The Pre-Lipid-Heart Period
The rising coronary mortality after WWII particularly in the USA (where in 1950, 51 percent of the total deaths were cardiac, 90 percent of which coronary deaths) spurred worldwide research activity and the formation of heart association's - national, international and regional. The World Congress of Cardiology was held fist in 1950 in Paris, then in 1954 in Washington D.C. and in 1958 in Brussels, Belgium and every four years thereafter.The Philippine Heart Association was formed in 1952; four years later, in 1956, the Asian Pacific Society of Cardiology (APSC) was organized in Manila by delegates from Australia, India, Indonesia, Iran, New Zealand, the Philippines and Taiwan.
The APSC’s Research Committee (with the author as chairman) decided to present a joint paper on heart disease in Asia at the Third World Congress of Cardiology in Brussels, Belgium. Three APSC countries, Australia, India and the Philippines, reported data that was the easiest to obtain in the short time available - the number of cases and kinds of heart diseases admitted in their teaching hospitals that can provide some idea of relative prevalences of heart diseases in the country. Rheumatic heart disease led in number of admissions, followed by hypertensive heart disease. There were almost as many admissions of congenital and syphilitic hearts as coronary heart patients in these teaching hospitals, indicating the influence that academic interests had on admission priorities. It was also showed how low the incidence of coronary heart disease was in the country; coronary heart disease was only number three in admissions. The Philippines was the only coconut-oil consuming nation in this survey because India’s data came from New Delhi hospitals in North INdia where coconuts do not grow. Yet the findings in these three diverse countries of Asia were similar - the highest hospital admissions were rheumatic and hypertensive, not coronary.
Four years later, at the 1962 International Seminar on Atherosclerosis in Bombay, India, Ancel Keys, the leading proponent of the Lipid-Heart Theory, invited us delegates from APSC to join him in his multination studies on coronary mortality and fat consumption. Only Japan was ready to participate. The other APSC countries could not for various reasons. In the case of the Philippines, the trained cardiologists were all in Manila and a few large cities. The provincial hospitals had no ECG machines. Nor had there been any study yet on the diet and type of fat intake in the twelve regions of the Philippines that differ in language, diet and culture. Keys proceeded with his study on the communities he selected in five European countries, like USA and Japan. This Seven Country study was published in 1970. It is interesting to speculate what would have happened had the Philippines joined this study and shown how low the incidence of coronary heart disease was in a coconut oil-eating country. Perhaps, the attacks of the U.S. edible-oil industry in the ‘80s would never have happened or succeeded as they did.
Heart Disease in Coconut-Oil Countries
Coconut oil is a staple only in the tropical/subtropical Pacific islands and coastal areas of Southeast Asia and South America where the Cocos nucifera Linn grows. The coconut tree thrives along the coast and some distance inland. Its cultivation as a crop, therefore, is restricted by geographic environment. Hence, relatively few populations subsist on coconut oil. The peoples of the Philippines, Indonesia, Sri Lanka and Polynesia are olive-oil consumers. The U.S. was coconut oil’s biggest importer before WWII until politics and the edible-oil industry’s vilification campaign against coconut and tropical oils stopped all coconut oil entry to that country.
To determine the effect, if any, of a coconut-oil diet on heart disease, an adequate numbre of cocinut oil-consuming subjects have to be observed for a long enough period extending into old age. Artificial feeding experiments can never be large enough nor endured by the subjects long enough to determine dietary effects on coronary morbidity or mortality. Hence, prolonged observations of peoples eating their usual diet, living their natural lives and dying their natural deaths, i.e., epidemiologic studies, are what are needed and not short-time ‘experiments’ on say, cholesterol levels. The data available from Polynesia, Sri Lanka, and the Philippines are precisely epidemiologic. Yet proponents of the Lipid-Heart and the enemies of coconut oil would still ask for ‘experimental evidence’ when they were so quick to accept the defect-ridden evidence for the Lipid-Heart proposal.
If it is true that coconut oil causes heart disease, then Polynesians, Sri Lankans, and Filipinos should be dying of heart disease right and left. But they are not - they, in fact, have the lowest coronary heart disease prevalence. This is most clearly seen in coconut-consuming people before they are exposed to the civilizing influence of the West. In these people, like the Maoris of Pukapuka and Tokelau, coconut oil’s unadulterated effects can be seen. The absence of heart disease in such people is absolute proof that their ways and diets - which of course include coconut oil - are all non-atherogenic, or specifically non-cardiopathogenic. Sri Lanka and the Philippines were not in such a pure state when surveyed but their remarkably low heart disease prevalence also are strong denials of cardiopoathogenicity of the medium chain
fats.
Among Filipinos, strokes outnumber heart attacks by 5:1 or more in hospital admissions. (The ration used to be 10:1 in the '30s to the '50s when the author was a medical student and later a young professor in the Philippine General Hospital.) Hypertension must have been prevalent before WwII but not recognized because systolic B.P. of 160 or 180 mm was considered quite normal at that time. Salt is an important ingredient of Filipino cooking. Could salt-stroke rather than lipid-heart be the important relationship? Pukapukans use no salt in their food and they have no hypertension (see next section).
The Maoris of Polynesia
Ian Prior directed and conducted the twenty-year epidemiologic survey of the Maoris of the Cook islands and New Zealand. The Maoris are seafaring Polynesians believed to have migrated southwestward in magnificent canoes, leaving settlements along the way. The group that reached New Zealand in the 1300s was colonized by the white man in the 19th century, and succumbed to the white man’s ways and his diseases - tuberculosis, hyperuricemia, gout, rheumatic infection, coronary heart disease, hypertension. diabetes. The group that inhabited Rarotonga (southmost Cook island) became partially westernized and developed some of the white man’s diseases but not to the same degree as the New Zealand Maoris. But far to the north in the Polynesian chain of islands are Maori settlements with little contact with civilization and that are continuing their old ways of living and eating. Prior and his group focused their attention on Pukapuka, an isolated atoll 730 miles north of Rarotonga with 800 people, and the Tokelau islands 300 miles west of Pukapuka. Prior described them as a "handsome, brave, intelligent, blisfully happy" people free of hypertension, gout, diabetes, or heart disease. To study these people, the New Zealand epidemiologic team had to transport by boat more than 700 cubic feet of gear including two generators for electric power, an X-ray machine, deep-freeze containers, an electrocardiograph, a centrifuge, a flame photometer to measure dietary salt and reagents. Blood samples and aliquot's of urine were stored in the deep-freeze container for subsequent analysis of electrolytes, uric acid, and cholesterol in New Zealand.
Table 4 shows the average composition of the Maoris' diet and their cholesterol level. They are very little meat and it was mostly canned. Coconut products, fish, taro and rice were their protein and calorie sources. Their fats came almost wholly from coconut oil and fish oil and ranged from 35 to 55 percent of total calories. The Pukapukans who took a little less fat (and no salt) had very normal cholesterol (170 mg/dl in males, 175 in females). The Tokelauans who consumed a very high 55 percent of fat calories had somewhat higher cholesterol levels. Both Maori populations had neither hypertension nor heart disease, proof that coconut oil in such high amounts does not cause heart disease and that cholesterol levels above 200 mg are not atherogenic.
Table 4
Coconut Diet - Polynesian Atolls
PUKAPUKA TOKELAU
Males
|
Females
|
Males
|
Females
| |
Total Calories
Carbohydrates (g)
*Protein (g)
**Fat (% of total calories)
Fat, saturated (g)
Fat, unsaturated (g)
Cholesterol (mg)
|
2,120
283
31
35.2%
63
*7
73
|
1,810
230
53
39.8%
64
4
70
|
2,520
229
34
55.7%
137
6
51
|
2,100
189
53
56.1%
120
4
48
|
Serum cholesterol (mg)
|
170
|
176
|
208
|
216
|
*mostly from fish
**mostly from coconut
Sri Lankans
The Sri Lankans or Ceylonese live on an island in the Indian Ocean near the coast of India. They too are regular coconut-oil users who have no heart disease. The United Nations’ Demographic Yearbook of 1985 reported that Sri Lanka had a coronary mortality rate of one per 100,000; other countries not using coconut oil had coronary mortalities of 16 to 187 per 100,000. Coconut oil obviously was not causing, but rather even preventing heart disease in Sri Lankans.
S. Mendis, R.W. Wissler, and coworkers, wanting to show the superiority of linoleic acid over coconut oil, took sixteen healthy Sri Lankan males and subjected them to two dietary interventions - a first phase lasting six weeks during which the free living subjects continued to eat their regular meals with coconut oil; a second phase lasting six weeks where the coconut oil was replaced with an equivalent amount of corn oil. The blood lipid values of the participants during each phase were compared. On coconut oil, the blood cholesterol averaged a very normal 179 mg/dl and a very good TC:HDL-C ratio of 3:1. With corn oil, an omega-6 polyunsaturated oil, the cholesterol came down to 145 mg and the HDL to 25 mg. The TC:HDL-C ratio rose to an undesirable 4:1 due to a drastic fall in HDL (Table 5). Low HDL is an independent risk factor for atherosclerosis. The lowering of serum cholesterol by omega-6 oils has been traced to cholesterol deposition in tissues and blood vessel walls. The greater beneficial effect of coconut oil over corn oil is evident in this study.
Other Clinical Studies on LDL and HDL
The findings on Sri Lankans are practically duplicated by two similar feeding studies, on normolipemic adults. K. Sundram, K.C. Hayes, and O.H. Siru found that palmitic acid lowers cholestrol and LDL more than coconut oil (a lauric-myristic acid mixture) in human subjects with normal blood lipid levels. Coconut oil lowered LDL-C by an insignificant 0.1 percent but it increased HDL-C by a good 6.3 percent. And T.K.W Ng et al., on feeding their eighty-three Malaysian adults a 75 percent fat ration of coconut oil, found a 21.4 percent increase in HDL-C, lowering the LDL:HDL ratio by 3.6 percent. In all these studies the very evident effect of coconut oil is to raise HDL-C and lower the LDL:HDL ratio, a most beneficial effect.