Folks, I’m excited to bring you this book excerpt from The Carnivore Code. Author Dr. Paul Saladino is one of the best informed thought leaders and advocates of the carnivore diet. Paul uses his experience in functional and traditional medicine to devise a holistic picture of healing. I think you’ll appreciate his detailed, well-researched, and measured approach to presenting and analyzing evidence.
We’ve reviewed study after study that’s correlated red meat consumption with mortality risk, atherosclerosis, heart disease, and more. Paul takes the topic to task in The Carnivore Code, hopefully proving once and for all the true physiological cause of these conditions.
You can purchase a copy of The Carnivore Code here. From February 24, 2020 until February 26, 2020, you can enter for your chance to win a signed copy of The Carnivore Code. Simply follow @marksdailyapple and @carnivoremd on Instagram, tag some friends in the comments of the Instagram giveaway announcement, and you’ll be automatically entered to win a signed copy of the book plus a canister of Primal Kitchen Collagen Peptides. Five winners will be selected and notified via DM; U.S. entrants only. Good luck, and enjoy the excerpt.
Few things conjure more fear in the hearts and minds of the general population than the big, bad cholesterol monster and the associated trepidation that red meat will cause our arteries to become filled with plaque. After all, we’ve been told by cardiac surgeons that when they scoop plaque out of the arteries in our heart or neck, it looks just like animal fat, eggs, or butter.
In this excerpt, we’ll debunk the notion that eating animal meat, fat, or organs is bad for our heart and blood vessels and slay this final beast once and for all. We’ll see that these false notions have been based on more misleading epidemiological literature and how interventional and mechanistic studies tell a very different story. Come, brave adventurers, our destiny of discarding unfounded ideologies and reclaiming the vibrant health of our ancestors awaits!
The Basics of Lipoproteins and Cholesterol
The word “cholesterol” is often used colloquially to refer to all of the lipoproteins in our blood, but technically, cholesterol is a steroid backbone type of molecule that is used to make all sorts of vital compounds in human physiology. Our body makes around 1,200 milligrams of cholesterol every day for many important purposes, including the proper formation of all of our cell membranes.
The fat we eat is absorbed from our intestines and packaged as triglycerides with dietary cholesterol into a type of lipoprotein known as chylomicrons, marked with apolipoprotein B48. These particles circulate in the blood stream, dropping off their contents to cells of the body before becoming chylomicron remnants and being taken up by the liver.
In medicine, the term “total cholesterol” refers to the sum of all the cholesterol molecules in the blood and is usually measured directly in laboratory tests. In order to know how much of this cholesterol resides in the different lipoproteins, these must be measured individually. Most current lipid testing measures HDL, LDL, VLDL, and triglycerides directly, but older assays measure only some of these and must calculate LDL, which you may see written as LDL-C. For this reason, many previous research studies have looked at total cholesterol levels rather than LDL. Historically, elevated levels of total cholesterol have been assumed to correlate with elevated levels of LDL, and unless triglycerides are extremely elevated, this is generally a reasonable assumption.
The Vital Role of LDL in Our Body
Most of the cells of our body can make a bit of cholesterol from scratch, but they also rely heavily on the delivered supply of this molecule to build membranes and hormones. In addition to its vital role transporting building blocks and nutrients, LDL also serves important roles within the immune system. Yes, you read that correctly, LDL plays a valuable part in our response to assault by infectious invaders, as do many of the lipoproteins, including HDL. When gram-negative bacteria seek to invade our body, they release a cell wall component known as endotoxin, which is quite inflammatory and can strongly trigger the immune system. But don’t worry, friendly neighborhood LDL is around to bind-up this toxin and prevent things from getting out of hand.
Is there evidence that higher levels of LDL could be protective against infection in us? You bet there is! There are many studies that show elevated levels of LDL are not a risk factor for increased all-cause mortality or cardiovascular mortality in the elderly.9 Furthermore, there are many studies suggesting that higher levels of LDL are protective as we age, which is most likely connected with its role in immune function.1,2,3-11
In a sample of 347 individuals over the age of sixty-five, those with low total cholesterol had a significantly higher risk of dying by non-vascular causes, while those with elevated total cholesterol had half the risk of the reference population.1 Another study of 105 individuals over the age of eighty living in Iceland found that those with the highest total cholesterol level had less than half the all-cause mortality of those with lower levels.12 An even larger investigation called the Leiden 85-plus study had even more striking results. This study included 724 elderly individuals living in the Netherlands in whom the correlation between total cholesterol and all-cause mortality was measured for ten years. The authors found that for every 38 milligrams per deciliter increase in the total cholesterol, there was a corresponding 15 percent decrease in the risk of dying over this time period.
Clearly, LDL is a valuable particle in our blood and serves many indispensable roles. How can LDL be both protective and harmful? This doesn’t seem to make any sense! The answer is that LDL itself is not harmful, but in certain situations, it can be involved in the process of responding to injury and inflammation—making it look like it’s a bad actor when it’s merely present at the scene of the crime.
So… What Causes Atherosclerosis?
There are more than a quintillion particles of LDL floating around in our bloodstream. If every LDL particle that entered the subendothelial space in our arteries led to the formation of a plaque, we’d be deader than a doornail long before our first birthday. Every second of every day, lipoproteins like LDL are moving in and out of the walls of both veins and arteries, delivering nutrients to the cells there for energy and the construction of membranes. Clearly, there must be another part of this equation that leads to retention of some of these LDL particles within the arterial wall.
Interestingly, HDL particles are smaller and ten times more numerous than LDL. They carry more cholesterol in our blood stream, but these particles do not participate in the formation of atherosclerotic lesions. Why not? Because they do not get stuck in the subendothelial space.
Within the arterial wall, it appears that only particles containing the APOB molecule are able to bind to the proteoglycans within the intima and be retained.13 It’s not the size of the particle, or the number of particles moving into the vessel wall that’s important, it’s how likely a lipoprotein is to be retained that determines whether or not it contributes to the process of plaque formation.
What determines how sticky the LDL particle and the intimal space are? Ah, my friends, this is truly the million-dollar question! There’s very good evidence that during the states of insulin resistance and inflammation, both the LDL particle and the intimal space get coated in “molecular velcro” and become more sticky.14,15,16-18
Specifically, studies looking at the arteries of diabetics and arterial wall injury have shown changes in the proteoglycan matrix that increase its affinity for LDL.19 Additional research reveals that the LDL particle becomes more likely to be bound to proteoglycans in the intimal space when it is enriched with apolipoprotein ApoC III—a process that occurs during states of insulin resistance—making for a dangerous combination that strongly predisposes to plaque formation. The risk of atherosclerosis is so high in diabetics that rates of heart attack are elevated in this population even with low levels of LDL.20
At this point, you may be saying, “Sure, I believe you on this, but doesn’t atherosclerosis occur in people without diabetes or pre-diabetes? How common is this scenario of insulin resistance?” Though diabetes and pre-diabetes are diagnosed in 35 percent of the American population, there’s strong evidence that insulin resistance is much more common than this! There is evidence that a whopping 88 percent of the American population has some degree of metabolic dysfunction.21 If the vast majority of people around us have insulin resistance, is it any wonder that some studies have shown a correlation between LDL levels and cardiovascular disease? Almost the entire population of the U.S. has velcro on their lipoproteins and within their arteries, and the tennis balls are getting stuck to the wall!
So to answer the previous question, there’s good evidence that when atherosclerosis does occur, it is almost always in the setting of insulin resistance and metabolic dysfunction.
One of the biggest mistakes Western medicine makes is to extrapolate these pathologies to the 12 percent of us who are not insulin resistant and not inflamed, warning us that certain cardiovascular disease will swiftly follow with an elevated LDL.
Those of us with good insulin sensitivity are essentially a different breed, and there are many striking stories of plaque regression among insulin-sensitive individuals with “elevated LDL” eating carnivore or ketogenic diets. In the absence of insulin resistance and inflammation, higher levels of LDL are probably protective because of their roles with the immune response. Want to live a long time? Eat in a manner that allows for insulin sensitivity, decreases inflammation, and leads to a robust amount of valuable LDL particles. Carnivore diet, anyone?
Excerpted (in a summarized format) from The Carnivore Code by Paul Saladino, MD.
1. Raiha, I., Marniemi, J., Puukka, P., Toikka, T., Ehnholm, C., & Sourander, L. (1997). Effect of serum lipids, lipoproteins, and apolipoproteins on vascular and nonvascular mortality in the elderly. Arteriosclerosis, Thrombosis, and Vascular Biology, 17(7), 1224-1232. doi:10.1161/01.atv.17.7.1224
2. Forette, F., De la Fuente, X., Golmard, J., Henry, J., & Hervy, M. (1982). The prognostic significance of isolated systolic hypertension in the elderly. Results of a ten year longitudinal survey. Clinical and Experimental Hypertension. Part A: Theory and Practice, 4(7), 1177-1191. doi:10.3109/10641968209060782
3. Forette, B., Tortrat, D., & Wolmark, Y. (1989). Cholesterol as risk factor for mortality in elderly women. The Lancet, 333(8643), 868-870. doi:10.1016/s0140-6736(89)92865-1
4. Risk of fatal coronary heart disease in familial hypercholesterolaemia. Scientific Steering Committee on behalf of the Simon Broome Register Group. (1991). BMJ, 303(6807), 893-896. doi:10.1136/ bmj.303.6807.893
5. Weijenberg, M. P., Feskens, E. J., & Kromhout, D. (1996). Total and high density lipoprotein cholesterol as risk factors for coronary heart disease in elderly men during 5 years of follow-up: The Zutphen elderly study. American Journal of Epidemiology, 143(2), 151-158. doi:10.1093/oxfordjournals.aje.a008724
6. Weuenberg, M. P., Feskens, E. J., Bowles, C. H., & Kromhout, D. (1994). Serum total cholesterol and systolic blood pressure as risk factors for mortality from ischemic heart disease among elderly men and women. Journal of Clinical Epidemiology, 47(2), 197-205. doi:10.1016/0895-4356(94)90025-6
7. Zimetbaum, P., Frishman, W. H., Ooi, W. L., Derman, M. P., Aronson, M., Gidez, L. I., & Eder, H. A. (1992). Plasma lipids and lipoproteins and the incidence of cardiovascular disease in the very elderly. The Bronx Aging Study. Arteriosclerosis and Thrombosis: A Journal of Vascular Biology, 12(4), 416-423. doi:10.1161/01.atv.12.4.416
8. Abbott, R. D., Curb, J., Rodriguez, B. L., Masaki, K. H., Yano, K., Schatz, I. J., … Petrovitch, H. (2002). Age-related changes in risk factor effects on the incidence of coronary heart disease. Annals of Epidemiology, 12(3), 173-181. doi:10.1016/s1047-2797(01)00309-x
9. Chyou, P., & Eaker, E. D. (2000). Serum cholesterol concentrations and all-cause mortality in older people. Age and Ageing, 29(1), 69-74. doi:10.1093/ageing/29.1.69
10. Menotti, A., Mulder, I., Nissinen, A., Feskens, E., Giampaoli, S., Tervahauta, M., & Kromhaut, D. (2001). Cardiovascular risk factors and 10-year all-cause mortality in elderly European male populations. The FINE study. European Heart Journal, 22(7), 573-579. doi:10.1053/euhj.2000.2402
11. Krumholz, H. M. (1994). Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause mortality in persons older than 70 years. JAMA: The Journal of the American Medical Association, 272(17), 1335-1340. doi:10.1001/jama.272.17.1335
12. Jónsson, Á., Sigvaldason, H., & Sigfússon, N. (1997). Total cholesterol and mortality after age 80 years. The Lancet, 350(9093), 1778-1779. doi:10.1016/s0140-6736(05)63609-4
13. Hurt-Camejo, E., & Camejo, G. (2018). ApoB-100 lipoprotein complex formation with intima proteoglycans as a cause of atherosclerosis and Its possible ex vivo evaluation as a disease biomarker. Journal of Cardiovascular Development and Disease, 5(3), 36. doi:10.3390/jcdd5030036
14. Hiukka, A., Stahlman, M., Pettersson, C., Levin, M., Adiels, M., Teneberg, S., … Boren, J. (2009). ApoCIII-enriched LDL in type 2 diabetes displays altered lipid composition, increased susceptibility for sphingomyelinase, and increased binding to biglycan. Diabetes, 58(9), 2018-2026. doi:10.2337/db09-0206
15. Olsson, U., Egnell, A., Lee, M. R., Lunden, G. O., Lorentzon, M., Salmivirta, M., … Camejo, G. (2001). Changes in matrix proteoglycans induced by insulin and fatty acids in hepatic cells may contribute to dyslipidemia of insulin resistance. Diabetes, 50(9), 2126-2132. doi:10.2337/diabetes.50.9.2126
16. Hulthe, J., Bokemark, L., Wikstrand, J., & Fagerberg, B. (2000). The metabolic syndrome, LDL particle size, and atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology, 20(9), 2140-2147. doi:10.1161/01. atv.20.9.2140
17. Wasty, F., Alavi, M. Z., & Moore, S. (1993). Distribution of glycosaminoglycans in the intima of human aortas: Changes in atherosclerosis and diabetes mellitus. Diabetologia, 36(4), 316-322. doi:10.1007/ bf00400234
18. Rodriguéz-Lee, M., Bondjers, G., & Camejo, G. (2007). Fatty acid-induced atherogenic changes in extracellular matrix proteoglycans. Current Opinion in Lipidology, 18(5), 546-553. doi:10.1097/ mol.0b013e3282ef534f
19. Srinivasan, S. R., Xu, J., Vijayagopal, P., Radhakrishnamurthy, B., & Berenson, G. S. (1993). Injury to the arterial wall of rabbits produces proteoglycan variants with enhanced low-density lipoprotein-binding property. Biochimica et Biophysica Acta (BBA) – Lipids and Lipid Metabolism, 1168(2), 158-166. doi:10.1016/0005-2760(93)90120-x
20. Howard, B. V., Robbins, D. C., Sievers, M. L., Lee, E. T., Rhoades, D., Devereux, R. B., … Howard, W. J. (2000). LDL cholesterol as a strong predictor of coronary heart disease in diabetic individuals with insulin resistance and low LDL. Arteriosclerosis, Thrombosis, and Vascular Biology, 20(3), 830-835. doi:10.1161/01. atv.20.3.830
21. Araújo, J., Cai, J., & Stevens, J. (2019). Prevalence of optimal metabolic health in american adults: National health and nutrition examination survey 2009–2016. Metabolic Syndrome and Related Disorders, 17(1), 46-52. doi:10.1089/met.2018.0105
})( jQuery );
eventCategory: ‘Ad Impression’,