly in the first year, 10% or less plaque growth is still a good result that predicts much reduced risk of heart attack. More than 20% per year and your program needs more work--or else you know what's ahead.
Lipids are snapshots in time; heart scans are cumulative 12. August 2006 William Davis (0) Let me paint a picture. It's fictional, though a very real portrait of how things truly happen in life. Michael is an unsuspecting 40-year old man. He hasn't undergone any testing: no heart scan, no lipids or lipoproteins. But we have x-ray vision, and we can see what's going on inside of him. (We can't, of course, but we're just pretending.) Average build, average lifestyle habits, nothing extraordinary about him. His lipids/lipoproteins at age 40:--LDL cholesterol 150 mg/dl--HDL cholesterol 38 mg/dl--Triglycerides 160 mg/dl--Small LDL 70% of all LDLAt age 40, with this panel, his heart scan score is 100. That's high for a 40-year old male. Fast forward 10 years. Michael is now 50 years old. Michael prides himself on the fact that, over the past 10 years, he's felt fine, hasn't gained a single pound, and remains as active at 50 as he did in 40. In other words, nothing has changed except that he's 10 years older. His lipids and lipoproteins:--LDL cholesterol 150 mg/dl--HDL cholesterol 38 mg/dl--Triglycerides 160 mg/dl--Small LDL 70% of all LDLSome of you might correctly point out that just simple aging can cause some deterioration in lipids and lipoproteins, but we're going to ignore these relatively modest issues for now.)Lipids and lipoproteins are, therefore, unchanged. Michael's heart scan score: 1380, or an approximate 30% annual increase in score. (Since Michael didn't know about his score, he took no corrective/preventive action.)My point: If we were to make our judgment about Michael's heart disease risk by looking at lipids or lipoproteins, they would'nt tell us where he stood with regards to heart disease risk. His lipids and lipoproteins were, in fact, the same at age 50 as they were at age 40. That's because measures of risk like this are snapshots in time. In contrast, the heart scan score reflects the cumulative effects of life and lipids/lipoproteins up until the day you got your scan. Which measure do you think is a better gauge of heart attack risk? I think the answer's obvious.
11. August 2006 William Davis (0) The recognition of the metabolic syndrome as a distinct collection of factors that raise heart disease risk has been a great step forward in helping us understand many of the causes behind heart disease. Curiously, there's not complete agreement on precisely how to define metabolic syndrome. The American Heart Association and the National Heart, Lung, and Blood Institute issued a concensus statement in 2005 that "defined" metabolic syndrome as anyone having any 3 of the 5 following signs:Waist size 40 inches or greater in men; 35 inches or greater in women Triglycerides 150 mg/dL or greater (or treatment for high triglycerides) HDL-C <40 mg/dL in men; <50 mg/dL in women (or treatment for reduced HDL-C) Blood Pressure >130 mmHg systolic; or >85 mmHg diastolic (or drug treatment for hypertension) Glucose (fasting) >100 mg/dL (or drug treatment for elevated glucose) Using this definition, it has become clear that meeting these criteria triple your risk of heart attack. But can you have the risk of metabolic syndrome even without meeting the criteria? What if your waste size (male) is, 36 inches, not the 40 inches required to meet that criterion; and your triglycerides are 160, but you meet none of the other requirements? In our experience, you certainly can carry the same risk. Why? The crude criteria developed for the primary practitioner tries to employ pedestrian, everyday measures. We see people every day who do not meet the criteria of the metabolic syndrome yet have hidden factors that still confer the same risk. This includes small LDL; a lack of healthy large HDL despite a normal total HDL; postprandial IDL; exercise-induced high blood pressure; and inflammation. These are all associated with the metabolic syndrome, too, but they are not part of the standard definition. I take issue in particular with the waist requirement. This one measure has, in fact, gotten lots of press lately. Some people have even claimed that waist size is the only requirement necessary to diagnose metabolic syndrome. Our experience is that features of the metabolic syndrome can occur at any waist size, though it increases in likelihood and severity the larger the waist size. I have seen hundreds of instances in which waist size was 32-38 inches in a male, far less than 35 inches in a female, yet small LDL is wildly out of control, IDL is sky high, and C-reactive protein is markedly increased. These people obtain substantial risk from these patterns, though they don't meet the standard definition. To me, having to meet the waist requirement for recogition of metabolic syndrome is like finally accepting that you have breast cancer when you feel the two-inch mass in your breast--it's too late. Recognize that the standard definition when you seen it is a crude tool meant for broad consumption. You and I can do far better.
What role DHEA? 9. August 2006 William Davis (2) DHEA, the adrenal gland hormone, has suffered its share of ups and downs over the years. Initially, DHEA was held up as the fountain of youth with hopes of turning back the clock 20 years. Such extravagant dreams have not held up. But DHEA can still be helpful for your program. All of us had oodles of DHEA in our bodies when we were in our 20s and 30s. Gradually diminishing levels usually reach nearly blood levels of around zero by age 70. In our heart disease prevention program, of course, we aim to stop or reduce your CT heart scan score. Does DHEA reduce your score? No, it most certainly does not. But it can be helpful for gaining control over some of the causes behind coronary plaque. For instance, DHEA can:--Help reduce abdominal fat and increase muscle mass (slightly)--Provide more physical stamina. --Boost mood.--It may modestly reduce some of the phenomena associated with the metabolic syndrome (high blood pressure, high blood sugar, high insulin, low HDL, small LDL, etc.)In my experience, people who feel better do better on their overall program. If you're always tired and run down and run out of steam by 3 pm, I won't see you riding your bicycle outdoors or at the aerobics class. But if you're bursting with energy until you put your head on the pillow, you're more inclined to walk, bike, dance, play with the kids, dance, take Tai Chi, etc. Some downsides to DHEA: Some people experience aggression. Backing off on the dose usually relieves it. Also, sleeplessness. Taking your DHEA in the morning usually fixes it. The dose is best tailored to your age and blood levels. People less than 40 years old should not take DHEA. The older you are, the higher the dose, though we rarely ever have to exceed 50 mg per day. If you've never had a blood level and your doctor refuses to obtain one, 25 mg per day is a reasonable dose (10-15 mg in women 40-50 years old). It's always best to discuss your supplement use, particularly agents like DHEA, with your doctor. Track Your Plaque Members: Stay tuned to the www.cureality.com website for a Special Report more completely detailing the hows and whys behind DHEA.
Brainwashed! 9. August 2006 William Davis (0) At a social gathering this weekend, as we humans like to do, someone asked me what I did for a living. I told him I was a cardiologist. "What hospital do you work at?" he asked. This is invariably the response I get whenever I tell people what I do. I wouldn't make much of it except that it happens just about every time. This indicates to me just how successful hospitals, my colleagues, cardiac device manufacturers, and others supporting the status quo in heart care, have been in persuading us that the place for heart disease is the hospital--period. Tense families, drama, high-tech...It all takes place in the hospital. Yet the people destined to be the fodder for hospital heart care are presently well, mostly unaware of what the future holds. Also unaware that heart disease is readily, easily, inexpensively, and accurately identifiable. Ask anyone in the Track Your Plaque program who's had a CT heart scan. We all need to rid ourselves of the idea that the hospital is the place for heart disease. If the coronary plaque behind heart attack is easy to detect and controllable, there's little or no need for the hospital for the vast majority of us.In the majority of instances of coronary disease, the hospital should be the place for the non-compliant and the ill-informed, and not for those of us sufficiently motivated to know and do better. The formula is simple: 1) Quantify plaque with a CT heart scan, 2) Identify the causes, then 3) Correct the causes.
The Fanatic Cook: A fabulous Blog about food and nutrition 7. August 2006 William Davis (0) I came across this Blog authored by a nutritionist when it was highlighted on Blogger as an interesting site:The Fanatic Cook at http://fanaticcook.blogspot.com/I was thoroughly impressed with the insightful and entertaining commentary. I'd highly recommend this site to you for reading on nutrition. In particular, her coenzyme Q10 column was exceptionally well written and clear.(http://fanaticcook.blogspot.com/2005/02/statins-and-not-well-publicized-side.html)Also read her column, Super NonFoods at http://fanaticcook.blogspot.com/2005/07/super-nonfoods.html.There's also oodles of recipes, all for the taking.
Eggs: Good, bad, or indifferent? 5. August 2006 William Davis (3) Eggs have been in the center of the cholesterol controversy almost from the very start. The traditional argument against eggs went that eggs, high in cholesterol (210-275 mg per egg)and with some saturated fat (1.5-2.5 grams per egg), raised blood cholesterol (and LDL). Out went the daily fried, scrambled, poached eggs that many Americans indulged in most mornings. (We replaced it with more breakfast cereals and other carbohydrate conveniences, then got enormously overweight.)A large Harvard epidemiologic study in 1999 called this observation into question. They tracked the fate of 117,000 thousand people and then compared the rate of heart attack, death, and other cardiovascular events among various people correlated to the "dose" of eggs they ate. Egg intake varied from none to 7 or more per week. Lo and behold, people who ate more eggs appeared to not suffer more events. This study, large and well-conducted by an internationally respected group of investigators, seem to reopen the gates for more egg consumption, though most Americans still consume eggs cautiously. Deeper down in this study, however, was another observation: People with diabetes who ate 1 egg per day had double the risk of heart attack. Because this study was observational, no specific conclusion as to why could be drawn. A new study conducted by a Brazilian group may shed some light. Healthy (non-diabetic) men were fed an emulsion of several eggs. Inclusion of plentiful yolks caused a dramatic slowing of fat clearance from the blood. Specifically, "chylomicron remnants" were abnormally persistent in the blood. Chylomicron remnants are potent causes of coronary plaque. (Chylomicron remnants can be measured fairly well by intermediate-density lipoprotein and VLDL by NMR, or IDL by VAP.)Diabetics are know to have substantial disorders of after-meal fat clearance, including an excess of chylomicron remnants. Could the Brazilian observation be the explanation for the increased event rate in diabetics in the Harvard study? Interesting to speculate. We continue to tell our patients that eating eggs in moderation is probably safe. After all, there are good things in eggs: the high protein in the egg white, lecithin in the yolk. It is the yolk's contents that are in question, not the white. Thus, you and I can eat all the egg whites (e.g., Egg Beaters) we want. It's the safety of yolks that are uncertain. The abnormal after-eating effect suggested by the Brazilians opens up some very interesting questions and confirms that we should still be cautious in our intake of egg yolks. One yolk per day is clearly too much. What is safe? The exisitng information would suggest that, if you have diabetes, pre-diabetes, or a postprandial disorder (IDL, VLDL), you should minimize your egg yolk use, perhaps no more than 3 or so per week, preferably not all at one but spaced out to avoid the after-eating effect.Others without postprandial disorders may safely eat more, perhaps 5 per week, but also not all at one but spaced out. Track Your Plaque Members: Be sure to read our upcoming Special Report on Postprandial Disorders. It contains lots of info on what this important pattern is all about. Postprandial disorders are largely unexplored territory that hold great promise for tools to inhibit coronary plaque growth and drop your heart scan score. The Brazilian study is just one of many future studies that are likely to be released in future about this very fascinating area. Hu FB, Stampfer MJ, Rimm EB, Manson JE, Ascherio A, Colditz GA, Rosner BA, Spiegelman D, Speizer FE, Sacks FM, Hennekens CH, Willett WC.A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA 1999 Apr 21;281(15):1387-94.Cesar TB, Oliveira MR, Mesquita CH, Maranhao RC. High cholesterol intake modifies chylomicron metabolism in normolipidemic young men. J Nutr. 2006 Apr;136(4):971-6.
Diabetes is Track Your Plaque's Kryptonite! 3. August 2006 William Davis (0) If there's one thing I truly fear from a heart scan score reduction/coronary plaque regression standpoint, it's diabetes. I saw a graphic illustration of this today. Roy came into the office after his 2nd heart scan. His first scan 14 months ago showed a score of 162. Roy started out weighing well over 300 lbs and with newly-diagnosed adult diabetes. Roy put extraordinary effort into his program. He lost nearly 70 lbs by walking; cutting processed carbohydrates, greasy foods, and slashing overall calories. His lipoproteins, disastrous in the beginning, were falling into line, though HDL was still lagging in the low 40s, as Roy remains around 60 lbs overweight, even after the initial 70 lb loss. Unfortunately, despite the huge loss in weight, Roy remains diabetic. On a drug called Actos, which enhances sensitivity to insulin, along with vitamin D to also enhance insulin response, his blood sugars remained in the overtly diabetic range. Roy's repeat heart scan showed a score of 482--a tripling of his original score. Obviously, major changes in Roy's program are going to be required to keep this rate of growth from continuing. But I tell Roy's story to illustrate the frightening power of diabetes to trigger coronary plaque growth. Like Kryptonite to Superman (remember George Reeves crumbling and falling to his knees when the bad guys got a hold of some?), diabetes is the one thing I fear greatly when it comes to reducing your heart scan score. As you see with Roy's case, diabetes can be responsible for explosive plaque growth, more than anything else I know. The best protection from diabetes is to never get it in the first place. (See my earlier Blog, "Diabetes is a choice you make".)