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There are three different types of muscle tissue in the human body: cardiac muscle, which is only in the heart; smooth muscle, which is found in organs & blood vessels; and of course skeletal muscle, which is found all over the body and is responsible for movement. All three of these muscle types have distinctly different anatomical structure and function in the body. We know that muscles get bigger and stronger when put under stress, which is called adaption. Which simply means that the muscle is preparing itself in case it’s put under the same type of stress again. An analogy is calluses on your hand, if you rub your hand on a course surface causing enough friction eventually the skin adapts by building up calluses, thus protecting it self from future happenings. Muscle reacts much the same way, if you train them or put them under enough stress they will adapt to this stress by growing bigger and stronger. So the next time you train them they will be capable of handling this new level of stress. Now obviously that is a very basic explanation, but hang on to your dumbbells we’ll get more in depth! Inside a muscle there are groups of motor units separated by membranes. Each motor unit consists of a single neuron and all of the muscle fibers it stimulates. In muscles such as the hand where fine motor control is necessary the ratio of nerves to fibers will be much higher than that of a muscle such as the calf. Muscle fiber consists of myofibrils, a myofibril is a small bundle of myofilaments. Myofilaments are mainly comprised of two types of proteins called actin and myosin. The myofilament is the part of the muscle that actually shortens upon contraction where the actin and myosin filaments slide over each other, which is called the sliding filament theory. Basically by the way of chemical bonds and receptor sites located on the myofilaments the actin and myosin attract each other thereby causing a contraction. A contraction can be held until fatigue sets in, and the strength of a contraction is determined by the number of motor units that are recruited. Inevitably, the more force that is necessary for muscle contraction requires an increased number of motor units to allow the muscle to contract. Within skeletal muscle there are three types of muscle fibers: Type I, Type IIa and Type IIb. Everyone has their own unique distribution of these fibers, some people are predominately Type I, and some Type IIa, however the “average person” has an even amount of red and white fiber. Type I muscle fiber often referred to as slow-twitch or red fiber and is highly resistant to fatigue and has a high oxidative capacity, This muscle fiber is responsible for aerobic exercises and activities, such as running. Type IIa muscle fiber often referred to as fast-twitch or white fiber is an intermediate fiber and they’re larger in size and much stronger than Type I fibers. Type IIb muscle fiber, which are also fast twitch & white fiber, are capable of producing more force than Type IIa, but they’re low in oxidative capacity, and fatigue very quickly. Fast twitch fibers have thicker nerves that give them an increased contractile impulse, which is measured by the number of twitches per second, hence the name fast twitch fiber. Slow twitch fibers have smaller nerves, thereby twitch much slower, however they have a higher number of mitochondria, which increases their oxidative capacity. Mitochondria are the cells in a muscle that synthesize ATP (Adenosine Triphosphate), often referred to as the cell’s “powerhouse”. Okay, so now you have a basic understanding of muscle physiology, let’s talk about how we make them grow! The enlargement of a muscle fiber is called hypertrophy. As I mentioned earlier muscle growth or hypertrophy is a result of adaption to a new stress placed upon the muscle. So, what is the best form of stress? Well, there really is no single best principle that will work for every person. This is where the muscle fiber type distribution that you posses becomes important. If you train using appropriate methods based on your individual body type you will ultimately get faster results. First I would like to define the 7 Laws (adapted from the writings of Fredrick C. Hatfield) that should be adhered to regardless of the type of training system you employ: Law I – The Principle Of Individual Differences We must recognize and accept that we are all different based on genetics. We all have different body types, often referred to as the somatotypes: ectomorph, mesomorph & endomorph (most people are a combination of all 3 body types). The somatotypes is a very general classification that can help you determine the best type of training for you, but it’s a very basic tool and there is much more involved in one’s genetic make-up and musculature. Somatotypes are defined as follows: - Ectomorph: Thin, light bone structure, difficult to gain mass. - Mesomorph: Muscular, lean, gains muscle mass relatively easy. - Endomorph: Heavy, large bone structure, propensity to weight gain. Law II – The Overcompensation Principle The body overcompensates in defense to the stress placed upon it. A muscle grows bigger and stronger when trained with heavy weights, just as your hand will develop calluses when friction is applied. If you do not change the form of stress the muscles will have no reason to further adapt. Law III – The Overload Principle Relates to Law II, in that to gain further size & strength, endurance, etc., you must use training that is greater than what the body would normally encounter. If you train with the same amount of weight and/or repetitions every workout your muscles will not continue to adapt. Thus, you must overload in some way to cause further adaption. Law IV – The SAID Principle Specific Adaption to Imposed Demands, basically this law states that in order to meet your training objectives, e.g. increase explosiveness, you must you use specific training methods that will increase explosiveness. Or, if your goal is to increase limit strength, you must train with heavy weights. Law V – The Use/Disuse Principle Very simply put: “use it, or lose it”! If you increase a muscle via weight training you must continue to place the same or more stress upon the muscle or it will inevitably return to it’s normal size, which is called atrophy. Law VI – The Specificity Principle This law states that you must progress from foundational training to specific training to meet your final objective, whether it be a competition or improving your game of golf. An example would be to increase your maximum squat you need to use squats in your training rather than leg presses. Law VII – The GAS Principle General Adaption Syndrome, there are three stages: the alarm stage (intense training), the resistance stage (adaption) and the exhaustion stage (over training). If one is not careful in their training regimen they will over train according to this law. To avoid over training you must use periods of high intensity training, followed by periods of low intensity training and/or rest. So, no matter what method of training you utilize, the 7 Laws should be adhered to as closely as possible to facilitate maximum gains and to avoid a state of over training. The two most common questions are how much weight and how many reps? Unfortunately there is no magic number; it will vary from individual to individual. An “ectomorph” who is predominantly red fiber will respond better to higher repetition training, whereas a “mesomorph” who is predominantly white fiber will respond better to lower repetitions and heavier weights. However, no one is any single somatotype, most of us are a combination of all three, so there is no canned program that will yield the best results. For overall size gains, the goal of a bodybuilder, using a multitude of rep ranges, poundage’s and varying intensity will be most beneficial as well as staying in your 55-85 percent maximum range. If your max on bench press were 200lbs, using varying weights of 110lbs up to 170lbs would be your “training zone”. That does not mean you should never go above or below those poundage’s, it just means that the majority of training you do should be within that range. Typically, for hypertrophy to take place your reps should be in the 4-8 range. There is no need to ever use a weight that you cannot perform at least 4 reps with, unless your goal is pure strength. There are a few reasons that I say this, one is that when you train at 90 percent or higher of your maximum weight Type IIb muscle fibers are doing the majority of the work, and this will not do much for hypertrophy. In fact, even power lifters and Olympic lifters do the majority of their training at around 85% of their max. You may be thinking that 55-85 percent is quite a difference in poundage, well it is. This is where periodization comes into play. Periodization is a concept where you use cycles to break up your training. Regardless of your ultimate goal you should have a plan, and this plan needs to be broken up into your daily, weekly, and monthly workouts. So, you may have a week of heavy intense training, then a maintenance week of lighter training, the light week allows the muscles to recuperate, yet because they’re still being trained atrophy will not occur from disuse. In order to avoid a state of over training, and continue to grow, we need to recover. Remember your muscles do not grow in the gym, they grow when at rest. Many factors contribute to over training, including inadequate rest, continued heavy training, and deficiencies in diet & nutrition. By using periodization to map out your training you will avoid over training and keep your muscles in a state of continued adaption. Principles that can be used when planning your training cycles: Cycle Training: this is where you break up your training into bulk cycles, strength cycles and cutting cycles; which will help keep your muscles in a responsive state. Split Training: this is breaking up your training into separate body parts each work-out which allows for shorter and more intense sessions. Muscle Confusion: your muscles adapt to stress, and ultimately you can reach a plateau. By constantly varying the exercises, weights, sets and reps you can ensure continued adaption. Progressive Overload: continue to increase different parameters in your training, whether it be more weight, increasing sets and reps, etc. Eclectic Training: using a variety of methods in your training, combining numerous techniques such as compound and isolation exercises. Principles that can assist you in arranging each workout: Supersets: alternating two opposing muscle groups with little rest in between sets. Giant Sets: performing several exercises for a single muscle group with little rest in between sets. Muscle Priority: training a weaker body part first in your work out. Pre-Exhaustion: this is where you perform an isolation exercise preceding a compound exercise, e.g. leg extensions before squats. Pyramiding: beginning with a lighter weight, gradually increasing weight and lowering reps, then work backwards, decreasing weight and increasing reps. Stripping: going from a heavy weight, and stripping off weight each set as fatigue sets in. Principles that can be used with each exercise: Forced reps: once failure has been reached on a set, your partner assists you in performing additional reps that could not be performed alone. Continuous tension: maintaining slow continuous tension thru out the rep, which will maximize red muscle fiber recruitment. Cheating: once failure is reached the weight is swung past your sticking point to complete the movement. (useful when you do not have a spotter) Partial reps: as the name implies only part of the full movement is performed, e.g. only curling a barbell half way up, which can be effective due to the varying points of leverage. Peak contraction: at the completion of a set holding the weight fully contracted for a few seconds. Super speed: using a lighter weight, reps are performed explosively yet controlled, called “compensatory acceleration”, which can help with white fiber recruitment. Another very important component of your training and growth is nutrition. Unfortunately, the scope of this article is not diet and nutrition, but I want to emphasize its importance. Since protein is required for anabolism, it’s crucial that your protein intake be adequate. The general rule of thumb for protein requirements is 1 to 1.5 grams of protein per pound of bodyweight. This means that a 200lb bodybuilder should be consuming 200-300 grams of protein per day spread across 5-6 meals each day (33 to 50 grams per meal). You should consume protein from a variety of sources, including red meat, chicken, eggs, milk, fish, cheese and whey to name a few. Many times people will say they just cannot gain weight; well the answer is simple “eat more calories”. In order to gain weight, including muscle mass, you must be consuming more calories than you’re burning, period. So, if you feel that you’re doing everything correctly in regards to training, and you’re not gaining weight, try increasing your calories by 200-300 per day. I am not saying the answer is that simple, although often times it is, I am just making the point that you cannot gain weight without adequate calories. 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If you’ve ever witnessed someone suffer a stroke, you understand the humbling nature of this disease. It can reduce the mightiest human being to an immobile, helpless creature. Impairment of crucial functions like speech, walking, and control of bowel and bladder can wrench control from the body in a moment. Even perpetually youthful TV personality Dick Clark was struck down by stroke at age 75, despite the outward appearance of perfect health. Clark’s stroke resulted in a six-week hospital stay and, judging from fragmented reports, significant disability. Stroke can be like a devastating fire that strikes without warning, leaving only smoldering rubble. Stroke can so ravage basic bodily functions that often all you can hope for is to regain a portion through rehabilitation. The disease process that underlies stroke requires decades—30 or 40 years—to develop. With that much lead time, why aren’t we better able to detect or stop this crippling disease? The truth is that we are able to predict many, if not most, strokes. Advances in imaging technology allow detection of atherosclerotic plaque that cause stroke years before it becomes a threat. Progress in deciphering the causes of stroke has also leapt forward. Unfortunately, your neighborhood physician still focuses on diagnosing the crisis rather than anticipating it. Physicians prefer to deal with catastrophes and are just not that interested in prevention. Most physicians ask: “Is it time to operate or not?” The medical community obsesses over procedures like carotid endarterectomy (surgical removal of plaque) or carotid stents. Even when a person is afforded the warnings of a “mini-stroke”, or transient ischemic attack (TIA), little more is done once it’s determined that surgery is not necessary—even though this person has high risk for future stroke (50% over 10 years). Let’s flip-flop this approach to stroke. Procedures represent a failure of prevention! Where do strokes come from? Stroke develops when some portion of the brain is deprived of blood. This usually results from a tiny bit of debris that dislodges from an atherosclerotic plaque along the walls of an artery (the same sort that accumulates in coronaries causing heart attack). The sources of debris have been a subject of controversy, but new imaging technologies have settled the question. Any blood vessel that leads from the heart to the brain can be a source. The two carotid arteries on both sides of your neck are a frequent source, as these arteries are prone to develop plaque. (Our discussion will be confined to what are called thromboembolic, or ischemic, strokes, i.e, strokes that occur from plaque that fragments, sending debris to the brain, and will not include the far less common hemorrhagic strokes due to rupture of small vessels in the brain, nor will we discuss atrial fibrillation and other heart causes of stroke. The thromboembolic strokes we discuss cause around 88% of all strokes.) Over the last 10 years, the aorta has been recognized as another important source of stroke. The aorta is the main artery of the body whose branches go to the head, arms, and legs. Atherosclerotic plaque is a live tissue that, through poor diet, inactivity, high cholesterol, overweight, etc., grows and becomes progressively more unstable. At some point, plaque fragments. Little bits break away, traveling to the brain. Fractured plaque also exposes its deeper structures to flowing blood, triggering blood clot formation, which in turn can also fragment and go to the brain. Atherosclerotic plaque is a prerequisite for the most common causes of stroke. If the majority of strokes originate from plaque, why not measure plaque to determine if you’re at risk for stroke? How can we easily, safely, and accurately measure plaque in the carotid arteries and aorta? And if plaque can be measured, can it be shrunk or inactivated to reduce or eliminate risk for stroke? How can plaque be measured? Just 20 years ago, the only practical method of identifying plaque in the carotids or aorta was through angiography, requiring catheters inserted into the body to inject x-ray dye. Angiography was impractical as a screening measure. CT scanning and magnetic resonance imaging (MRI) are emerging as exciting methods of imaging both carotids and aorta. Unfortunately, most centers and physicians are much more focused on the diagnostic uses of these technologies for people who have already suffered stroke or other catastrophe, and application of these devices for preventive uses is still evolving. One exception is when aortic calcification or aortic enlargement is incidentally noted on the increasingly popular CT heart scans; this is an important finding that can signal presence of aortic plaque. The one test that is widely available and can be performed in just about any center is carotid ultrasound. It’s simple, painless, and precise. Two basic observations can be made: 1. Plaque detection—Atherosclerotic plaque can be clearly visualized. If plaque blocks more than 70% of the diameter of the vessel, or if there are “soft” (unstable) elements in plaque, then stroke risk may be high enough to justify surgery or stents. However, if there are plaques that are less severe, substantial risk for stroke may still be present that can be reduced with preventive measures. 2. Carotid intimal-medial thickness—This is a measure of the thickness of the lining of the carotid artery in areas not involved by plaque, but often precedes the development of mature plaque. Carotid intimal-medial thickness also provides an index of body-wide potential for atherosclerotic plaque that can place you at risk for stroke. The aorta, for instance, cannot be well imaged by surface ultrasound but can still be a source for stroke. Increased carotid intimal-medial thickness and carotid plaque are closely associated with likelihood of aortic plaque. The Rotterdam Study of 4000 participants demonstrated that if carotid intimal-medial thickness is greater than normal (1.0 mm), then you can be at risk for stroke (and heart attack), even if no carotid plaques are detected. Carotid ultrasound is the one test you should consider that provides the most information with least effort. Ultrasound is harmless, painless, and can be obtained just about anywhere. Even if your doctor disagrees with your request for a carotid ultrasound, an increasing number of mobile services are popping up nationwide that make this test available for around $100. One important point: many scanners and interpreters will only report whether plaque is present or not. While this is important information, you should request that the carotid-intimal medial thickness be made as well. Not all centers can make this simple measure (because of software requirements), but it doesn’t hurt to try. Any amount of carotid plaque is reason to follow a preventive program, even if the plaque is insufficient to justify surgery. Can plaque be reduced? Can we shrink plaque in carotid arteries and aorta and thereby reduce, perhaps eliminate, these sources of stroke? That question is gaining momentum as effective therapies become available that pack real punch for reducing plaque. Study after study has now documented that plaque can be reduced and, with it, risk for stroke. Reduction in plaque of 10–20% is possible within a year or two. Let’s consider the most potent influences on carotid and aortic plaque growth that need to be considered in a plaque-reducing program. (I assume that you are a non-smoker—if you are a smoker, you first need to concentrate on quitting.) Hypertension Considerable experience documents the power of blood pressure-lowering for prevention of stroke. The most recently updated guidelines, the JNC–VII, recommends a blood pressure of 407 mg/dl heightens stroke risk six-fold. C-reactive protein (CRP) This measure of inflammation is proving to be a useful marker for identifying people at risk for stroke, with increased risk beginning at a level of 0.5 mg/l. High CRP also predicts more rapidly growing carotid plaque. Homocysteine Homocysteine is an important marker of increased likelihood of both carotid and aortic plaque, as well as stroke. In 1997, the European Concerted Action Project reported more than a doubling of stroke when homocysteine levels exceeded 12 mol/l. As homocysteine increases to 20 μmol/l, risk for stroke and heart attack increases an amazing 10-fold over that at a level of 9 μmol/l. Asymmetric dimethylarginine (ADMA) ADMA is recently discovered amino acid whose blood levels can skyrocket up to 10-fold in the presence of hypertension, metabolic syndrome, diabetes, high cholesterol and triglycerides, obesity, and high homocysteine levels. ADMA blocks the action of the amino acid, l-arginine. This mimicry reduces the availability of nitric oxide, a powerful dilator and protector of arteries. ADMA levels in the top 10% predict a six-fold heightened risk for future stroke, and ADMA levels in people with strokes are double that in other people. A carotid ultrasound study in 116 subjects showed that higher blood levels of ADMA are associated with more severe carotid plaque. Because of ADMA’s shared role across a variety of abnormal conditions, correction or blocking the action of ADMA has been suggested as a unique therapeutic tool to reduce stroke risk. Cholesterol Data suggest that lowering cholesterol with statin cholesterol-lowering drugs slows carotid plaque growth and reduce stroke risk approximately 22%. An interesting study from the Cardiovascular Institute at Mt. Sinai School of Medicine in New York using the precise measuring ability of MRI of the carotids and thoracic aorta showed an impressive 20% regression of plaque area with simvastatin (Zocor®) taken for two years. Although guidelines for cholesterol treatment recommend reduction of LDL cholesterol to 100 mg/dl in high-risk persons, a report from the Walter Reed Army Medical Center in Washington, DC, showed that carotid plaque was more effectively reduced when LDL cholesterol of 70 mg/dl or lower was achieved with statin cholesterol drugs. Lower LDL cholesterol may, therefore, be better. Treatment Strategies to Reduce Carotid and Aortic Plaque The essential question: How do we reduce carotid and aortic plaque? If we make this the focus of our efforts, many pieces begin to fall into place. If you’ve had any measure of carotid or aortic plaque such as a carotid ultrasound or aortic calcification on a CT heart scan, you know that you’re at increased risk for stroke. You also have a baseline for future comparison to gauge whether your program is working or not. Because most people have not one but several causes of carotid and aortic plaque, there is no one single treatment that effectively eliminates risk for stroke. Instead, most people require a comprehensive program of healthy diet, exercise, supplements, and medication when indicated. Here, we focus on the nutritional supplements that can be critical components of your plaque-reduction program. Fish oil Fish oil is a cornerstone of your stroke prevention program. Epidemiological observations suggest a strong relationship of fish intake and reduction of stroke risk. Carotid ultrasound studies demonstrate less carotid plaque with greater intakes of fish. A cleverly designed University of Southampton study made the fascinating observation that fish oil transforms the structure of carotid plaque. 150 people with severe carotid plaque scheduled for carotid endarterectomy (surgical removal of the plaque) were given fish oil, sunflower oil, or no treatment over several months while waiting for their procedure. (Delays in the British health system permitted this unique design.) Plaque was removed at surgery and examined. Participants taking fish oil had reduced inflammation in plaque and thicker tissue covering the fatty core, markers of more stable plaque. Those taking sunflower oil or no treatment had unstable plaques with greater inflammation and thinner, less sturdy covering tissue. This suggests that fish oil stabilizes carotid plaque, making it less likely to rupture and fragment. A standard capsule of fish oil (containing 300 mg of EPA + DHA) contains the same amount of omega-3s as a 3 oz serving of cod or halibut; three capsules (900 mg DHA + EPA) contain the equivalent of a serving of farm-raised salmon. The dose that seems to provide greatest protection from stroke, lowers triglycerides (that form abnormal lipoproteins; see above), and reduces fibrinogen, is four capsules per day (1200 mg EPA + DHA). Coenzyme Q10 (CoQ10) Although there are no data specifically addressing whether CoQ10 reduces plaque, it is a marvelously effective way to reduce blood pressure, one of the crucial factors causing carotid and aortic plaque growth. A pooled analysis of eight studies showed that, on average, CoQ10 in daily doses of 50–200 mg reduced systolic blood pressure by 16 mm Hg, diastolic pressure by 10 mm Hg. Data suggest that CoQ10 can reverse abnormal heart muscle thickening (hypertrophy), another manifestation of high blood pressure, strongly suggesting that CoQ10 has benefits beyond just reducing pressure. Supplements to correct the metabolic syndrome Weight loss is, without question, the most immediate and direct path to correction of this dangerous pre-diabetic condition. A drop of even 10–20 lbs yields improvements across the board: increased sensitivity to insulin, increased HDL, and reductions in triglycerides, CRP, fibrinogen, small LDL particles, and blood pressure. Diet and exercise are fundamental components of an effort to lose weight; low carbohydrate or reduced glycemic index diets (e.g., South Beach or Mediterranean) rich in fibers are clearly effective. Several supplements can amplify weight-reduction efforts and be useful adjuncts to your lifestyle program. Among them: White bean extract White bean extract blocks intestinal absorption of carbohydrates by 66%. 1500 mg twice a day with meals yields, on average, 3–7 lbs of weight loss in the first month of use. The only side-effect is excessive gas, due to unabsorbed starches. Glucomannan This unique fiber taken prior to meals absorbs many times its weight in water and thereby fills your stomach. You consequently take in less food. Most people lose around four lbs per month using 1500 mg prior to each meal. Interestingly, glucomannan also blunts the rise in blood sugar after meals, an effect that, by itself, may lead to weight loss. Be sure to take with plenty of water. DHEA This adrenal hormone is key to maintaining physical stamina, mood, muscle mass in men, and libido in women. A recent randomized, placebo-controlled study at Washington University in 56 subjects showed a 13% decline in abdominal fat (fat that drives resistance to insulin) measured by MRI with 50 mg of DHEA per day at bedtime, along with improved sugar control and lower insulin levels. Pectin, beta-glucan Pectin is the soluble fiber in citrus rinds, green vegetables, and apples, also available as a supplement. Beta-glucan is the soluble fiber of oats and is also available as a supplement. Both are wonderful fibers that provide feelings of fullness, lower cholesterol, slow release of sugars, and can yield modest weight reduction. A USC study in 573 subjects using carotid ultrasound showed that greater intake of healthy fibers like pectin and beta-glucan is associated with less carotid plaque growth. Folic acid, vitamins B6 and B12 Dr. Daniel Hackam at the Stroke Prevention and Atherosclerosis Research Centre in Ontario conducted a study using carotid ultrasound in 101 participants treated with folic acid 2.5 mg, vitamin B6 25 mg, and B12 250 mcg per day. Treatment resulted in plaque reduction, especially when homocysteine levels exceeded 14μmol/l at the start, compared to untreated participants who experienced substantial plaque growth. An attempt to clarify the role of homocysteine treatment was made through a National Institute of Health-sponsored study of stroke prevention. 3680 participants with a prior history of stroke were enrolled and given either a “low-dose” (20 mcg folic acid, 0.2 mg B6, 6 mcg B12) or a “high-dose” (2.5 mg folic acid, 25 mg B6, 400 mcg B12) regimen. Although starting homocysteine levels showed a graded association with stroke risk (higher homocysteine levels predicted greater stroke risk), the treatment groups experienced, on average, only a 2 μmol drop in homocysteine levels and no reduction in stroke risk over two years. The study investigators as well as critics have suggested that the study failed due to an insufficient treatment period and that the doses were too low. (The doses we use in our plaque reduction program are folic acid 2.5–5.0 mg, B6 50–100 mg, B12 1000–2500 mcg.) L-arginine L-arginine can be used to overpower the adverse effects of ADMA. L-arginine is emerging as an important carotid plaque-reversing tool. Early reports in animals showed that l-arginine completely halted growth of aortic plaque, and did so more effectively than lovastatin (a cholesterol-lowering drug). In humans, L-arginine reduces blood pressure, abnormal constriction of carotid and coronary arteries, blocks entry of inflammatory cells into plaque, increases sensitivity to insulin, and heightens exercise capacity. Following coronary angioplasty or stent placement, l-arginine results in up to 36% reduction in plaque growth. The average American takes in 5400 mg of l-arginine through food every day. Supplementing with doses of 3000–12,000 mg per day has proven useful to correct many of these phenomena. (We use a dose of 6000 mg of l-arginine powder, twice a day on an empty stomach, dissolved in water, for our plaque regression program.) Does this result in a reduction of stroke risk? The emerging data suggest that l-arginine is likely to exert a powerful plaque-reducing and stroke-preventing benefit, but we await more clinical trial data. Conclusion Reducing stroke risk by reversing carotid and aortic plaque is becoming an everyday reality, with better tools becoming available. To know whether you’re at risk, the best and most available imaging tool is carotid ultrasound, aiming to identify intimal-medial thickness >1.0 mm, or carotid plaque. Any degree of calcification of the aorta, such as on a CT heart scan, is another useful measure of risk. Treatment to reduce risk is multi-faceted but is based on examining all your sources of risk, including metabolic syndrome, small LDL, lipoprotein(a), and C-reactive protein. Fish oil is the one absolutely crucial ingredient in any stroke prevention program. Other supplements can be used in a targeted fashion, depending on the causes identified for your carotid or aortic plaque. 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