Diagnosis Diet - Cholesterol - Georgia Ede
"Poor cholesterol—so misunderstood. All animal cells require cholesterol for proper structure and function. The vast majority of cholesterol in the body does not come directly from foods like eggs and meat, but from the liver, which can make cholesterol out of anything we eat. So, if cholesterol-rich foods don’t cause high cholesterol, what does?"
A very good primer about what cholesterol is and how it works - by Dr. Georgia Ede from Diagnosis Diet
"Poor cholesterol—so misunderstood. All animal cells require cholesterol for proper structure and function. The vast majority of cholesterol in the body does not come directly from foods like eggs and meat, but from the liver, which can make cholesterol out of anything we eat. So, if cholesterol-rich foods don’t cause high cholesterol, what does?"
A very good primer about what cholesterol is and how it works - by Dr. Georgia Ede from Diagnosis Diet
Assessing cardiovascular disease: looking beyond cholesterol - Kendrick, Malcolm - August 18, 2022
"We now have a greater understanding of the endothelial/glycocalyx function and how endothelial damage links to thrombus formation and lysis, and these new findings strongly suggest that Rokitansky, Duguid, Ross and Elspeth Smith, and others, may well have been correct.
Thus, whilst this article is entitled “Assessing cardiovascular disease: looking beyond cholesterol”, it may have been more accurate to call it, ‘Assessing cardiovascular disease, looking before cholesterol’, because the thrombogenic hypothesis precedes the cholesterol hypothesis by many years. It is fascinating that recent research now provides an increasing evidence base."
"We now have a greater understanding of the endothelial/glycocalyx function and how endothelial damage links to thrombus formation and lysis, and these new findings strongly suggest that Rokitansky, Duguid, Ross and Elspeth Smith, and others, may well have been correct.
Thus, whilst this article is entitled “Assessing cardiovascular disease: looking beyond cholesterol”, it may have been more accurate to call it, ‘Assessing cardiovascular disease, looking before cholesterol’, because the thrombogenic hypothesis precedes the cholesterol hypothesis by many years. It is fascinating that recent research now provides an increasing evidence base."
What We Know About Cholesterol
Cholesterol goes up heart disease goes down - Malcolm Kendrick
"It is also exceedingly difficult for mainstream researchers to attack this current data, as the Japanese were once held up as poster boys for the cholesterol hypothesis. ‘Look at the Japanese’the researchers shouted loudly in the 1960s. ‘Very low cholesterol levels and very low rates of heart disease… case proven.’ In fact, the Japanese data were one of the strongest drivers of the cholesterol hypothesis. It is entirely possible that, without the Japanese data, the cholesterol hypothesis would never have been accepted in the first place."
"It is also exceedingly difficult for mainstream researchers to attack this current data, as the Japanese were once held up as poster boys for the cholesterol hypothesis. ‘Look at the Japanese’the researchers shouted loudly in the 1960s. ‘Very low cholesterol levels and very low rates of heart disease… case proven.’ In fact, the Japanese data were one of the strongest drivers of the cholesterol hypothesis. It is entirely possible that, without the Japanese data, the cholesterol hypothesis would never have been accepted in the first place."
Is Cholesterol Bad? Cholesterol Explained in 500 Words
Cholesterol is a healing agent in the body. Cholesterol levels rise during stress and when it is needed to aid a healing process. The body sends cholesterol from the liver to damaged tissue for repair. When the cholesterol is no longer required for tissue repair, it returns to the liver.
Cholesterol travels to the artery to repair inflamed tissue, but it does not block the artery. If the inflammation is not addressed, then polyunsaturated fats and plaque form an arterial block. Inflammation, not cholesterol, causes heart disease.
Overwhelming research shows that consuming cholesterol-rich saturated fats (1 2) does not cause heart disease. Interestingly, low cholesterol levels are:
Because [LDL] cholesterol travels from the liver to the wound in the form of LDL, our “science,” in its wisdom calls LDL “bad” cholesterol. When the wound heals and the cholesterol is removed, it travels back to the liver in the form of HDL cholesterol (high-density lipoprotein cholesterol). Because this cholesterol travels away from the artery back to the liver, our misguided “science” calls it “good” cholesterol. This is like calling an ambulance traveling from the hospital to the patient a “bad ambulance,” and the one traveling from the patient back to the hospital a “good ambulance.”
LDL cholesterol is not created equal. Dense, small, heavy LDL particles are correlated to an increased risk of heart disease. Large fluffy LDL particles are not. Consuming cholesterol-rich foods like eggs and butter raises the ratio of benign fluffy LDL particles to dense LDL. For about 2/3 of the population, cholesterol-rich eggs are shown to have no effect on blood cholesterol levels. For the other 1/3, it raises cholesterol levels – by raising the benign HDL and the particle size of LDL (11, 12).
Some foods like canola oil, touted by the American Heart Association as cholesterol-reducing, actually worsen the cholesterol profile. These foods reduce the beneficial fluffy LDL and the healthful HDL cholesterol (13). Vegetable oils also create dangerous oxidized LDL, which can build up in the arteries (14).
Cholesterol-rich saturated fats are nutrient-dense and a foundational component of a healthy diet. Saturated fat raises HDL cholesterol, which is associated with a reduced risk of heart disease. Saturated fat is correlated to a mild increase in the benign, fluffy LDL (15, 16). Research shows that saturated fat intake from old-fashioned fats like butter are beneficial, not dangerous, to heart health.
There is no correlation between dietary saturated fat intake and heart disease (17). Cholesterol is a nutrient required for health. Unprocessed, whole-food sources of cholesterol, including butter, egg yolks, and seafood are time-honored foods that have nourished humanity for millennia.
Cholesterol is a healing agent in the body. Cholesterol levels rise during stress and when it is needed to aid a healing process. The body sends cholesterol from the liver to damaged tissue for repair. When the cholesterol is no longer required for tissue repair, it returns to the liver.
Cholesterol travels to the artery to repair inflamed tissue, but it does not block the artery. If the inflammation is not addressed, then polyunsaturated fats and plaque form an arterial block. Inflammation, not cholesterol, causes heart disease.
Overwhelming research shows that consuming cholesterol-rich saturated fats (1 2) does not cause heart disease. Interestingly, low cholesterol levels are:
- correlated with a higher risk of cancer (1)
- correlated with criminal acts of violence and suicide (2, 3)
- correlated with a higher risk of mortality (4, 5. 6)
- correlated with a higher risk of dementia and Alzheimer’s disease (7, 8)
- correlated with a higher risk of depression (9, 10)
Because [LDL] cholesterol travels from the liver to the wound in the form of LDL, our “science,” in its wisdom calls LDL “bad” cholesterol. When the wound heals and the cholesterol is removed, it travels back to the liver in the form of HDL cholesterol (high-density lipoprotein cholesterol). Because this cholesterol travels away from the artery back to the liver, our misguided “science” calls it “good” cholesterol. This is like calling an ambulance traveling from the hospital to the patient a “bad ambulance,” and the one traveling from the patient back to the hospital a “good ambulance.”
LDL cholesterol is not created equal. Dense, small, heavy LDL particles are correlated to an increased risk of heart disease. Large fluffy LDL particles are not. Consuming cholesterol-rich foods like eggs and butter raises the ratio of benign fluffy LDL particles to dense LDL. For about 2/3 of the population, cholesterol-rich eggs are shown to have no effect on blood cholesterol levels. For the other 1/3, it raises cholesterol levels – by raising the benign HDL and the particle size of LDL (11, 12).
Some foods like canola oil, touted by the American Heart Association as cholesterol-reducing, actually worsen the cholesterol profile. These foods reduce the beneficial fluffy LDL and the healthful HDL cholesterol (13). Vegetable oils also create dangerous oxidized LDL, which can build up in the arteries (14).
Cholesterol-rich saturated fats are nutrient-dense and a foundational component of a healthy diet. Saturated fat raises HDL cholesterol, which is associated with a reduced risk of heart disease. Saturated fat is correlated to a mild increase in the benign, fluffy LDL (15, 16). Research shows that saturated fat intake from old-fashioned fats like butter are beneficial, not dangerous, to heart health.
There is no correlation between dietary saturated fat intake and heart disease (17). Cholesterol is a nutrient required for health. Unprocessed, whole-food sources of cholesterol, including butter, egg yolks, and seafood are time-honored foods that have nourished humanity for millennia.
Dave Feldman's Cholesterol Calculator
for assessing your numbers
for assessing your numbers
The following journal paper has caused much controversy on the Internet.
It is hard to imagine why our body might want to kill itself, but that is what we are expected to believe if we read the following study. Cholesterol is a vital part of our metabolism and the low density lipoproteins have their role in protecting us as do the high density ones.
The important consideration in my mind is what is causing LDL-C to get to a point when it starts to cause harm to our body. Rather than using a drug to artificially restrict our production of cholesterol (which is still vitally required for a host of other functions in our body), we need to look to what is causing it to be high in the first place.
If LDL is what causes heart disease then I would ask "what causes LDL?" When you can find what causes the LDL then I would suggest eliminating that.
In the meantime blaming LDL for heart disease is like blaming fuel for causing the fire.
Speaking of using drugs to lower cholesterol - why don't we take a look at the Conflict Of Interest statement for the writers of this article - it is longer than the Abstract and the Conclusions!
It is hard to imagine why our body might want to kill itself, but that is what we are expected to believe if we read the following study. Cholesterol is a vital part of our metabolism and the low density lipoproteins have their role in protecting us as do the high density ones.
The important consideration in my mind is what is causing LDL-C to get to a point when it starts to cause harm to our body. Rather than using a drug to artificially restrict our production of cholesterol (which is still vitally required for a host of other functions in our body), we need to look to what is causing it to be high in the first place.
If LDL is what causes heart disease then I would ask "what causes LDL?" When you can find what causes the LDL then I would suggest eliminating that.
In the meantime blaming LDL for heart disease is like blaming fuel for causing the fire.
Speaking of using drugs to lower cholesterol - why don't we take a look at the Conflict Of Interest statement for the writers of this article - it is longer than the Abstract and the Conclusions!
Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel
Aims To appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD). Methods and results We assessed whether the association between LDL and ASCVD fulfils the criteria for causality by evaluating the totality of evidence from genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized trials of LDL-lowering therapies. In clinical studies, plasma LDL burden is usually estimated by determination of plasma LDL cholesterol level (LDL-C). Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. Both the naturally randomized genetic studies and the randomized intervention trials consistently demonstrate that any mechanism of lowering plasma LDL particle concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the achieved reduction in LDL-C is concordant with the reduction in LDL particle number and that there are no competing deleterious off-target effects. Conclusion Consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD. |
Here is the counter argument:
LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature
LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature
The idea that high cholesterol levels in the blood are the main cause of CVD is impossible because people with low levels become just as atherosclerotic as people with high levels and their risk of suffering from CVD is the same or higher. The cholesterol hypothesis has been kept alive for decades by reviewers who have used misleading statistics, excluded the results from unsuccessful trials and ignored numerous contradictory observations. |
Ivor Cummins - The Cholesterol Conundrum
Conclusion: Our result indicates that high level of LDL-C is inversely associated with dementia. High level of LDL-C may be considered as a potential protective factor against cognition decline.
LDL-cholesterol is unable to predict future cardiovascular events
Cardiovascular diseases are the leading cause of death worldwide. In 2015, coronary heart disease affected 110 million people and resulted in 8.9 million deaths. Common belief is that coronary heart disease (CHD) patients are at an equally high risk for cardiovascular events such as heart attack. Published in the European Heart Journal, the study showed that LDL-cholesterol was not able to identify those CHD patients who were at the highest risk of cardiovascular death.
Cardiovascular diseases are the leading cause of death worldwide. In 2015, coronary heart disease affected 110 million people and resulted in 8.9 million deaths. Common belief is that coronary heart disease (CHD) patients are at an equally high risk for cardiovascular events such as heart attack. Published in the European Heart Journal, the study showed that LDL-cholesterol was not able to identify those CHD patients who were at the highest risk of cardiovascular death.
Leading Scientists Agree: Current Limits on Saturated Fats No Longer Justified - February 25, 2020
- Numerous recent meta-analyses of both controlled randomized trials and observational studies have found no significant evidence for effects of saturated fat consumption on cardiovascular or total mortality. Furthermore, there is evidence that saturated-fat intake may be associated with a lower risk of experiencing a stroke.
- Recommendations to lower saturated fat consumption have been based primarily on the evidence that this will lower LDL, the type of cholesterol in the blood that has been linked to heart disease risk. However, it is now known that there is more than one type of LDL, and that in the majority of individuals, reducing dietary saturated fat does not lower the type (small dense LDL) that is most strongly associated with heart-disease risk. This may help to explain why lowering saturated fat intake in trials has not been found to reduce cardiovascular mortality.
A Standard Lipid Panel is Insufficient for a Patient on a High Fat, Low Carbohydrate Diet
- Herein, we reported on a subject who adopted a ketogenic diet for ulcerative colitis that successfully put his condition into remission but was also associated with an ostensibly adverse change in his serum lipid profile. A deeper analysis of these lipid profile changes revealed that many parameters might, in fact, be positive. Therefore, rather than recommending the subject abandon the diet that has proved successful in treating his disease, we have recommended a slight nutritional adaptation to see if that optimizes his lipid profile and health.
- The significance of this report is threefold: (i) Although clinical anecdotes reveal that ketogenic diets can improve the symptoms of patients struggling with inflammatory bowel diseases, there is little published data on the topic (possibly owing to the high variability among human microbiomes and, thus, patient responsiveness). This report documents an instance in which a ketogenic diet clearly improved a patient's colitis symptoms and laboratory inflammatory markers. (ii) We herein provide data that strongly suggest, at least in the case of subjects on ketogenic diets, standard lipid panels may not be sufficient, and that analyses of lipid subfractionations may be required, in order to inform optimal clinical recommendations. In closing, (iii) this case represents an example of the positive trend in medicine away from formulaic care and toward holistic, personalized, and integrative care.