Simple changes in diet can protect you against friendly fire

What you eat can fuel or cool inflammation, a key driver of heart disease, diabetes, and other chronic conditions.

Inflammation is an essential part of the body’s healing system. Without it, injuries would fester and simple infections could be deadly. Too much of a good thing, though, is downright dangerous. Chronic low-grade inflammation is intimately involved in all stages of atherosclerosis, the process that leads to cholesterol-clogged arteries. This means that inflammation sets the stage for heart attacks, most strokes, peripheral artery disease, and even vascular dementia, a common cause of memory loss. Think of it as friendly fire — yourself attacking yourself.

Inflammation doesn’t happen on its own. It is the body’s response to a host of modern irritations that our Stone Age genes haven’t quite caught up to. The main ones are smoking, lack of exercise, high-fat and high-calorie meals, and highly processed foods.

Medical researchers and pharmaceutical companies are hot on the trail of inflammation-busting drugs. Don’t bother waiting — they are a long way off, are bound to be expensive, and will almost certainly have side effects. Instead, you can turn to simple tools that ease inflammation. We’ll focus on diet here, but don’t forget about avoiding cigarette smoke (yours or someone else’s), exercising, watching your weight, and taking care of your teeth.

What is inflammation?

Inflammation is an intricate dance involving different types of white blood cells, the antibodies they make, and a dizzying array of chemical messengers known as cytokines. Its aim is to defend the body against bacteria, viruses, and other foreign invaders, to remove debris, and to help repair damaged tissue. Inside arteries, inflammation helps kick off atherosclerosis and keeps the process smoldering. It even influences the formation of artery-blocking clots, the ultimate cause of heart attacks and many strokes.

Simple changes

What you eat may fan the fires of inflammation. With some small changes — no crazy new foods involved — you can douse them. Here are some suggestions:

Get an oil change. Eating a lot of saturated fats and/or trans fats is linked with higher levels of inflammation. Swap them for olive oil, which has potent anti-inflammatory properties, or polyunsaturated fats, especially omega-3 fats from fish.

Don’t be so refined. The bolus of blood sugar that accompanies a meal or snack of highly refined carbohydrates (white bread, white rice, French fries, sugar-laden soda, etc.) increases levels of inflammatory messengers called cytokines. Eating whole-grain bread, brown rice, and other whole grains smooths out the after-meal rise in blood sugar and insulin, and dampens cytokine production.

Promote produce. The more fruits and vegetables you eat, the lower the burden of inflammation. Why? They contain hundreds, perhaps thousands, of substances that squelch inflammation-rousing free radicals; some act as direct anti-inflammatory agents.

Go nuts. Adding walnuts, peanuts, almonds, and other nuts and seeds to your snacks and meals is another tasty way to ease inflammation.

Cocoa lovers rejoice? In laboratory studies, cocoa and dark chocolate slow the production of signaling molecules involved in inflammation. The trick is to get them without too much sugar and fat.

Alcohol in moderation. A drink a day seems to lower levels of C-reactive protein (CRP), a powerful signal of inflammation. Too much alcohol has the opposite effect on CRP.

Spice it up. Herbs and spices such as turmeric, ginger, garlic, basil, pepper, and many others have anti-inflammatory properties.

Putting it all together

If you are a do-it-yourselfer, pick and choose foods that ease inflammation and eat them instead of those that promote it. If you’d rather follow a plan, the so-called Mediterranean diet encompasses many inflammation-fighting foods. I love this diet!

If you adopt an anti-inflammatory diet, you probably won’t see or feel any different. Angina won’t suddenly disappear or heart failure reverse itself. But you will be doing your heart, arteries, and the rest of you a huge favor that will pay off in many ways.

Recovering from an Ankle Sprain

Ankle AnatomyTake it easy, but keep moving.

All it takes is a simple misstep, and suddenly you have a sprained ankle. It’s one of the most common musculoskeletal injuries in people of all ages, athletes and couch potatoes alike. The injury occurs when one or more of the ligaments in the ankle are stretched or torn, causing pain, swelling, and difficulty walking. Many people try to tough out ankle injuries and don’t seek medical attention. But if a sprain causes more than slight pain and swelling, it’s important to see a clinician. Without proper treatment and rehabilitation, a severely injured ankle may not heal well and could lose its range of motion and stability, resulting in recurrent sprains and more downtime than you’d like.

Anatomy of an ankle sprain

The most common type of ankle sprain is an inversion injury, or lateral ankle sprain. The foot rolls inward, damaging the ligaments of the outer ankle — the anterior talofibular ligament, the calcaneofibular ligament, and the posterior talofibular ligament. (Ligaments are bands of fibrous tissue that connect bone to bone; see illustration.)

Ankle ligaments

Less common are sprains affecting the ligaments of the inner ankle (medial ankle sprains) and syndesmotic sprains, which injure the tibiofibular ligaments — the ligaments that join the two leg bones (the tibia and the fibula) just above the ankle. Syndesmotic sprains, which occur most often in contact sports, are especially likely to cause chronic ankle instability and subsequent sprains.

The severity of an ankle sprain depends on how much damage it does and how unstable the joint becomes as a result. The more severe the sprain, the longer the recovery (see “Grades of ankle sprain severity”).

Grades of ankle sprain severity

Severity

Damage to ligaments

Symptoms

Recovery time

Grade 1

Minimal stretching, no tearing

Mild pain, swelling, and tenderness. Usually no bruising. No joint instability. No difficulty bearing weight.

1-3 weeks

Grade 2

Partial tear

Moderate pain, swelling, and tenderness. Possible bruising. Mild to moderate joint instability. Some loss of range of motion and function. Pain with weight bearing and walking.

3-6 weeks

Grade 3

Full tear or rupture

Severe pain, swelling, tenderness, and bruising. Considerable instability and loss of function and range of motion. Unable to bear weight or walk.

Several months

Source: Adapted from Maughan KL, “Ankle Sprain,” UpToDate, version 14.3, and Ivins D, “Acute Ankle Sprain: An Update,” American Family Physician (Nov. 15, 2006), Vol. 74, No. 10, pp. 1714-20.

Immediate treatment

The first goal is to decrease pain and swelling and protect the ligaments from further injury. This usually means adopting the classic RICE regimen — rest, ice, compression, and elevation. If you have severe pain and swelling, rest your ankle as much as possible for the first 24-48 hours. During that time, immerse your foot and ankle in cold water, or apply an ice pack (be sure to cover the ankle with a towel to protect the skin) for 15-20 minutes three to five times a day, or until the swelling starts to subside.

To reduce swelling, compress the ankle with an elasticized wrap, such as an ACE bandage or elastic ankle sleeve. When seated, elevate your ankle as high as you comfortably can — to the height of your hip, if possible. In the first 24 hours, avoid anything that might increase swelling, such as hot showers, hot packs, or heat rubs. Nonsteroidal anti-inflammatory drugs such as ibuprofen can help reduce pain and swelling and may also speed recovery.

There are several great Oriental medical remedies and nutrients you need to take in order to reduce the swelling and promote healing and enhance the tensil strength of the joint.

Medical evaluation

Contact your clinician as soon as possible. He or she may want to see you immediately if your pain and swelling are severe, or if the ankle feels numb or won’t bear weight. He or she will examine the ankle and foot and may manipulate them in various ways to determine the type of sprain and the extent of injury. This examination may be delayed for a few days until swelling and pain improve; in the meantime, continue with the RICE regimen.

X-rays aren’t routinely used to evaluate ankle injuries. Ligament problems are the source of most ankle pain, and ligaments don’t show up on regular x-rays. To screen for fracture, clinicians use a set of rules — called the Ottawa ankle rules, after the Canadian team that developed them — to identify areas of the foot where pain, tenderness, and inability to bear weight suggest a fracture. A review of studies involving more than 15,000 patients concluded that the Ottawa rules identified patients with ankle fractures more than 95% of the time.

Functional treatment

To recover fully, you’ll need to restore the normal range of motion to your ankle joint and strengthen its ligaments and supporting muscles. Studies have shown that people return to their normal activities sooner when their treatment emphasizes restoring ankle function — often with the aid of splints, braces, taping, or elastic bandages — rather than immobilization (such as use of a plaster cast). Called functional treatment, this strategy usually involves three phases: the RICE regimen in the first 24 hours to reduce pain, swelling, and risk of further injury; range-of-motion and strengthening exercises within 48-72 hours; and training to improve endurance and balance once recovery is well under way.

Generally, you can begin range-of-motion and stretching exercises within the first 48 hours, and should continue until you’re as free of pain as you were before your sprain. Start to exercise seated on a chair or on the floor. As your ankle improves, you can progress to standing exercises. If your symptoms aren’t better in two to four weeks, you may need to see a physical therapist or other specialist.

Exercises to help restore function and prevent injury

Range-of-motion, stretching, and strengthening: First 1-2 weeks

Flexes. Rest the heel of the injured foot on the floor. Pull your toes and foot toward your body as far as possible. Release. Then point them away from the body as far as possible. Release. Repeat as often as possible in the first week.

Ankle alphabet. With the heel on the floor, write all the capital letters of the alphabet with your big toe, making the letters as large as you can.

Press down, pull back. Loop an elasticized band or tubing around the foot, holding it gently taut (A). Press your toes away and down. Hold for a few seconds. Repeat 30 times. Tie one end of the band to a table or chair leg (B). Loop the other end around your foot. Slowly pull the foot toward you. Hold for a few seconds. Repeat 30 times.

Ankle eversion. Seated on the floor, with an elasticized band or tubing tied around the injured foot and anchored around your uninjured foot, slowly turn the injured foot outward. Repeat 30 times.

Ankle inversion. Seated on the floor, cross your legs with your injured foot underneath. With an elasticized band or tubing around the injured foot and anchored around your uninjured foot, slowly turn the injured foot inward. Repeat 30 times.

Stretching and strengthening: Weeks 3-4

Standing stretch. Stand one arm’s length from the wall. Place the injured foot behind the other foot, toes facing forward. Keep your heels down and the back knee straight. Slowly bend the front knee until you feel the calf stretch in the back leg. Hold for 15-20 seconds. Repeat 3-5 times.

Seated stretch. Loop an elasticized band or tubing around the ball of the foot. Keeping the knee straight, slowly pull back on the band until you feel the upper calf stretch. Hold for 15 seconds. Repeat 15-20 times.

Rises. Stand facing a wall with your hands on the wall for balance. Rise up on your toes. Hold for 1 second, then lower yourself slowly to the starting position. Repeat 20-30 times. As you become stronger, do this exercise keeping your weight on just the injured side as you lower yourself down.

Stretches. Stand with your toes and the ball of the affected foot on a book or the edge of a stair. Your heel should be off the ground. Use a wall, chair, or rail for balance. Hold your other foot off the ground behind you, with knee slightly bent. Slowly lower the heel. Hold the position for 1 second. Return to the starting position. Repeat up to 15 times, several times a day. This exercise can place a lot of stress on the ankle, so get your clinician’s go-ahead before trying it.

New drug fizzles at raising HDL

Tried-and-true strategies are still excellent ways to boost good cholesterol.

When pharmaceutical giant Pfizer pulled the plug on torcetrapib, its experimental HDL-raising drug, media reports made it sound like we were losing our last, best ally in the battle against heart disease. The decision was unquestionably a huge setback for Pfizer, which had sunk $800 million into developing torcetrapib. And it was a big bump in the road for researchers hoping that high-density lipoprotein (HDL, the so-called good cholesterol) would be the next big thing in cholesterol-targeted drug therapy. But it shouldn’t be taken as a sign that raising HDL is a bad or dangerous strategy for preventing heart disease and stroke — just that torcetrapib isn’t the way to do it.

The torcetrapib story starts in the late 1970s with the discovery of cholesteryl ester transfer protein (CETP), a protein that circulates in the bloodstream attached to HDL particles. Its job is to shuttle cholesterol and other fats between different types of cholesterol-carrying lipoprotein particles.

Although cholesterol is a four-letter word when it comes to heart disease, it is essential for good health. The body uses it to build cell membranes, bile acids for digestion, vitamin D, and hormones such as estrogen and testosterone. As is the case for any vital nutrient, the body has systems that give it great flexibility in handling cholesterol during feast, famine, and everything in between. CETP is part of such a system. But for most Americans, who are overloaded with cholesterol, CETP’s action is counterproductive. It pulls cholesterol out of protective HDL, which sponges up excess cholesterol from artery walls and ferries it to the liver for disposal, and puts it into harmful LDL, which is responsible for creating artery-clogging plaque.

The discovery of CETP raised an interesting question: Could blocking or disabling this molecule increase the amount or activity of HDL and thus reduce plaque? Statins have taken us about as far as we can go with lowering harmful LDL. Boosting helpful HDL represents another tantalizing target for slowing or preventing heart disease. Every 1% increase in HDL translates into a 2%-3% decrease in heart disease risk. Existing drugs raise HDL by 35% at best. Kicking it up a notch or two should theoretically save lives. It would also be worth billions of dollars to the drug company that gets there first.

Classifying HDL
Low: below 40 mg/dL

Average: 40-60 mg/dL

High: above 60 mg/dL

Warning signs

Early studies of CETP in humans were hard to decipher. People with mutations that led to low levels of CETP had higher than average HDL. When their HDL was really high, above 80 milligrams per deciliter of blood (mg/dL), they seemed to be protected against heart disease. When it only got moderately high, though, some studies showed an increase in heart disease, while others showed a decrease.

Despite the contradictions, the search was on for drugs that could inhibit CETP. A Japanese company developed one, called JTT-705, that raised HDL by 34% and lowered LDL by 7%; it is still being investigated. Pfizer scientists developed a different CETP inhibitor, called torcetrapib, in 1992. An early test of the drug’s safety showed that it boosted HDL a whopping 106%.

That was enough for Pfizer to start the kind of large-scale clinical trial the FDA needs for approving a new heart disease drug. Dubbed ILLUMINATE, the trial included 15,000 people at high risk of heart disease. Half took torcetrapib plus Lipitor (Pfizer’s blockbuster cholesterol-lowering statin), and the other half took an identical pill containing Lipitor alone. The trial was supposed to last until 2009.

An early look at the data raised some concerns about torcetrapib. It appeared to elevate blood pressure, a bad sign for a medicine designed to prevent heart trouble. The death knell came about halfway through the trial, when independent overseers found that 82 volunteers taking torcetrapib and Lipitor had died, compared to 51 taking Lipitor alone. They determined that the difference wasn’t due to chance, and that the situation wasn’t likely to reverse itself. Pfizer stopped the trial and all further work on torcetrapib.

Meanwhile, Cleveland Clinic researchers were doing a parallel study in which they threaded tiny ultrasound cameras through the coronary arteries of 1,200 volunteers taking torcetrapib plus Lipitor or Lipitor alone. Their findings, which they present at the American College of Cardiology meeting in New Orleans in March 2007, may offer some clues as to how or why torcetrapib increases the risk of heart disease even as it raises protective HDL.

It could be that this particular drug does something else that’s harmful in addition to boosting blood pressure. It is also possible that blocking CETP in any way may have unintended consequences. We won’t know for sure until results are in from ongoing trials of other CETP inhibitors.

Hurrah for HDL

The demise of torcetrapib shouldn’t tarnish HDL’s reputation as part of the body’s natural protection against heart disease. In numerous large studies, people with naturally high HDL have less heart disease than those with low HDL. And evidence from earlier clinical trials shows that raising HDL lowers the risk of heart attack or premature death from cardiovascular disease.

There are several things you can do right now to boost your HDL (see “Raising HDL today”). These strategies work, though none offers a huge increase in HDL. Lifestyle changes are the place to start, since they don’t have negative side effects. For people with low HDL, doctors sometimes prescribe niacin (generic, Niaspan) or a fibrate such as fenofibrate (generic, Tricor, Lofibra, others), gemfibrozil (generic, Lopid), or clofibrate (generic, Atromid). Both of these drug types have been used for years. Statins can also modestly boost HDL.

Raising HDL today

There’s no need to wait for the development of new HDL-raising drugs. You can boost yours now with several tried-and-true methods.

Exercise. Moderate to vigorous exercise can boost HDL by 3%-9%.

Smoking cessation. On average, HDL rises by about 4 mg/dL after stopping smoking.

Trans fats. Eating trans fats increases LDL (bad) cholesterol and decreases HDL. Avoiding them and switching to unsaturated fats improves HDL.

Weight control. In clinical trials, HDL increased 1.6 mg/dL for every 10 pounds lost.

Alcohol. One alcoholic drink a day, regardless of the beverage, boosts HDL by about 4 mg/dL.

Medicines. Niacin, fibrates, and statins all increase HDL. Of these, niacin is the most powerful, with increases of 20% to 35%.

Sooner or later a new HDL-raising drug will come along. No matter how well it seems to work, heed the lesson from torcetrapib, drug-coated stents, and other new drugs and devices: Don’t be an “early adopter.” Instead, wait until the hazards are as well known as the benefits.

What the latest diet trial really means…

Any diet that helps you take in fewer calories will help you shed pounds.

The “Atkins is best” headlines you may have seen in March 2007 had champions of the low-carbohydrate, high-fat diet smiling — and hoping that people wouldn’t read the study on which the news reports were based.

An article in the March 7, 2007, Journal of the American Medical Association compared weight loss over the course of a year in 311 overweight but healthy women who used one of four popular diet plans: Atkins, the Zone (balanced protein, carbohydrate, and fat), Ornish (very low fat, very high carbohydrate), and the LEARN program (standard low fat, moderately high carbohydrate).

The women in all four groups steadily lost weight for the first six months. The most substantial weight loss occurred among women assigned to the Atkins plan, who lost an average of 14 pounds, compared with 6-8 pounds for the other three plans. After six months, most of the participants started to regain weight. At the end of a year, the women in the Atkins group were about 10 pounds lighter than when they had started, compared with 5.7 pounds for the LEARN group, 4.9 pounds for the Ornish group, and 3.5 pounds for the Zone group.

Read the fine print, though, and you realize that few of the women actually stuck with their assigned diets. Those in the Atkins group were aiming for 50 grams of carbohydrate a day but took in almost triple that amount. The Ornish dieters were supposed to limit their fat intake to under 10% of their daily calories, but got about 30% from fat. There were similar deviations for the Zone and LEARN groups.

Beyond carbs, protein, and fat

The real message of this and other head-to-head diet comparisons isn’t that one type of nutrient is better than another. Instead, it is that you can lose weight with any diet that helps you eat less. “In the long run, finding strategies that guide you to match your food intake to the calories you burn matters far more than macronutrients like protein, fat, or carbohydrates,” says Dr. George Blackburn, director of the Center for the Study of Nutrition Medicine at Harvard-affiliated Beth Israel Deaconess Medical Center. Diet books that focus on individual nutrients may be good for short-term weight loss but don’t necessarily offer good advice for a lifetime.

One worry about the Atkins diet is that eating meat, cheese, and other fatty foods will be bad for cholesterol and heart disease. In this trial, though, cholesterol levels in the Atkins dieters were fine.

To make the Atkins approach work for your heart as well as your waist, make smart protein choices. A study published in 2006 in the New England Journal of Medicine showed that over a 20-year period, women who followed low-carb diets high in plant protein and good (meaning unsaturated) fats were less likely to have developed heart disease than those whose low-carb diets were high in animal protein and fat. “If you plan to follow a low-carb diet, skip the butter and sausage and go for olive oil and fish,” says Dr. Walter C. Willett, professor of nutrition at the Harvard School of Public Health.

There is a lot more to it than just the diet though - my goal is to help you shed pounds and feel great by following nutrition plan that you can continue for a lifetime. Education is the key to success. I hope to provide you with the tools needed. On top of that, is is essential to look at many contributing factors that can cause weight gain and cause one to struggle with sheding the pounds - sometimes lab work and potential supplemetation can aid the process.

Give me a call and we can discuss your goals.