Clearing the Cholesterol and Honey Controversy…the Story of Two Villains Turned Superfood-Superheroes

cholesterol labs and healthEven in the world of medicine, stories prevail between villains and heroes. Two such tales exist between cholesterol and heart disease and honey and diabetes. In this blog, I’m going to discuss one of the most famous, most-wanted enemies in medicine, cholesterol. This sterol has been falsely blamed due to the fact that it has been the wrong place at the wrong (diagnostic) snapshot in time. After we clear cholesterol, we’ll move forward to freeing honey’s good name.


Cholesterol- No Longer Enemy Number 1

In medicine, as in some of the best Marvel comics and Disney movies, sometimes when it appears that the no-good-doers should be destroyed entirely, more evidence comes to light that the beast may, in fact, have only appeared to be a scoundrel mistaken as the criminal.

The controversy over cholesterol and lipid foes verses sterol lovers is strong! Advocates beg us not to ignore all the roles that cholesterol has in fat-soluble vitamin formation, hormone production, bile salt production, cognitive health, and as cellular membrane building blocks. Haters of this fatty lipid want us to suppress the bugger and make it go as low as possible, because they’ve seen it at the scene of the crime and nothing that should be floating around in our blood.

However, more evidence has shown that, when cholesterol gets too low, our body implodes into various side effects. This was recently made evident in safety label changes on statin drugs warning of cognitive impairment and elevations in hemoglobin A1c (a measurement of blood sugar by glycation (“sugaring”). Risks were expanded by the FDA in 2014 and reported in this consumer update.

In fact, a recent study in May 2015, concluded “Statin treatment increased the risk of type 2 diabetes by 46%, attributable to decreases in insulin sensitivity and insulin secretion.” Here are the results from the abstract:

Participants on statin treatment (N?=?2,142) had a 46% increased risk of type 2 diabetes (adjusted HR 1.46 [95% CI 1.22, 1.74]). The risk was dose dependent for simvastatin and atorvastatin. Statin treatment significantly increased 2 h glucose (2hPG) and glucose AUC of an OGTT at follow-up, with a nominally significant increase in fasting plasma glucose (FPG). Insulin sensitivity was decreased by 24% and insulin secretion by 12% in individuals on statin treatment (at FPG and 2hPG <5.0 mmol/l) compared with individuals without statin treatment (p?<?0.01). Decreases in insulin sensitivity and insulin secretion were dose dependent for simvastatin and atorvastatin.

Furthermore, a 2015 study in Movement Disorders reported a link between low cholesterol and Parkinson’s disease. This was the exact opposite correlation of what was previously believed to be true.

Another hit to statin lovers was in a current review of statin therapy that proposed that cholesterol reduction with statins may actually be “causative in coronary artery calcification and can function as mitochondrial toxins that impair muscle function in the heart and blood vessels through the depletion of coenzyme Q10 and ‘heme A’, and thereby ATP generation.” The authors felt this occurred through various mechanisms:

Statins inhibit the synthesis of vitamin K2, the cofactor for matrix Gla-protein activation, which in turn protects arteries from calcification. Statins inhibit the biosynthesis of selenium containing proteins, one of which is glutathione peroxidase serving to suppress peroxidative stress. An impairment of selenoprotein biosynthesis may be a factor in congestive heart failure, reminiscent of the dilated cardiomyopathies seen with selenium deficiency. Thus, the epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin treatment guidelines be critically reevaluated.

This was further supported in March 2015 with the release of a critical assessment of various research articles on the effect of lowering cholesterol with statin medications on cardiovascular health outcomes. The authors concluded,

Our opinion is that although statins are effective at reducing cholesterol levels, they have failed to substantially improve cardiovascular outcomes. We have described the deceptive approach statin advocates have deployed to create the appearance that cholesterol reduction results in an impressive reduction in cardiovascular disease outcomes through their use of a statistical tool called relative risk reduction (RRR), a method which amplifies the trivial beneficial effects of statins. We have also described how the directors of the clinical trials have succeeded in minimizing the significance of the numerous adverse effects of statin treatment.

Of course, we have to look at the fact that statins also block other vital components of cellular function such as coQ10 and the other mevalonate pathway non-sterol isoprenoids (intermediates of cholesterol synthesis), such as dolichol, heme-A, isopentenyl tRNA, which are related to cell growth and differentiation.

In this article, Chris Kresser does a wonderful review offering further evidence of studies that dietary cholesterol and saturated fat are not the enemy. High cholesterol, in itself, is not necessarily an issue, unless it’s extremely high. The cardiovascular issues present when the cholesterol gets dysfunctional and becomes oxidized or inflamed and sticks to artery walls. Correcting hormonal imbalances, high blood sugar, sources of infection and inflammation, sleep imbalances, diet, toxins, and addressing stress are some ways to prevent this unwanted effect.


Does that mean we ignore high cholesterol levels?

Cholesterol is important to look at in context with other factors. Some of these factors include:

  • Genetic profiles, such as ApoAE gene variations to assess if statins would be helpful based on one’s ability to clear lipids
  • Inflammatory and nutritional markers such as hsCRP, various cytokine levels, fibrinogen, homocysteine, and ferritin
  • Insulin and leptin resistance
  • Oxidative stress markers
  • NMR Lipoprofile to assess LDL particle size number
  • Apo B
  • Checking for heavy metals
  • Assessing hormonal levels, such as cortisol, testosterone, thyroid, and estrogen levels
  • Liver and kidney function

Furthermore, the root cause of why cholesterol is elevated should be addressed. A Naturopathic or Functional Doctor can help you navigate which tests might be helpful to run for you. They can also evaluate risk factors mentioned above.

Now, let’s take a look at the not-so dark side of fructose-Nature’s golden sweetener.



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FDA: For Consumers. FDA Expands Advice on Statin Risks. Updated August 31, 2015.

Cederberg H, Stan?áková A, Yaluri N, Modi S, Kuusisto J, Laakso M. Increased risk of diabetes with statin treatment is associated with impaired insulin sensitivity and insulin secretion: a 6 year follow-up study of the METSIM cohort. Diabetologia. 2015 May;58(5):1109-17. doi: 10.1007/s00125-015-3528-5. Epub 2015 Mar 10.

Huang, X., Alonso, A., Guo, X., Umbach, D. M., Lichtenstein, M. L., Ballantyne, C. M., Mailman, R. B., Mosley, T. H. and Chen, H. (2015), Statins, plasma cholesterol, and risk of Parkinson’s disease: A prospective study. Mov. Disord. 2015; 30: 552–559. doi: 10.1002/mds.26152

David McNamee. Statins may not protect against Parkinson’s after all, study finds. Medical News Today. February 20, 2015.

Okuyama H, Langsjoen PH, Hamazaki T, Ogushi Y, Hama R, Kobayashi T, Uchino H. Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms Expert Rev Clin Pharmacol. 2015 Mar;8(2):189-99. doi: 10.1586/17512433.2015.1011125. Epub 2015 Feb 6.

Diamond DM, Ravnskov U. How statistical deception created the appearance that statins are safe and effective in primary and secondary prevention of cardiovascular disease. Expert Rev Clin Pharmacol. 2015 Mar;8(2):201-10. doi: 10.1586/17512433.2015.1012494. Epub 2015 Feb 12.