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The coronary cardiopathy is the main cause of premature death and is responsible for 50% of all deaths.

Estimates for year 2006 are that 81.100.000 people in the United States have one or more forms of cardiovascular disease:

 

High blood pressure:73.600000

Coronary artery disease :17.600000

Myocardial infarction(acute heart attack) :8.500000

Angina pectoris :10.200000

Stroke: 6.400000

Heart failure:5.800000.

MORE:

1)CORONARY ARTERY DISEASE CAUSED 425.426 DEATHS IN 2006.

2)17.600000 ALIVE TODAY HAVE A HISTORY OF HEART ATTACK.

3)THIS YEAR AN ESTIMATED 1.260.000 MILLIONS OF AMERICANS WILL HAVE A NEW  O RECURRENT HEART ATTACH.

 

A vegetarian diet with less than 10% fat prevents development of coronary desease, stops development of existing damages, and regresses desease in many patients.

Even dough, cardiopatic patients mantain total cholesterol below 200 mg/dl, as recommended by THE AMERICAN HEARTH ASSOCIATION, millions of them will suffer and die  of cardiovascular disease.

Many studies show that to arrest the epidemics of coronary disease we must hold total cholesterol below 150 mg.

 A RISK ANALYSIS, DONE IN A BIG U.S. COURT TRIAL( MRFIT STUDY,316000 PATIENTS), SHOWS THAT THERE ARE LESS DECEASED WITH A LEVEL OF TOTAL CHOLESTEROL OF 122 MG/DL.(18)

THE MORTALITY RATE AMONG PATIENTS WITH HIGH CHOLESTEROL ABOVE 275 MG/DL IS TWICE THAT OF PEOPLE WITH LOWER CHOLESTEROL LEVEL.(19)

A 1% reduction of plasm cholesterol lead a risk reduction of 2-3%.

THE LESSER THE CHOLESTEROL LEVEL, THE MORE ARE THE BENEFITS

THE SAYING LOWER IS BETTER HAS BEEN DEMONSTRATED IN THOUSANDS OF CLINICAL STUDIES

 

 

 

 

 

RISKS FACTORS FOR HEART ATTACK INCLUDE:

 

 

 

INCREASING AGE (OVER AGE 65)

MALE GENDER

DIABETES

FAMILY HISTORY OF CORONARY DISEASE

HIGH BLOOD PRESSURE

SMOCKING

TO MUCH FAT IN YOUR DIET

UNHEALTY CHOLESTEROL LEVELS ESPECIALLY LDL CHOLESTEROL AND LOW HDL CHOLESTEROL

CRONIC KIDNEY DISEASE

 

 

 

 

PREVENTION:

 

 

1)KEEP YOUR BLOOD PRESSURE, BLOOD SUGAR , WEIGHT AND CHOLESTEROL UNDER CONTROL

2)DON'T SMOKE

3)CONSIDER DRINKING1 TO 2 GLASSES OF ALCHOOL OR WINE EACH DAY.HOWEVER DRINKING LARGER AMOUNT DOES MORE HARM THAN GOOD.

4)EAT A LOW FAT DIET RICH IN RAW FRUITS AND VEGETABLES  AND LOW IN ANIMAL FAT.

5)EAT FISHESTWICE A WEEK, BAKED OR GRILLED IS BETTER THAN FRIED FISH.

6)EXERCICE DAILY OR SEVERAL TIMES A WEEK.

7)LOSE WEIGHT IF YOU ARE OVERWEGHT.

 

 

 

 

THE SHANGHAI STUDY, THAT CARED THOUSAND OF CHINESE FOR MANY YEARS DEMONSTRATED THAT LOW LEVELS OF CHOLESTEROL (140 MG/187 MG) ARE NOT HAZARDOUS TO HEALTH

Reducing LDL cholesterol to 70MG/DL is key.

A recent study (Asteroid Trial, 2006 of Dr. Ballantyne of Baylor College Huston, TX on 507 patients) has demonstrated that reducing ldl cholesterol to 60 mgr/dl reduces plates in 2/3 of patients.

In this study a statin the rosuvastatin with 40 mg dosage per day.

With this dosage the rosuvastatina has determined a reduction of LDL cholesterol and increse of HDL cholesterol.

The rosuvastatin has determined after 2 years on average a decrease  of 53% LDL cholesterol and an increase of about 14,7% of HDL cholesterol from 42,8 mg/dl to 48,3 mg/dl.

Dr. Ballantyne claims that 97% of patients of trial has obtained regression and stabilization of plaques.

Usage of niacin from 1500 mg to 2500 mg a day, measeured increase of alchool, physical exercise are the most important means to augment HDL colesterol.

A long experience with coronaric patients demonstrates  that total cholesterol level should be under (150 mg), with a reduced fat diet and eventually with drugs.

A reduced fat diet hinders progression of coronary desease and can regress it.

A 200 mg level of cholesterol and a diet with 30% of fats is too high.

When talking about cholesterol moderation is a killer.

WHEN CHOLESTEROL LEVEL IS LOW AS IT IS IN ALL PRIMATES THE CORONARY DISEASE DOESN' T EXIST OR IF THERE IS IT DOESN' T PROGRESS.

 

 

EXPERIMENTAL STUDIES

 

 

SEVERAL STUDIES ON ARTERIOSCLEROSIS THAT WAS INDUCED BY HIGHLY LIPIDIC DIETS HAVE DEMONSTRATED THAT DAMAGES CAN REGRESS.

THESE STUDIES HAVE BEEN CONDUCTED ON APES, PIGS, RABBITS, ETC,  USING FAT RICH DIETS AND CHOLESTEROL. AFTER CHOLESTEROL WAS ELIMINATED FROM DIET, ITS CONCETRATION WAS NORMALIZED AND DAMAGES WERE RAPIDLY REGRESSING. LESIONS WERE SHOWING SMALLER LIPIDIC CONTENT, WITH REDUCED COLESTEROL, AND REDUCED COLLAGEN CONTENT (CLARCSON E COLL.)

 IN MEN, IT HAS BEEN WIDELY DEMONSTRATED  THAT ADVANCED LESIONS AND SEMICLOSED CAN REGRESS.

 

 

OMEGA 3 AND PROTEIN C

 

 

AS CO-AGENTS TO DIET AND THERAPY OMEGA 3 HAVE PROVEN HELPFUL WITH THEIR ACTION ON PROSTAGLANDINE, ESPECIALLY WITH ANTI AGREGGANT, ANTI INFLAMMATORY AND  VASODILATOR ACTION.

 

 

 

TOTAL TRIALS RESULTS

 

 

1) A 1% REDUCTION IN COLESTEROLEMIA DECREASES CHD RISK BY 2%.

2) A 1% INCREASE OF HDL DECREASES CHD RISK BY 2-4%.

3)A DECREASE IN TRIGLICERIDS IS ASSOCIATED WITH A VARIABLE DECREASE OF CHD RISK.

4) AN EFFECTIVE LIPIDIC REDUCTION SLOW ATEROMATOSE PLAQUE PROGRESSION AND IN SOME CASES CAN LEAD TO THEIR REGRESSION.

 

5)SEVERAL STATIN STUDIES HAVE DEMONSTRATED A GENERAL MORTALITY REDUCTION.

THE 4S STUDY HAS POINTED OUT IN POST HEART-STROKE PATIENTS WITH 212/309 CHOLESTEROL A TOTAL MORTALITY REDUCTION OF 30%, A CORONARIC MORTALITY OF 42% , AND REDUCTION OF CORONARIC EVENTS OF 34%.

 

 

 

SATURATED FATS  

 

 

 

 

SATURATED FATTY ACIDS ARE THOSE WITHOUS DOUBLE LINKS WITH CARBONIC ATOMS.

IT HAS BEEN DEMOSTRATED THAT SATURATED FATS INCREASE CHOLESTEROL LEVEL IN THE BLOOD.

ALMOST ALL SATURATED FATS ORIGINATE FROM ANIMALS BUT ALSO VEGETABLE OILS ARE RICH IN SATURATED FATS ( IS. PALM SEED OIL,COCONUT OIL, COTTON SEED OIL ),AND ALSO OLIVE OIL HAS 16% OF SATURATED FATS. TREE FATTY ACIDS INCREASE IN A MARKED WAY THE CHOLESTEROL LEVEL: PALMITIC ACID(16 CARBON ATOMS) MIRISTIC ACID(14), AND lAURIC ACID.

FOR EVERY 1% INCREASE ON CALORIES FROM SATURATED FATTY ACIDS TOTAL CHOLESTEROL IN SERUM INCREASE OF ABOUT 2,7 MG/DL.

MAIN SOURCES OF SATURATED FATS ARE DAIRY PRODUCTS, MEATS AND CAKES.

MILK FAT(BUTTER, CHEESE, ICE CREAM) IS THE MOST HYPERCHOLESTEROLEMIC DUE TO ITS HIGH CONTENT IN PALMITIC AND MIRISTIC ACID. SOME SATURATED FATS DON'T INCREASE CHOLESTEROL LEVELS, AMONG THESE ARE: CAPRILIC ACID WITH 8  CARBONIC ATOMS AND  CAPROIC ACID WITH 10  CARBONIC ATOMS, AS WELL AS STEARIC ACID WITH 18  CARBONIC ATOMS .

 

 

ATEROGENICS INDEX

 

 

 

 THECHOLESTEROL/SATURATED FATS INDEX (CSI) HAS BEEN DEVELOPED TO PROVIDE AN ATEROGENIC SCORE TO VARIOUS FOODS.

CSI INDEX FOR SOME FOODS:

WHITE SEAFOOD =4

PEANUTS BUTTER=5

SKINLESS CHICKEN=6

WHOLE MILK=7

MAYONNAISE=10

 VEGETABLE MARGARINE =10

ICE CREAM=13

BEEF MEAT, LAMB =13

CHEESE=26

EGGS=29

COCONUTAND PALM OIL, COCOA BUTTER=49

 

 

TRANS FATS

 

 

 

SOME FATTY ACIDS HAVE BEEN DISCOVERED RECENTLY, MONOINSATURATED TRANS, ABLE TO INCREASE CHOLESTEROL.

THE MOST IMPORTANT IS ELAIDIC ACID WITH 18 CARBON ATOMS AND A DOUBLE LINK IN OMEGA 9 POSITION.  TRANS ACIDS DEVELOP THROUGH HYDROGENIZATION OF THE LINOLEIC ACID AND ARE FOUND IN MARGARINES AND PASTRY FATS.  

 

 

 

OBESITY

 

 

 

OBESITY IS THE THIRD FACTOR ABLE TO INCREASE CHOLESTEROL LEVELS.

AMONG OBESE PEOPLE HYPERCHOLESTOLIC CONDITIONS CONCERN BOTH THE VLDL AND LDL SECTIONS.

OBESITY IS NOT SOLELY RESPONSIBLE TO INCREASE THE VLDL, BUT ALSO REDUCE HDL CHOLESTEROL.

 

 

DIETS

 

Patients must reduce in or in most serious cases eliminate from their diets oil, meat, cheese, ice cream, pastries, bacon, egg yolks,liver ,brain , etc...

 

Dietary cholesterol has to decrease,  and gathering data from several studies was observed that a total cholesterol increase is about 8/10mg every 100mg of intake colesterol/1000 calories.

 

Increase of haematic cholesterol cause removal of the syntesis ability of LDL receptors.

Patients can eat hard-boiled egg white, skimmed milk, skimmed yoghurt, 0 fat cheese, green beans, tofu ,legumes, fish, whole cereals, soy, fruit and vegetables. 

Flax seed oil can be used as it is a rich source of linoleic acid (omega 3), so can nuts, almonds, peanuts in limited amounts. 

Seed oil rich in omega 6 and hydrogenated fats should be avoided.

If diet is not enough to mantain cholesterol  below 150mg. patient have to associate anti cholesterol drugs (statin).

Fruits and vegetables would be eaten mainly raw (up to 10 portions a day) to preserve enzymes (is. catalyse, glutation, sod)   and thermo fleeting vitamins  (folic acid , C, B6, B1) minerals(potassium,magnesium, selenium, boron, etc.

It is helpful to eat 25 mg of fiber every day.

Salt has to be reduced especially in high blood pressure sufferers, because of their hydroretentive and constrictive actions. 

Magnesium and potassium intake should be increased.  

Physical activity should be increased up to burn 2000 calories a week.

 

 

 

ANTIOXIDANTS

 

 

STUDIES CONDUCED ON WATANABE RABBITS WITH HIGH CHOLESTEROL HOMO-ZYGOT WITH HUGE LEVELS (800/1000MG), AND SUFFERING OF MULTIPLE, HAVE DEMONSTRATED THAT PROBUCOL, A DRUG WITH MARKED ANTI OXIDANT ACTION  REDUCE ARTERIOSCLEROSIS DAMAGE

  ARTERIOSCLEROSIS PLAQUES CONTAIN EXCLUSIVELY LDL OXIDIZED AND LIPID OXIDIZED.

INDEED ONLY LDL OXIDIZED ( NOT NORMAL LDL) ARE CATCHED BY MACROFAGOUS AND START FOAM CELLS AND LIPIDIC STRIPS, A FOREGOING STEP OF ATEROMS.

LDL ARE LIPOPROTEIN THAT TRANSPORT CHOLESTEROL FROM LIVER TO TISSUES AND ARE KNOWN AS BAD CHOLESTEROL.

THE LDL OXIDATE  WHEN THEY REACT TO FREE RADICALS.  LDL CAN OXIDATE FOR DEGRADATION OF APOB- 100 OR UNDERGO GLYCOLYSIS.

SMOKING, HYDROGENATED FATS, JUNKFOOD, HIGH GLYCEMIC CONDITION, METABOLIC SYNDROME FAVOUR OXIDATE LDL FORMATION.

IS THEREFORE EVIDENT THAT AN ANTIOXIDANT RICH DIET CAN STOP LDL OXIDATION.

 SOD ( SUPEROSSID DISMUTASI ) GIVING,THE MOST IMPORTANT ANTIOXIDANT OF LIVE ORGANISMS IS EXTRACTED FROM YELLOW MELON ASSOCIATED TO GLIADINA, ACCORING TO FRENCH AUTORS, HAS LEAD REGRESSION ARTERIOSCLEROTIC DAMAGE.

IT IS BELIVED THAT ANTIOXIDANTS OF RAW FRUIT AND VEGETABLE CAN PREVENT OXIDATION OF LDL AND ARTERIOSCLEROSIS DAMAGE.

SOME OF THE RICHEST ORAC UNIT VEGETABLE, THAT MESURE ANTIOXIDANT ANCTIVITY WE MENTION: POMEGRANATE, BLUEBERRIES, DRIED PLUMS, ORANGES, RASPBERRIES, STRAWBERRIES, SPINACH, GARLIC, BROCCOLI, CABBAGES.

 

THIS FOODS ARE PARTICULARLY RICH OF ELECTRONS AND HENCE EASLY HINDER FREE RADICALS.

VITAMIN E AND A AND VITAMIN C ARE USED AS ANTIOXIDANTS.

THE Q 10 COENZYME, LIPOIC ACID, SELENIUM, THROUGH GLUTATIONE TRANSPORT AND YELD HYDROGEN, PROVIDING A STRONG ANTIOXIDANT FUNCTION.

 

 

COMFIRMATION FROM STUDIES:

 

 

Several studies confirmed the benefits of a low cholesterol level.

For instance 35 % of coronarysclerosis cases of the FRAMINGHAM study was occurring among patients with cholesterol level between 150 mg and 200 mg.  In contrast few cases happened in subjects with 150 mg choleterol level and none of them had mortal strokes (3).

Arteriosclerosis develop itself silently after many years of fat diet, as demonstrate autoptic studies of young soldiers who died in Korea and Vietnam (4-5) who were found with serious coronary stenosic damage.

In Cina where the average colesterol rate is among 90mg/dl and 150 mg/dl,and nutrition is almost vegetarian, coronary disease is almost unknown (6-7).

Over 10 years ago BLANKEHORN and his colleagues demontrated that arteriosclerosis can stop and regress if you lower colesterol with drugs (8-11).

More recently DEAN ORNISH and others confirmed these results wih a poor fat diet.  So this study confirmed that the best results are obtained with poor fat diet associated to ipocolesterolic drugs (9).

 

The AVERT study has demonstrated that an agressive ipocolesterolis theraphy is effective as an angioplastic theraphy.

Patients examined in the Avert study cured with drugs and ipolipidic diet had 13% of complications, this means that pharmacologic treatment is not enough(12).

A RECENT STUDY SHOWED THAT OBTAINED BENEFITS ARE PROPORTIONAL TO COLESTEROL LEVEL THAT IS REACHED WITH TREATMENT(13).

 ARTERIOSCLEROSIS TREATMENT

 

 

Operations (bypass and angioplasty) on coronaric arteries are done to treat serious coronary stenoses. (14)

Anyhow 85 % of stroke cases are due from breakage of small instable plaques, that are not visible on coronar- graphy.

The costly surgeries don' t reduce coronary sclerosis, that without diet and teraphy keep to progress year after year.

On the other hand lowering the total colesterol level of of LDL prevent lesions and their progress.

Lowering colesterol level reduce foam cells amount in plaques and reduce ptoteolytic enzymes. As a result plaques can shrink , their cap stabilize and become less subject to rupture.

 

 RESISTENCE TO A LOW FAT DIET

 

 

Despite a strong evidence that a low fat and colesterol diet reduces stroke risk, coronaropatics continue to increase fat consumption. 
TV and press media  promote consumption of delightful, colored food very rich in fats.

At every occasion: baby showers, weddings, congresses, foods become more and more fat and damaging.

Slimming diets promise lower weight increasing protein and fats. It is evident that we leave in an extremely toxic environment. 
If we consider coronary disease as an exposive fire, and colesterol and fats as their fuel that it is necessary to reduce the fuel.  

 

 

 The real solution to the problem is to stop the causes: reduce colesterol and saturated fats to prevent and regress coronary disease.

 Increase antioxidants of raw fruit and vegetables to stop LDL oxidation and aggregation of platelets.

Also the decrease of body weight and reduction of sistolic pressure, as shown in many studies, favour regression of arteriosclerotic damage.