To Hell With Cholesterol.

ToHellWithCholesterol 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 many observations that conflict with the LDL [high LDL cholesterol causes atherosclerosis]…hypothesis, may be explained by the idea that high serum cholesterol and/or high LDL is protective against infection and atherosclerosis.”

“We have demonstrated a relationship between higher levels of cholesterol and increased survival in patients with CHF…Reducing cholesterol may be deleterious in CHF…”

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.

“Hypothyroidism leads to an increase of plasma low-density lipoprotein (LDL) cholesterol levels. Oxidation of LDL particles changes their intrinsic properties, thereby enhancing the development of atherosclerosis…”

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.

“MDA-modified LDL estimation has a diagnostic accuracy and may be used as an independent biochemical marker for atherosclerosis.”

“…circulating MDA-LDL level is increased in CAD [coronary artery disease], independent of the serum LDL cholesterol level…The measurement of serum MDA-LDL level may be useful for the identification of patients with advanced atherosclerosis.”

“Our study shows increased serum concentrations of MDA-LDL in patients with CAD. MDA-LDL is an independent risk factor of CAD as there was no association with other risk factors such as hypertension, hyperlipidaemia, smoking habit, or sex.”

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.

“…findings imply a direct influence of dietary polyunsaturated fatty acids on aortic plaque formation and suggest that current trends favouring increased intake of polyunsaturated fatty acids should be reconsidered.”

“…products of…linoleic acid and arachidonic acid oxidation in human atherosclerotic plaque…lipid peroxidation products in plaque may be important given the potential biological activity of these compounds and their possible relationship to plaque pathogenesis and instability.”

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.

“Recent data on the processes underlying atherogenesis indicate the significant role of endotoxin (lipopolysaccharide – LPS) of the intestinal microflora in the development of vascular lesions.”

“…the degree of circulating endotoxemia was related to the severity of systemic inflammation and features of atherosclerosis….result suggests that endotoxemia may contribute to the systemic inflammatory state and accelerated atherosclerosis…”

“Human trials have indicated that bacterial decontamination of the gut with concomitant decrease in lipopolysaccharide (LPS) has a positive outcome on heart disease patients.”

“…excess of bacterial lipopolysaccharides (endotoxin aggression) is observed in the general blood circulation of volunteers with the presence of atherosclerotic risk factors (obesity, diabetes, stress, pathology of haemostasis, kidney, intestines, etc.)”

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.

“In a study of critically ill trauma patients, mean cholesterol levels were significantly lower than expected values. In patients who died, final cholesterol levels fell by 33% versus a 28% increase in survivors…Because lipoproteins can bind and neutralize lipopolysaccharide [endotoxin], hypocholesterolemia can negatively impact outcome.”

“Lipoproteins would contribute to a reduction of LPS bioactivity and consequently lead to lower levels of inflammatory cytokines.”

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.

“…the increase in bacteria/bacterial toxin translocation arising from a more permeable intestinal wall causes a low-grade inflammatory state…”

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.

“The cardiovascular risk in patients with hypothyroidism is related to an increased risk of functional cardiovascular abnormalities and to an increased risk of atherosclerosis. The pattern of cardiovascular abnormalities is similar in subclinical and overt hypothyroidism, suggesting that a lesser degree of thyroid hormone deficiency may also affect the cardiovascular system.”

“Hypothyroidism is a commonly encountered clinical condition with variable prevalence. It has profound effects on cardiac function that can impact cardiac contractility, vascular resistance, blood pressure, and heart rhythm.”

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.

“…our findings support the hypothesis that hypercholesterolemia is a compensatory mechanism for life-cycle related down-regulation of steroid hormones…”

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…”

“These data suggest that serotonin plays a major role in the pathogenesis of the cardiac plaque formation observed in carcinoid patients.”

“…stimulation of inducible nitric oxide synthase (iNOS) and NO overproduction causes metabolic insulin resistance and characterises atherosclerosis, heart failure and cardiogenic shock in humans…”

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

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Hypothyroidism and the Heart

Human Monocytes Engage an Alternative Inflammasome Pathway

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Serotonin Mechanisms in Heart Valve Disease I

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High cholesterol may protect against infections and atherosclerosis

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HDL, lipid peroxidation, and atherosclerosis1

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Endotoxemia is Related to Systemic Inflammation and Atherosclerosis in Peritoneal Dialysis Patients

Changes in oxidized low-density lipoprotein cholesterol are associated with changes in handgrip strength in Japanese community-dwelling persons.

The risk of acute suicidality in psychiatric inpatients increases with low plasma cholesterol.

Immunopathogenesis of atherosclerosis: endotoxin accelerates atherosclerosis in rabbits on hypercholesterolemic diet.

Circulating malondialdehyde modified LDL is a biochemical risk marker for coronary artery disease

Nitric Oxide Measurements during Endotoxemia

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The Colorado thyroid disease prevalence study.

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Rare variant in scavenger receptor BI raises HDL cholesterol and increases risk of coronary heart disease

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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Glycemic control, oxidative stress, and lipid profile in children with type 1 diabetes mellitus.

Non-enterobacterial endotoxins stimulate human coronary artery but not venous endothelial cell activation via Toll-like receptor 2

Cardiac function and circulating cytokines after endotoxin exposure in neonatal mice.

Is low total cholesterol levels associated with suicide attempt in depressive patients?

Extreme high high-density lipoprotein cholesterol is paradoxically associated with high mortality in men and women: two prospective cohort studies

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High cholesterol diet supplemented with sunflower seed oil but not olive oil stimulates lipid peroxidation in plasma, liver, and aorta of rats

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The effect of endotoxin on the controllability of cardiac rhythm in rats.

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Suicidal behaviour and lipid levels in unipolar and bipolar depression

Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms.

High Level of Endotoxemia Following Out-of-Hospital Cardiac Arrest Is Associated With Severity and Duration of Postcardiac Arrest Shock.

Deposition and hydrolysis of serine dipeptide lipids of Bacteroidetes bacteria in human arteries: relationship to atherosclerosis

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Metabolic endotoxemia: a molecular link between obesity and cardiovascular risk.

Serum levels of remnant lipoprotein cholesterol and oxidized low-density lipoprotein in patients with coronary artery disease.

Increased atherogenic low-density lipoprotein cholesterol in untreated subclinical hypothyroidism.

LDL in patients with subclinical hypothyroidism shows increased lipid peroxidation

Oxidised LDL/LDL-cholesterol ratio and coronary artery calcification in haemodialysis patients.

Serum lipid levels in relation to serum thyroid-stimulating hormone and the effect of thyroxine treatment on serum lipid levels in subjects with subclinical hypothyroidism: the Tromsø Study.

Dietary lipid emulsions and endotoxemia

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The effect of L-thyroxine replacement therapy on lipid based cardiovascular risk in subclinical hypothyroidism.

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TSH-controlled L-thyroxine therapy reduces cholesterol levels and clinical symptoms in subclinical hypothyroidism: a double blind, placebo-controlled trial (Basel Thyroid Study).

Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73)

Regulation effect of Aspirin Eugenol Ester on blood lipids in Wistar rats with hyperlipidemia

The correlation between markers of oxidative stress and risk factors of coronary artery disease in Thai patients.

Elevated serum lipoprotein(a) in subclinical hypothyroidism.

Hypocholesterolemia in sepsis and critically ill or injured patients

Positive correlation between malondialdehyde-modified low-density lipoprotein cholesterol and vascular inflammation evaluated by 18F-FDG PET/CT

Serum levels of remnant lipoprotein cholesterol and oxidized low-density lipoprotein in patients with coronary artery disease

Oxidative stress influences cholesterol efflux in THP-1 macrophages: Role of ATP-binding cassette A1 and nuclear factors

The Nitric Oxide Theory of Aging Revisited

Hypothyroidism as a risk factor for cardiovascular disease.

Endotoxin theory of atherosclerosis.

Orange juice neutralizes the proinflammatory effect of a high-fat, high-carbohydrate meal and prevents endotoxin increase and Toll-like receptor expression.

Associations of egg and cholesterol intakes with carotid intima-media thickness and risk of incident coronary artery disease according to apolipoprotein E phenotype in men: the Kuopio Ischaemic Heart Disease Risk Factor Study

#cholesterolprotects
#sugarfeedsthyroid
#sugarsaves
#raypeat

Image: “A recent Milk and Cheese pin-up where they do what they do.” by Evan Dorkin

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