Cholesterol vs Blood Sugar in Heart Disease

Is Cholesterol Associated with Heart Disease?

If older people with higher cholesterol live longer, then it seems unlikely that high cholesterol causes heart disease.

Adding to the evidence, or lack of it, regarding cholesterol, the average patient admitted to the hospital with coronary artery disease had:

  • total cholesterol: 174
  • LDL: 105
  • HDL: 40
  • triglycerides: 161

Of these numbers, the total and LDL cholesterol are considered either optimal or nearly so. The HDL and triglycerides are considered abnormal. The number of patients in this study was 136,905, so I think we can say it’s representative.

Further evidence against cholesterol being involved in heart disease comes from Luca Mascitelli and co-authors, who state that “other cholesterol-reducing treatments different from statins have no effect on subsequent coronary mortality.” These other treatments include clofibrate and hormone replacement therapy in women.

The Lyon Diet Heart Study achieved a 70% reduction in mortality in patients with heart disease without lowering cholesterol.

“Furthermore, a dose-response relationship between the degree of cholesterol lowering and clinical outcome has not been demonstrated in statin trials where the dose-response was calculated using individual data.” (Mascitelli et al.)

To summarize so far:

  • The average patient hospitalized for coronary heart disease has normal cholesterol.
  • Cholesterol-lowering treatments other than statins do not reduce mortality.
  • The Lyon study reduced cardiovascular and all-cause death rates dramatically without lowering cholesterol.
  • There’s no correlation between degree of cholesterol lowering and clinical outcomes in individuals.

Still think cholesterol causes heart disease?

Blood Sugar and Heart Disease

Acute coronary syndrome is either a heart attack or unstable angina, and among people hospitalized for it, 57% had abnormal glucose metabolism, based on a simple fasting blood glucose (sugar) test. Of those, 66% had not been diagnosed or treated for diabetes.

Approximately 25-30% of patients with acute coronary syndrome have diabetes. Of the remaining patients, most have a spectrum of abnormal glucose metabolism, including previously undiagnosed impaired fasting glucose and diabetes mellitus. (Source.)

When over 1300 patients with impaired glucose tolerance were treated with the diabetes drug acarbose, risk of major cardiovascular events dropped by over 50%.

Acarbose doesn’t just reduce glucose, it reduces insulin and increases insulin sensitivity.

The rate of fatal coronary heart disease among diabetics is from 2 (in men) to 3 (in women) times higher than in non-diabetics.

Check out the following graph, which I discussed here. It shows the results when a team led by Gerald Reaven divided a group of men into tertiles (thirds) by steady state plasma glucose, a measure of insulin resistance. Those with the highest insulin resistance had the most heart disease (CHD). Those with the best insulin sensitivity (lowest insulin resistance) had zero cases of coronary disease — not to mention cancer, stroke, and the rest.

In the lowest tertile of insulin resistance, no one got sick.

To summarize the relation between blood glucose and heart attacks:

  • Most patients with acute coronary syndrome have abnormal fasting blood glucose
  • Lowering glucose and insulin decreases the risk of major cardiovascular events
  • Diabetics have much higher rates of heart disease
  • Men with insulin resistance have much higher rates of heart disease

Why high blood glucose relates to heart disease

Hyperglycemia — high blood glucose — is a cause of blood vessel disease. When blood glucose gets too high, it causes dysfunction of blood vessel walls (endothelial dysfunction), inflammation, and oxidative stress, eventually leading to plaques.

The old model, that somehow high cholesterol clogs up the arteries like sludge clogs a pipe, makes little sense.

 

PS: A good way to avoid heart disease is to do strength training, as in my book Muscle Up.

PPS: You can support this site by purchasing through my Supplements Buying Guide for Men. No extra cost to you.

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7 comments
Cholesterol vs Blood Sugar in Heart Disease says November 18, 2016

[…] Original Article: Cholesterol vs Blood Sugar in Heart Disease […]

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Joe S says November 18, 2016

Thanks for the amazing website! I try to remember to use your links to amazon whenever I buy supplements.
I have a family history of both diabetes and cancer. Since reading your blog I have been doing 36 hour fasts once a week. It makes me feel rejuvenated!
Also, have you heard/read about Lauricidin? A supplement to boost the immune system. I’m curious about your thoughts!

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    P. D. Mangan says November 18, 2016

    Hi Joe, glad you like this place, thanks for reading and for buying through the supplements page. And it’s also great you feel much better. As to Lauricidin, yes, I know of it, and tried it back when I had chronic fatigue. I couldn’t say much else about it, other than that those particular fatty acids in it do indeed have antiviral and antibacterial action. It’s also very non-toxic. Trial use of it may be helpful for those with mysterious, chronic illnesses.

    Reply
Ted says November 18, 2016

Thank you for the article.
What are your thoughts on Vitamin C (either ascorbic acid or wholefood Vitamin C) and its role in preventing/reversing atherosclerosis? It goes back to Linus Pauling, the supporters claim unlike most animals, humans (and some monkeys) cannot produce/synthesize their own Vitamin C, which repairs arteries. So cholesterol plaque and Lp(a) have evolved as substitutes in order to keep the arteries together in Vitamin C deficiency. In other words atherosclerosis is a mild form of scurvy (when sailors bled to death on ships due to lack of Vit C).
Some studies/websites I found (hope you forgive the long comment):

https://www.ncbi.nlm.nih.gov/pubmed/8821982 – Numerous in vitro studies have demonstrated that ascorbic acid (vitamin C) strongly inhibits LDL oxidation by a variety of mechanisms.

https://www.ncbi.nlm.nih.gov/pubmed/8692035 – We suggest that in latent scurvy, large blood vessels use modified LDL–in particular lipoprotein(a)–in addition to collagen to maintain macrovascular integrity. … The foam-cell phenotype of atherosclerosis is identified as a mesenchymal genetic program, regulated by the availability of ascorbate. When vitamin C is limited, foam cells develop and induce oxidative modification of LDL, thereby stabilizing large blood vessels via the deposition of LDL. The structural similarity between vitamin C and glucose suggests that hyperglycemia will inhibit cellular uptake of ascorbate, inducing local vitamin C deficiency.

https://www.ncbi.nlm.nih.gov/pubmed/16118484 – hyperglycemia inhibits uptake of ascorbate. Vitamin C exists in 2 forms: The charged form, ascorbate, is taken up into cells via sodium-dependent facilitated transport. The uncharged form, dehydroascorbate, enters cells via glucose transporter and is then converted back to ascorbate within these cells. Because dehydroascorbate and glucose compete for glucose transporters, hyperglycemia will exclude vitamin C from the cell and resulted in a decreased antioxidant capacity in some cell type that is dehydroascorbate dependent.

http://www.pnas.org/content/87/16/6204.full.pdf?sid=7d097127-31ba-41a1-846f-4d8cf4b9fdc2 – Lp(a) is found generally in the blood of primates and the guinea pig, which have lost the ability to synthesize ascorbate, but only rarely in the blood of other animals. Lp(a) has similar properties to ascorbate, i.e. wound healing and other cell-repair mechanisms, the strengthening of the extracellular matrix (e.g., in blood vessels), and the prevention of lipid peroxidation. High plasma Lp(a) is associated with coronary heart disease and other forms of atherosclerosis in humans, and the incidence of cardiovascular disease is decreased by elevated ascorbate. Similar observations have been made in cancer and diabetes. We have formulated the hypothesis that Lp(a) is a surrogate for ascorbate in humans and other species.

https://www.ncbi.nlm.nih.gov/pubmed/26064792 – Deficiency of ascorbate increases serum levels of Lp(a) in mouse model with two characteristics of human metabolism: the expression of Lp(a) and the lack of endogenous ascorbate (vitamin C) production. Moreover, chronic hypoascorbemia and complete depletion of ascorbate (scurvy) leads to Lp(a) accumulation in the vascular wall and parallels atherosclerotic lesion development. The results suggest that dietary ascorbate deficiency is a risk factor for atherosclerosis independent of dietary lipids. We provide support for the concept that Lp(a) functions as a mobile repair molecule compensating for the structural impairment of the vascular wall, a morphological hallmark of hypoascorbemia and scurvy.

http://www.whole-dog-journal.com/issues/1_7/features/5309-1.html – The average dog produces 18 mg of vitamin C per pound of body weight per day. So a 60lbs dog produces 1.08gm of vitamin C per day.

https://www.wddty.com/magazine/2006/march/atherosclerosis-scurvy-in-disguise.htm – A 70-kg goat makes about 13,000 mg (13 g) of vitamin C every day, a large dog about 2.5 g/day. The Committee on Animal Nutrition has also shown that monkeys (which, like us, can’t produce their own vitamin C) need around 55 mg/kg body weight/day of vitamin C for optimal health. In human terms, this means an average 70-kg person needs to take nearly 4 g/day.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1823880/?page=3 – in guinea pigs atherosclerosis is reversible with vitamin C (in summary). Early lesions resorbed quickly, advanced lesions more resistanct, possibly due to only point of contact being at the surface (or maybe due to calcification – K2 would help).

https://www.ncbi.nlm.nih.gov/pubmed/18335267 – vitamin C inhibits serum cholesterol oxidation in rats.
http://jn.nutrition.org/content/133/10/3047.full – vitamin C inhibits lipid oxidation in HDL and preserves its antioxidant activity in vitro.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2682928/ – Supplementation with at least 500 mg/d of vitamin C, for a minimum of 4 weeks, can result in a significant decrease in serum LDL cholesterol and triglyceride concentrations.

https://www.youtube.com/watch?v=DnvnKnu7YBI – explanation of full wholefood Vitamin C complex contents, byt Dr Eric Berg.

http://www.sciencedirect.com/science/article/pii/S0140673600889692 – in 3/10 patients ascorbic acid (orally or IV) did not cure haemorrhagic diathesis nor elevate seruc ascorbic acid levels to normal, but after that lemon juice cured both issues. Suggests that something else may work in conjunction with ascorbic acid for its absopbtion/effect.

https://www.ncbi.nlm.nih.gov/pubmed/2147514 – induced atherosclerosis in this guinea pigs by dietary ascorbate depletion and identified Lp(a) as accumulating in the atherosclerotic plaque. Adequate amounts of ascorbate (40 mg per kg of body weight per day) prevent the development of atherosclerotic lesions in this animal model and the accumulation of Lp(a) in the arterial wall.

Reply
    Ted says November 24, 2016

    Here’s another study from different authors: Aortic wall damage in mice unable to synthesize ascorbic acid
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC15418/

    As plasma ascorbic acid decreased, small, but significant, increases in total cholesterol and decreases in high density lipoprotein cholesterol were observed. The most striking effects of the marginal dietary vitamin C were alterations in the wall of aorta, …… Thus, marginal vitamin C deficiency affects the vascular integrity of mice unable to synthesize ascorbic acid, with potentially profound effects on the pathogenesis of vascular diseases.

    Reply
      P. D. Mangan says November 25, 2016

      Thanks, Ted. Something I was wondering: one reads about primates not producing vitamin C and the effects on our physiology. While I’m not denying the undoubted health effects of C deficiency, the idea that, e.g., “dogs make 5 grams of C daily” (or whatever amount) therefore that’s x g/kg and we should take that much too. Doesn’t follow. Primates have almost certainly adapted to making less C. The adaptation itself must have occurred because we didn’t need the C. Anyway, I’m not knocking the idea of C involvement in healing blood vessels.

      Reply
        ted says November 25, 2016

        Good point. http://orthomolecular.org/library/jom/1992/pdf/1992-v07n01-p005.pdf here’s the A Unified Theory of Human Cardiovascular Disease paper by Pauling, he talks about how Lp(a) and plaque compensates for loss of GLO gene to keep one alive until reproduction age is lower, most CVD deaths happen after 40s.
        So it could be a growth(reproduction) vs longevity tradeoff, favoring reproduction. If early humans lived in Vitamin C rich environment, and liver used glucose to convert it into C, and glucose competes with C to enter cells, maybe evolution preferred that humans did not have a lot of C and died not long after reproduction was over. Of course it would be interesting to study how humans adapted to loss of GLO gene.
        And I don’t see a way to get 3-5 grams of Vitamin C from food every day, that’s like 50 oranges. Richest food in C that I know is Camu Camu berries – 2g of Vit C per 100g.

        Reply
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