To Hell With Cholesterol.
Explanations and interpretations regarding blood cholesterol levels and their significance in relation to metabolic health, can be extremely confusing and misleading, and the part played by sugar in relation to this, is very often misrepresented and misunderstood.
It is far from unusual to hear it said that sugar causes ‘high cholesterol’, and the implication here is that sugar is bad because high cholesterol it is then claimed, causes disease.
Unfortunately that is only partly correct, and most likely not the part many are imagining.
The physiological importance of cholesterol is not in dispute, however the relationship between ‘high cholesterol’ and disease outcomes is not anywhere near as black and white as is made out to be the case.
Cholesterol is one of the building blocks – in combination with thyroid hormone and vitamin A – for many important and highly protective substances including pregnenolone, progesterone, dhea, and testosterone. The production of cholesterol is fundamental to the maintenance of optimal health.
Cholesterol is a precursor to bile – as well as vitamin D – and many studies have shown that it plays an important role in the protection against infection, numerous kinds of toxins as well as radiation damage. It is also generally anti-inflammatory and plays a role in the prevention of oxidative damage. Cholesterol production tends to rise in response to stress.
It’s true that fruit sugar – or sucrose – helps to promote the production of cholesterol when more is needed for protection against stress of any kind. But it is also true that sugar helps to increase the rate at which cholesterol is converted into the protective substances (such as pregnenolone) mentioned above.
A healthy thyroid metabolism is a central factor enabling cholesterol to carry out many of its more specialized, highly protective anti-aging functions. Sugar consumption supports thyroid activity and energy metabolism in general.
Thus sugar helps to encourage the efficient use of cholesterol and as a result, helps to lower levels detectable in the blood.
When thyroid and energy metabolism is suppressed – on the other hand – as a result of stress and aging, blood cholesterol levels often increase.
High cholesterol levels have been demonstrated in a number of studies – especially in aging populations – to protect against mortality from all causes (but particularly from cancer). This makes a lot of sense because cancer (and disease in general) has been demonstrated to be fueled by stress and inflammation, and cholesterol is one of the basic anti-stress anti-inflammatory materials.
There are studies which suggest that high cholesterol can also be protective against heart disease.
The polyunsaturated fats (PUFAs) – which are (more and more today) released into the blood under conditions of stress or insufficient sugar – interfere with the production of cholesterol, with thyroid function generally, and with cholesterol turnover.
When metabolism is suppressed and cholesterol turnover is slowed (allowing for it to be exposed to greater amounts of polyunsaturated free fatty acids) it can more easily be degraded and damaged, thereby reducing its protective capability.
Under such circumstances high cholesterol can be seen as something which is, in and of itself, potentially problematic. Experimental evidence suggests however, that in the absence of the polyunsaturated fats (and other related promoters of oxidative damage) this is less likely to be the case.
The PUFA breakdown products interact with cholesterol in such a way as to make the modification of cholesterol a fairly accurate measure of the progression and severity of atherosclerosis. This is quite possibly a major reason for confusion regarding cholesterol and cardiovascular health and disease.
Apart from possibly causing the formation of plaque, the inflammatory PUFA breakdown products found in human atherosclerotic plaque, may be responsible for what makes formation more dangerous.
The metabolically suppressive impact of stress (and exposure to PUFA) encourages bacterial issues and a subsequent increase in circulating levels of bacterial endotoxin (LPS). Endotoxin is highly inflammatory and rising levels in the blood are increasingly being understood to be a significant factor promoting inflammatory disease, including cardiovascular disease.
Interference with the production of cholesterol in the liver – as a result of cholesterol lowering drugs or exposure to the polyunsaturated fats and endotoxin – can lead to a situation where cholesterol production is too low. Low cholesterol has been shown to be directly connected to increased mortality from many causes including cancer, suicide, infection and heart failure.
PUFA and exdotoxin have each been shown to promote inflammatory conditions independently, however there is evidence suggesting that in combination they have a synergistically inflammatory and thyroid impeding impact.
Cholesterol is also known to play an important role in the neutralization of bacterial endotoxin, and so it is easy to see why a low cholesterol, high stress, low thyroid state with lots of exposure to PUFA and other inflammatory substances can be so dangerous.
Sugar consumption, seen from this perspective, can more easily be understood to be protective, both by its ability to assist with increasing as well as decreasing blood cholesterol levels.
Sufficient sugar availability, by promoting thyroid energy metabolism (and subsequnetly improving intestinal barrier function), can also be seen as an important element in the protection against the inflammatory effects of too much endotoxin making its way into the main system.
Interference with the production of cholesterol (rather than healthy turnover of cholesterol) – or greater exposure of cholesterol to factors which promote its degradation – is what can more obviously be viewed as harmful. Context is very important.
I’m not a doctor or a nutritionist. I don’t get paid to be a scientist, and I’m not telling you what to do. In fact, I don’t think you should take what I say on face value. Have a look through the science. Read though it, and search for more. Look for opposing views and see if they have a valid argument. They often don’t have an argument at all, just a conclusion.
I believe it is physiologically rational to suggest that sugar consumption is helpful and very important. For one thing it helps to encourage sufficient production of cholesterol, and this is necessary for the proper functioning of the organism. It’s necessary for protection against stress and disease in general.
Sugar fuels thyroid energy metabolism and this is central to protection against stress and disease in many different ways. An under performing thyroid metabolism has been shown to be involved in the progression of cardiovascular issues.
Also related to thyroid function is the fact that sugar plays an important part in ensuring optimal (or improved) conversion of cholesterol into the highly protective anti-aging substances which defend against the effects of stress and promote metabolic health.
Maintaining glycogen stores so as to provide a stable supply of blood sugar, helps to limit the release of PUFA into the blood (and limit stress hormone release), and based on the findings of many studies and experiments, this may end up being fundamental to protection against heart disease.
The fact that high cortisol has been shown to be an accurate predictor of death from cardiovascular disease, should be enough information to make people, at least question the anti-sugar rhetoric.
Cardiovascular disease has also been shown to be connected to rising levels of estrogen and serotonin and nitric oxide, and there is plenty of good quality evidence which shows that these substances rise in response to stress and inflammation and a suppressed thyroid energy system. Sugar can be seen as protective here, and PUFA is a powerful promoter of chronic inflammation and the stress substances.
“The mean serum estradiol level was significantly higher in the subjects with coronary disease…”
It has been argued that estrogen protects women from heart disease, partly because it is common to believe that menopause is a low estrogen state, and because women are far more susceptible to heart disease post menopause. Biological evidence shows, however, that menopause is actually a state driven by estrogen dominance. Unfortunately estrogen blood tests do not necessarily accurately reflect estrogen levels, and so it is easy to be mislead.
Any discussion relating to ideal cholesterol levels is likely to be far more diagnostically relevant after consideration of the particular history and circumstances of the individual, taking into account numerous other informative measures of stress and metabolic function.
In light of biological understanding and experimental evidence in relation to heart disease, it makes sense to see rising cholesterol as part of a physiologically defensive and protective process responding to metabolic stress, rather than the cause of the problem. That doesn’t mean that high cholesterol is never intertwined in the disease process, but there seems to be little justification for popular cholesterol lowering methodologies.
Promoting the use of PUFA ingestion as ‘heart healthy’ because it lowers blood cholesterol levels, is beyond irresponsible once you consider the available science.
A diet restricting PUFAs and providing sufficient protein – from milk, cheese and gelatin – as well as plenty of sugar – from sweet ripe juicy fruits, fruit juice, white sugar and honey – is one rational approach encouraging healthy production of cholesterol, and promoting the conversion of cholesterol into the specialized, protective substances which help to fight stress and prevent degeneration and disease.
Some other things which might be protective against the damaging effects of stress and inflammation include things that promote thyroid metabolism and reduce levels of estrogen, serotonin, cortisol, nitric oxide and other stress substances. Things like aspirin, cyproheptadine, thyroid hormone, pregnenolone, progesterone, methylene blue, certain antibiotics, glycine and a number of other things mentioned in my other articles, have been shown to be effective.
It’s easy to blame cholesterol for disease when you see it hanging around, especially if you never ask why it’s high. And if you ignore how it rises under stress. And if you ignore the benefits of it being high. And if you ignore what happens when stress is high and cholesterol is low. And if you ignore hypothyroidism and free fatty acids, and chronic inflammation, and the impact of rising levels of the substances of stress. Basically, if you ignore the things that cause stress and inflammation in the first place.
See more here
Hypercholesterolemia treatment: a new hypothesis or just an accident?
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Cardiovascular risk factors in patients with subclinical hypothyroidism.
Risk factors for cardiovascular disease in women with subclinical hypothyroidism.
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Hypothyroidism in coronary heart disease and its relation to selected risk factors
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Human Monocytes Engage an Alternative Inflammasome Pathway
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Low Serum Cholesterol Level and Increased Ischemic Stroke Mortality
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Is low cholesterol a risk factor for cancer mortality?
Serotonin Mechanisms in Heart Valve Disease I
High cholesterol may protect against infections and atherosclerosis
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Stress Induces Endotoxemia and Low-Grade Inflammation by Increasing Barrier Permeability
HDL, lipid peroxidation, and atherosclerosis1
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Urinary Cortisol and Six-Year Risk of All-Cause and Cardiovascular Mortality
Endotoxemia is Related to Systemic Inflammation and Atherosclerosis in Peritoneal Dialysis Patients
The risk of acute suicidality in psychiatric inpatients increases with low plasma cholesterol.
Circulating malondialdehyde modified LDL is a biochemical risk marker for coronary artery disease
Nitric Oxide Measurements during Endotoxemia
Systemic inflammation in heart failure–the whys and wherefores.
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Low plasma cholesterol predicts an increased risk of lung cancer in elderly women.
Lipid peroxidation, antioxidants and cardiovascular disease: how should we move forward?
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Is low total cholesterol levels associated with suicide attempt in depressive patients?
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LDL in patients with subclinical hypothyroidism shows increased lipid peroxidation
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Dietary lipid emulsions and endotoxemia
Chronic stress in mice remodels lymph vasculature to promote tumour cell dissemination
Regulation effect of Aspirin Eugenol Ester on blood lipids in Wistar rats with hyperlipidemia
Elevated serum lipoprotein(a) in subclinical hypothyroidism.
Hypocholesterolemia in sepsis and critically ill or injured patients
The Nitric Oxide Theory of Aging Revisited
Hypothyroidism as a risk factor for cardiovascular disease.
Endotoxin theory of atherosclerosis.
#cholesterolprotects
#sugarfeedsthyroid
#sugarsaves
#raypeat
Image: “A recent Milk and Cheese pin-up where they do what they do.” by Evan Dorkin