Cary G Dean.
WHO European Coronary Prevention Study The results of the World Health Organisation's European Coronary Prevention Study were called "depressing" because once again no correlation between fats and heart disease was found.
They had cut saturated fats down to only eight percent of calorie intake daily, yet in the UK section there were more deaths in the intervention group than in the control group.
The North Karelia Project North Karelia, which had Finland's highest rates of heart disease, was compared with neighbouring Kuopio in The North Karelia Project.
In North Karelia, risk factors were cut by seventeen percent over the period of the study.
In North Karelia there was a reduction in both CHD mortality and total mortality.
However, that in Kuopio, the control group, where there were no restrictions, there was an even bigger decline in both CHD and total mortality.
This suggest that adopting a 'healthy' lifestyle may actually have inhibited the decline in heart disease.
They certainly give it no support.
This paper does not allow me to go through the more minor studies but they all show little convincing correlation between either the amount of fat eaten and heart disease or the type of fat eaten and heart disease.
A review of twenty-six studies published in 1992 concluded that:
"Lowering serum cholesterol concentrations does not reduce mortality and is unlikely to prevent coronary heart disease.
Claims of the opposite are based on preferential citation of supportive trials.
" One that seemed to support the 'healthy' recommendations was a Finnish trial published in 1975.
In the five years that the trial ran, cholesterol levels were lowered significantly, and the study was hailed as a success.
But in December 1991 the results of a 10-year follow-up to that trial found that those people who continued to follow the carefully controlled, cholesterol-lowering diet were twice as likely to die of heart disease as those who didn't.
"Some Success"!!!
Professor Michael Oliver, writing in the British Medical Journal commenting on the results, writes.
"As multiple intervention against risk factors for coronary heart disease in middle aged men at only moderate risk seem to have failed to reduce both morbidity and mortality, such interventions become increasingly difficult to justify".
This runs counter to the recommendations of many national and international advisory bodies which must now take the recent findings from Finland into consideration.
Not to do so may be ethically unacceptable
" Despite this wealth of evidence, nutritionists and the media continue to mislead us.
They tell us, for example, that the recent fall in the numbers of heart deaths in the USA is because Americans are eating less fat.
However, while CHD in the USA peaked in the 1950s and has fallen consistently since, this is against a background of rising fat intake.
I find difficulty understanding how the fat hypothesis gained such credibility in the USA as its history more than most does not support it.
The North American continent had been opened up by explorers and trappers who lived, very healthily, as did the Amerindians, almost entirely on fresh meat and pemmican.
As real pemmican is half dried lean meat and half rendered animal fat, and as fat has over twice the calorific value of protein, more than seventy percent of the energy in their diet came from fat.
Dieticians also say that the British had less CHD in the 1940s when fat was rationed.
However, the decade of rationing went on into the early 1950s with fat being the last food to come off ration in 1954.
Again the most rapid rise in CHD occurred during that period.
Also, during the period of rationing, British farmers had a very low incidence of heart disease when one would have expected their intake of fats, particularly animal fats, to have been higher than most.
Experience in other countries Keys based his fat-causes-heart disease hypothesis on a comparison between countries.
When we are told that we are 'the sick man of Europe', we are also compared to other countries.
So let me do a similar comparison.
In Japan, intakes of animal fat have more than doubled since the end of the Second World War.
Over the same period their incidence of coronary heart disease has fallen consistently.
In Israel too an increased consumption of saturated fats was followed by a fall in coronary deaths.
The dietary changes in Sweden parallel those in the USA, yet heart disease mortality in Sweden was rising while American rates were falling.
There is also a threefold variation in rates of heart disease between France and Finland even though fat intake in those two countries is very similar.
Among south Asians in Britain there is an unusually high incidence of heart disease, yet living on largely vegetarian diets, they have low levels of blood cholesterol and eat diets that are low in saturated fat.
Indians in South Africa have probably the highest rates of coronary disease in the world yet there is no apparent reason why they should, based on the current dietary hypotheses.
Until recently, Indians in India had a very low incidence of heart disease while using ghee (clarified butter) and coconut oil, which are highly saturated, and mustard seed oil which is largely monounsaturated.
The epidemic of heart disease in India began only after these were replaced with peanut, safflower, sunflower, sesame and soybean oils, all of which are high in polyunsaturated oils.
Lastly, the World Health Organisation is apparently in ignorance of epidemiological data that do not support its recommendation to reduce dietary saturated fat.
While it talks of coronary heart disease being responsible for most deaths in Caribbean countries, fat intake there is remarkably low.
Polyunsaturated fats The arguments for the polyunsaturated fat hypothesis are no more convincing than those for the cholesterol theory.
The claim is that unsaturated fats have a protective or preventative effect on CHD.
But in Israel, when consumption of polyunsaturated fats was about twice that of most Western countries, there was a very high incidence of CHD.
Those given high polyunsaturated diets in a trial in New South Wales fared significantly worse than those on a free diet.
And this is the finding in most trials that have increased the ratio of polyunsaturated fats.
From as early as 1971, an excess of cancer deaths has been reported in trials using diets that were high in polyunsaturated fats.
Polyunsaturated fats are also blamed for a doubling in the incidence of gallstones in the general public.
One of the pioneers of the polyunsaturated-fat-prevents-CHD hypothesis was the American cardiologist E. H. Ahrens Jr.
After twenty-five years of further research, however, he concluded that it was "irresponsible" to continue to press the polyunsaturated fat recommendations on the general public.
He went on:
"If the public's diet is going to be decided by popularity polls and with diminishing regard for the scientific evidence, I fear that future generations will be left in ignorance of the real merits, as well as the possible faults in any dietary regimen aimed at prevention of coronary heart disease.
" Another of the original proponents of the low-fat, low-cholesterol hypothesis, and a member of the Norwegian Council for Diseases of the Heart and Arteries, Professor Jens Dedichen of Oslo, also changed his mind.
In the 1950s Norway launched a cholesterol-lowering regimen in which soy margarine, that is high in polyunsaturated fatty acids, replaced butter, and soy oil was used extensively.
During the subsequent 20 years the increase in the use of soy-based products was accompanied by a steep and continuing rise in deaths from coronary thrombosis.
Professor Dedichen drew attention to the failure of the programme - and received a very hostile reaction from his colleagues.
Also castigated were members of the National Academy of Sciences and the National Research Council of America when in a report of May 1980, they stated that prevention of heart disease could not be achieved by reducing blood cholesterol using either diet or drugs, and said that such measures should be abandoned.
Margarine - a natural food?
The polyunsaturated fats used to make margarine are generally obtained from vegetable sources such as sunflower seed, cottonseed, and soybean.
As such they might be thought of as natural foods.
Usually, however, they are pressed on the public in the form of highly processed margarines, spreads and oils and, as such, they are anything but natural.
In 1989, the petroleum-based solvent, benzene, that is known to cause cancer, was found in Perrier mineral water at a mean concentration of fourteen parts per billion.
This was enough to cause Perrier to be removed from supermarket shelves.
The first process in the manufacture of margarine is the extraction of the oils from the seeds, and this is usually done using similar petroleum-based solvents.
Although these are then boiled off, this stage of the process still leaves about ten parts per million of the solvents in the product.
That is 700 times as much as fourteen parts per billion.
The oils then go through more than ten other processes:
Degumming, bleaching, hydrogenation, neutralization, fractionation, deodorisation, emulsification, interesterification, that include heat treatment at 140 o -160 o with a solution of caustic soda.
The use of nickel, a metal that is known to cause cancer, as a catalyst, with up to fifty parts per million of the nickel left in the product.
The addition of antioxidants such as butylated hydroxyanisol (E320).
These antioxidants are again usually petroleum based and are widely believed to cause cancer.
The hydrogenation process, that solidifies the oils so that they are spreadable, produces trans -fatty acids that rarely occur in nature.
The heat treatment alone is enough to render these margarines nutritionally inadequate.
When the massive chemical treatment and unnatural fats are added, the end product can hardly be called either natural or healthy.
Recent United States studies showed that heart disease worsened in those who switched from butter to polyunsaturate-rich margarine.
Research published in March 1993, confirmed this.
In a study that involved 85,000 nurses, women who ate just four teaspoons of polyunsaturated margarine a day had a sixty-six percent increased risk of CHD compared to those who ate none.
A review of men's experience in the Framingham Study published in 1995 also found that 6 teaspoons a day (mean of lowest intake vs mean of highest), increased risk by nearly a third.
The authors conclude:
"Intake of margarine may predispose to development of CHD in men".
And CHD is the one disease eating this sort of margarine was supposed to reduce!
You may be interested in a list of the ingredients that may be present in butter and margarine:
Butter:
Milk fat (cream), a little salt Margarine: Edible oils, edible fats, salt or potassium chloride, ascorbyl palmitate, butylated hydroxyanisole, phospholipids, tert-butylhydroquinone, mono- and di-glycerides of fat-forming fatty acids, disodium guanylate, diacetyltartaric and fatty acid esters of glycerol, Propyl, octyl or dodecyl gallate (or mixtures thereof), tocopherols, propylene glycol mono- and di-esters, sucrose esters of fatty acids, curcumin, annatto extracts, tartaric acid, 3,5,trimethylhexanal, ß-apo-carotenoic acid methyl or ethyl ester, skim milk powder, xanthophylls, canthaxanthin, vitamins A and D.
Dietary fat patterns The total amount of fats in our diet today, according to the MAFF National Food Survey, is almost the same as it was at the beginning of this century.
What has changed, to some extent, is the types of fats eaten.
At the turn of the century we ate mainly animal fats that are largely saturated and monounsaturated.
Now we are tending to eat more polyunsaturated fats - it's what we are advised to do.
It is interesting to compare the growth of heart disease in this country with intakes of different fats.
The birth of CHD in Britain together with the intake of animal fat since the beginning of the century.
If we plot CHD together with intakes of margarines and vegetable shortenings, we find a different story.
Margarine use began around the turn of the century.
Butter was expensive.
The poor bought margarine as a substitute for butter and sales were brisk.
The rapid rise in margarine consumption was followed a couple of decades later by that dramatic rise in heart disease deaths.
If there is a causal relationship between fat intake and heart disease, it suggest's to me that it is the margarines that are the more likely candidates for suspicion.
They had cut saturated fats down to only eight percent of calorie intake daily, yet in the UK section there were more deaths in the intervention group than in the control group.
The North Karelia Project North Karelia, which had Finland's highest rates of heart disease, was compared with neighbouring Kuopio in The North Karelia Project.
In North Karelia, risk factors were cut by seventeen percent over the period of the study.
In North Karelia there was a reduction in both CHD mortality and total mortality.
However, that in Kuopio, the control group, where there were no restrictions, there was an even bigger decline in both CHD and total mortality.
This suggest that adopting a 'healthy' lifestyle may actually have inhibited the decline in heart disease.
They certainly give it no support.
This paper does not allow me to go through the more minor studies but they all show little convincing correlation between either the amount of fat eaten and heart disease or the type of fat eaten and heart disease.
A review of twenty-six studies published in 1992 concluded that:
"Lowering serum cholesterol concentrations does not reduce mortality and is unlikely to prevent coronary heart disease.
Claims of the opposite are based on preferential citation of supportive trials.
" One that seemed to support the 'healthy' recommendations was a Finnish trial published in 1975.
In the five years that the trial ran, cholesterol levels were lowered significantly, and the study was hailed as a success.
But in December 1991 the results of a 10-year follow-up to that trial found that those people who continued to follow the carefully controlled, cholesterol-lowering diet were twice as likely to die of heart disease as those who didn't.
"Some Success"!!!
Professor Michael Oliver, writing in the British Medical Journal commenting on the results, writes.
"As multiple intervention against risk factors for coronary heart disease in middle aged men at only moderate risk seem to have failed to reduce both morbidity and mortality, such interventions become increasingly difficult to justify".
This runs counter to the recommendations of many national and international advisory bodies which must now take the recent findings from Finland into consideration.
Not to do so may be ethically unacceptable
" Despite this wealth of evidence, nutritionists and the media continue to mislead us.
They tell us, for example, that the recent fall in the numbers of heart deaths in the USA is because Americans are eating less fat.
However, while CHD in the USA peaked in the 1950s and has fallen consistently since, this is against a background of rising fat intake.
I find difficulty understanding how the fat hypothesis gained such credibility in the USA as its history more than most does not support it.
The North American continent had been opened up by explorers and trappers who lived, very healthily, as did the Amerindians, almost entirely on fresh meat and pemmican.
As real pemmican is half dried lean meat and half rendered animal fat, and as fat has over twice the calorific value of protein, more than seventy percent of the energy in their diet came from fat.
Dieticians also say that the British had less CHD in the 1940s when fat was rationed.
However, the decade of rationing went on into the early 1950s with fat being the last food to come off ration in 1954.
Again the most rapid rise in CHD occurred during that period.
Also, during the period of rationing, British farmers had a very low incidence of heart disease when one would have expected their intake of fats, particularly animal fats, to have been higher than most.
Experience in other countries Keys based his fat-causes-heart disease hypothesis on a comparison between countries.
When we are told that we are 'the sick man of Europe', we are also compared to other countries.
So let me do a similar comparison.
In Japan, intakes of animal fat have more than doubled since the end of the Second World War.
Over the same period their incidence of coronary heart disease has fallen consistently.
In Israel too an increased consumption of saturated fats was followed by a fall in coronary deaths.
The dietary changes in Sweden parallel those in the USA, yet heart disease mortality in Sweden was rising while American rates were falling.
There is also a threefold variation in rates of heart disease between France and Finland even though fat intake in those two countries is very similar.
Among south Asians in Britain there is an unusually high incidence of heart disease, yet living on largely vegetarian diets, they have low levels of blood cholesterol and eat diets that are low in saturated fat.
Indians in South Africa have probably the highest rates of coronary disease in the world yet there is no apparent reason why they should, based on the current dietary hypotheses.
Until recently, Indians in India had a very low incidence of heart disease while using ghee (clarified butter) and coconut oil, which are highly saturated, and mustard seed oil which is largely monounsaturated.
The epidemic of heart disease in India began only after these were replaced with peanut, safflower, sunflower, sesame and soybean oils, all of which are high in polyunsaturated oils.
Lastly, the World Health Organisation is apparently in ignorance of epidemiological data that do not support its recommendation to reduce dietary saturated fat.
While it talks of coronary heart disease being responsible for most deaths in Caribbean countries, fat intake there is remarkably low.
Polyunsaturated fats The arguments for the polyunsaturated fat hypothesis are no more convincing than those for the cholesterol theory.
The claim is that unsaturated fats have a protective or preventative effect on CHD.
But in Israel, when consumption of polyunsaturated fats was about twice that of most Western countries, there was a very high incidence of CHD.
Those given high polyunsaturated diets in a trial in New South Wales fared significantly worse than those on a free diet.
And this is the finding in most trials that have increased the ratio of polyunsaturated fats.
From as early as 1971, an excess of cancer deaths has been reported in trials using diets that were high in polyunsaturated fats.
Polyunsaturated fats are also blamed for a doubling in the incidence of gallstones in the general public.
One of the pioneers of the polyunsaturated-fat-prevents-CHD hypothesis was the American cardiologist E. H. Ahrens Jr.
After twenty-five years of further research, however, he concluded that it was "irresponsible" to continue to press the polyunsaturated fat recommendations on the general public.
He went on:
"If the public's diet is going to be decided by popularity polls and with diminishing regard for the scientific evidence, I fear that future generations will be left in ignorance of the real merits, as well as the possible faults in any dietary regimen aimed at prevention of coronary heart disease.
" Another of the original proponents of the low-fat, low-cholesterol hypothesis, and a member of the Norwegian Council for Diseases of the Heart and Arteries, Professor Jens Dedichen of Oslo, also changed his mind.
In the 1950s Norway launched a cholesterol-lowering regimen in which soy margarine, that is high in polyunsaturated fatty acids, replaced butter, and soy oil was used extensively.
During the subsequent 20 years the increase in the use of soy-based products was accompanied by a steep and continuing rise in deaths from coronary thrombosis.
Professor Dedichen drew attention to the failure of the programme - and received a very hostile reaction from his colleagues.
Also castigated were members of the National Academy of Sciences and the National Research Council of America when in a report of May 1980, they stated that prevention of heart disease could not be achieved by reducing blood cholesterol using either diet or drugs, and said that such measures should be abandoned.
Margarine - a natural food?
The polyunsaturated fats used to make margarine are generally obtained from vegetable sources such as sunflower seed, cottonseed, and soybean.
As such they might be thought of as natural foods.
Usually, however, they are pressed on the public in the form of highly processed margarines, spreads and oils and, as such, they are anything but natural.
In 1989, the petroleum-based solvent, benzene, that is known to cause cancer, was found in Perrier mineral water at a mean concentration of fourteen parts per billion.
This was enough to cause Perrier to be removed from supermarket shelves.
The first process in the manufacture of margarine is the extraction of the oils from the seeds, and this is usually done using similar petroleum-based solvents.
Although these are then boiled off, this stage of the process still leaves about ten parts per million of the solvents in the product.
That is 700 times as much as fourteen parts per billion.
The oils then go through more than ten other processes:
Degumming, bleaching, hydrogenation, neutralization, fractionation, deodorisation, emulsification, interesterification, that include heat treatment at 140 o -160 o with a solution of caustic soda.
The use of nickel, a metal that is known to cause cancer, as a catalyst, with up to fifty parts per million of the nickel left in the product.
The addition of antioxidants such as butylated hydroxyanisol (E320).
These antioxidants are again usually petroleum based and are widely believed to cause cancer.
The hydrogenation process, that solidifies the oils so that they are spreadable, produces trans -fatty acids that rarely occur in nature.
The heat treatment alone is enough to render these margarines nutritionally inadequate.
When the massive chemical treatment and unnatural fats are added, the end product can hardly be called either natural or healthy.
Recent United States studies showed that heart disease worsened in those who switched from butter to polyunsaturate-rich margarine.
Research published in March 1993, confirmed this.
In a study that involved 85,000 nurses, women who ate just four teaspoons of polyunsaturated margarine a day had a sixty-six percent increased risk of CHD compared to those who ate none.
A review of men's experience in the Framingham Study published in 1995 also found that 6 teaspoons a day (mean of lowest intake vs mean of highest), increased risk by nearly a third.
The authors conclude:
"Intake of margarine may predispose to development of CHD in men".
And CHD is the one disease eating this sort of margarine was supposed to reduce!
You may be interested in a list of the ingredients that may be present in butter and margarine:
Butter:
Milk fat (cream), a little salt Margarine: Edible oils, edible fats, salt or potassium chloride, ascorbyl palmitate, butylated hydroxyanisole, phospholipids, tert-butylhydroquinone, mono- and di-glycerides of fat-forming fatty acids, disodium guanylate, diacetyltartaric and fatty acid esters of glycerol, Propyl, octyl or dodecyl gallate (or mixtures thereof), tocopherols, propylene glycol mono- and di-esters, sucrose esters of fatty acids, curcumin, annatto extracts, tartaric acid, 3,5,trimethylhexanal, ß-apo-carotenoic acid methyl or ethyl ester, skim milk powder, xanthophylls, canthaxanthin, vitamins A and D.
Dietary fat patterns The total amount of fats in our diet today, according to the MAFF National Food Survey, is almost the same as it was at the beginning of this century.
What has changed, to some extent, is the types of fats eaten.
At the turn of the century we ate mainly animal fats that are largely saturated and monounsaturated.
Now we are tending to eat more polyunsaturated fats - it's what we are advised to do.
It is interesting to compare the growth of heart disease in this country with intakes of different fats.
The birth of CHD in Britain together with the intake of animal fat since the beginning of the century.
If we plot CHD together with intakes of margarines and vegetable shortenings, we find a different story.
Margarine use began around the turn of the century.
Butter was expensive.
The poor bought margarine as a substitute for butter and sales were brisk.
The rapid rise in margarine consumption was followed a couple of decades later by that dramatic rise in heart disease deaths.
If there is a causal relationship between fat intake and heart disease, it suggest's to me that it is the margarines that are the more likely candidates for suspicion.
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