Colorectal Cancer is in the News Again. Don't Blame Red Meat

 

Colorectal Cancer in the News

NBC News and other prominent outlets are currently reporting on a dramatic increase in both rates of colon cancer and colon cancer mortality among young adults.¹ These news reports, based on a recent publication from the American Cancer Society, suggest a substantial uptick in the disease but can only theorize as to what might be driving it.² While the ACS report itself is only a dry statistical report, various news outlets and the public health experts they interview hypothesize a number of potential causes, typically of an environmental or dietary nature. One of these potential causes, is of course, meat consumption. So now seems like as good of time as any to discuss why I believe there is no legitimate evidence whatsoever linking meat (most specifically, red meat) consumption to colon and colorectal cancer (CRC) incidence.

Lets start with the ACS report itself, which reports increasing incidence of 6 of the top 10 cancers. For example, cancers of the breast and pancreas ticked up very slightly (less than 1% over five years), while cancers of the prostate and kidney were among those increasing most rapidly (upwards of 3% over five years). Colorectal cancer, on the other hand…is not increasing. So why all the headlines? I think part of it is that CRC makes for a trendy headline of sorts, as its been a particular mainstream focus in the last decade or so (more on that in a minute). The other reason is that, while CRC rates are not increasing overall, they are indeed increasing (between 1 and 2 percent) among people in their 30s and 40s. Perhaps even more relevantly, rates of CRC morality in that demographic are increasing as well.

 

Rates of CRC and other select cancers in adults under the age of 50

So rates are increasing among younger adults in which the disease tends to be relatively rare, but are not increasing overall. What might cause this to be the case? I certainly have a suggestion, but it won’t be the same you see in traditional medical and health circles. If you search the internet for CRC prevention advice, you’ll quickly find (along with advice to exercise and refrain from smoking) advice from the American Cancer Society to limit red and processed meat, from the CDC to limit animal fats, and from Harvard to remove as much meat as possible from your diet (“Red and processed meat has been the dietary factor most consistently linked to colon cancer”). ^3–5

None of these claims and none of these recommendations, though, are based on more than weak epidemiology (i.e. survey data). And while potential explanations (curing nitrates in processed meat, for example) have been sought to explain the association between meat consumption and CRC, I believe a much more obvious causal explanation exists both to explain the general association between red meat consumption and CRC AND the recent uptick in young adult incidence of the disease.

 

Increasing Focus on the Meat-CRC Link

 

It’s often presented as an obvious cause and effect, that red meat consumption is tightly linked to and often instrumental in causing CRC to develop. But the evidence does not support these typical claims. Let’s start in 2015, when the International Agency for Research on Cancer (IARC) prepared a study for the World Health Organization on the potential carcinogenic properties of meat. ⁶ Based (ostensibly) on this paper, the WHO issued a report declaring red meat to be a Category 2A carcinogen, describing it as “probably carcinogenic to humans.” This notion, that beef and other red meat may be cancer-causing, has become increasingly prevalent in the years since.

 

However, I would argue that the claims made by the IARC/WHO are deeply flawed for a number of reasons:

1.       The IARC report did not, in fact, find significant evidence that red meat consumption is linked to cancer in humans

2.       The epidemiological studies that do link meat consumption to cancer are very limited, and typically find only a small effect

3.       The studies linking meat consumption to cancer fail to take into account significant confounding variables.

             

When you first saw the alarming report on the nightly news in late 2015, you’d have been mistaken for believing the WHO made their claims on the back of a significant body of evidence. After all, the WHO is quick to point out that more than 800 studies were examined as part of the report. How many of these 800 studies detailed a significant link between red meat consumption and CRC, you might wonder…

Its certainly not 800. In fact it certainly doesn’t even appear to be 8. Included among those 800 studies were 29 that examined CRC specifically, and of those 29 only 14 showed positive associations between red meat consumption and CRC. But read that sentence again…. Its 14 studies that showed a positive association, not 14 studies that showed a statistically significant connection between CRC and red meat consumption. In fact, in their public report the very first study the IARC references among those 14 says this:

 

“Intake of red meat was positively but not statistically significantly associated with colorectal cancer"⁷

 

So, again, to be very clear – there were not 14 studies that found a scientific, statistical link between red meat consumption and CRC. There were instead 14 studies that demonstrated some vague, uncertain positive relationship between the two. However, the IARC and WHO made the choice in their reports to misrepresent these weak relationships as scientifically valid, when in fact they are anything but. And since every piece of epidemiology is going to pick up a vague, uncertain trend in one way or the other, we can be fairly confident the other 15 demonstrate some vague, weak, unscientific trend in the opposite direction. So while the totality of the evidence examined found no scientific link between CRC and red meat consumption, and the weak, non-significant trends were equally split between positive and negative, the WHO still made the decision, based on jaw-droppingly weak evidence, to label red meat a probable human carcinogen.

 

Why The CRC-Red Meat Link Still Sometimes Exists

 

Ok, ok….the IARC report didn’t support its own conclusions or its headlines. But there are, indeed, some epidemiological studies out there that show a genuine, significant scientific link between CRC and red meat consumption. There was even one in the public IARC report!⁸ So now let’s talk about why that link still isn’t what it seems, and what dietary factor I ultimately think is to blame for the uptick in young adult CRC.

**A quick aside – if you aren’t familiar with the concept of healthy user bias, now would be a good time to acquaint yourself. You can do so in detail HERE, but in short – healthy user bias is the concept by which people who want to be healthy do things they believe to be of benefit to their health. The opposite is "unhealthy user bias," in which people who don't care about their health don't mind doing things that are considered unhealthy. Because recommendations to avoid meat predate nutritional epidemiology by more than two decades, there has never been a study unbiased by the widespread belief that meat and fat are unhealthy. Healthy user bias is a massive problem in epidemiology because its effectively impossible to account for all the habitual differences between “healthy” and “unhealthy” individuals. It’s a problem made all the more massive by the fact that so many researches apparently don’t even make an attempt. For example, failure to adjust for a multitude of factors is how you end up with the consistent finding that red meat consumption “causes” as many or more accidents than it does cases of chronic disease^9–11**

 

Ok, now…A case study –

The same year as the IARC report, researches at Loma Linda University released a study claiming that "Vegetarian diets are associated with an overall lower incidence of colorectal cancers."¹² This study, basically, followed nearly 100,000 Seventh-Day Adventists for six years and compared self-reported diet to incidence of colon cancer. Because meat consumption is frowned upon in the religion, only half of the participants were meat-eaters. What they concluded is that vegetarians, compared to those who consume meat, were 22% less likely to develop colorectal cancer. This translates to roughly a 5% chance that a vegetarian, and a 6% chance that a meat-eater, would develop colorectal cancer during adulthood. And yes, this finding was statistically significant. 

 But it still doesn't mean meat causes cancer. Why? Healthy user bias and confounding variables. It is standard scientific practice to attempt to adjust for HUB, but is not possible to do so completely. Lets specifically examine meat-eaters vs. vegans, using the data from this study, to illustrate why. 

 

 

 

What you might notice at first is that the vegans in the study actually had more cases of colorectal cancer than did the meat-eaters. 7 percent more, to be accurate. But just stopping there would be very bad science indeed, as there are a number of other factors that can influence the results. For example, the meat-eaters are slightly younger and thus less likely, all things considered, to develop cancer of any kind. When the researchers apply the statistical process known as "adjustment" to the age variable, they can eliminate age as a factor and find that, age-adjusted, the vegans actually had 11 percent FEWER cases of colorectal cancer. 

But we can't just adjust for age. You'll also notice that meat-eaters are more overweight, more likely to smoke, more likely to drink, more likely to have diabetes, less likely to exercise, etc. This is (un)healthy user bias in action. Researchers adjust for these as well, with little impact on the final numbers. But what I want to focus on is not what they do adjust for, but what they don’t – namely, sugar and processed carb consumption, blood sugar, and insulin levels. You’ll note in the chart above that I specifically highlighted the diabetes rate of the meat eating group, and with good reason -

 

1. Diabetes is fundamentally a disease of insulin resistance and increased insulin production tightly related to prolonged overconsumption of high-glycemic (sugary) carbohydrates and obesity

        2. Insulin is a potent growth factor

        3. Cancer is a disease of uncontrolled growth, and cancer cells typically overexpress insulin receptors

 

It should not be surprising then, to find that individuals with increased insulin levels are far more likely to develop colorectal cancer. For example..

"An increased concentration of plasma C-peptide was statistically significantly associated with an increased risk of colorectal cancer (relative risk [RR] for the highest versus lowest quintile of plasma C-peptide = 2.7, 95% confidence interval [CI] = 1.2 to 6.2; P-trend = .047)"¹³

"Colorectal cancer risk increased with increasing levels of C-peptide (P-trend = .001), up to an odds ratio (OR) of 2.92 (95% confidence interval [CI] = 1.26–6.75) for the highest versus the lowest quintiles"¹⁴

"Cancer mortality was significantly higher in those with hyperinsulinemia than in those without hyperinsulinemia (adjusted HR 2.04)"¹⁵

*Note that C-Peptide is a measure of insulin production

 

In fact, a long list of studies show that individuals with high levels of insulin production are as much as 200 to 400 percent more likely to develop colorectal cancer.^16–24 But despite insulin's massive role in the development and progression of cancer, it is partially unaccounted for in the study above. We know, with a high level of certainty, that the meat-eating group had higher insulin levels, largely due to the drastically higher rate of diabetes but also the increased obesity (tightly connected to insulin levels) and the great likelihood that the meat eaters are also consuming more sugar and processed carbohydrate (healthy user bias).

Now it is true that obesity and a clinical diagnosis of diabetes are adjusted for, but the vast majority of meat-eaters did not have diabetes. Still, the massively increased rate of diabetes doesn't exist in a vacuum. Diabetes as a clinical diagnosis really just reflects a certain threshold of insulin resistance, not a discrete state. Which is to say that the meat-eating group has more diabetics because the entire group has higher insulin levels, meaning more people will be past the diabetic threshold. The critical point, then, is that this group will also have more "pre-diabetics" and more people with moderately elevated insulin. But without any adjustment made for the consumption of sugar, the consumption of processed grains, actual blood sugar levels, or actual insulin levels, the influence of insulin is allowed to persist. Certainly, then, the meat-eating group is to at least some degree more likely to develop colorectal cancer for reasons that have nothing to do with the consumption of meat. 

In fact, the end result of the study suggests, based on indirect survey data, that meat-eaters are 14% more likely than vegans to develop CRC. Contrast this with the consistent direct findings that individuals with the highest insulin levels are more like 2-300% more likely to develop CRC. These studies together suggest that high insulin is something like 15-20 times more powerful than high meat consumption in predicting the development of future CRC. When insulin is that much more powerful a predictor, it only takes a small degree of negligence in accounting for it to end up with results like the one is this study. Are meat-eaters 14% more likely to develop CRC because meat is driving the disease or because their more sedentary, processed-carb lifestyle results in elevated insulin that isn’t fully being accounted for?

You can see how glaring an oversight it is, then, to ignore the impact of insulin when you attempt to link meat consumption to CRC using only epidemiological survey data. Remember when I pointed out the one study in the IARC report linking red meat to CRC at a statistically significant level? Not only did that study not measure or adjust for sugar consumption, processed carb consumption, blood sugar, or insulin levels, they didn't even adjust for diabetes! If you then further layer in the pile of direct, controlled trials that demonstrate the capacity of a high fat, low-carb diet to improve blood sugar and lower insulin levels, the claims that meat consumption is causing CRC become even more difficult to believe.^25–35  

Conclusion

The following facts are all true:

1.      The link between meat consumption and CRC development is based only on a small number of epidemiological surveys, and the degree to which these studies suggest meat ostensibly increases one’s risk is quite small.  

2.      Elevated insulin levels predict CRC development as much as 20 times more strongly than does high levels of meat consumption.

3.     Epidemiological studies incompletely account for insulin levels to varying degrees, with some ignoring blood sugar, insulin levels, and diabetes entirely.

4.     Replacing sugar and carbohydrates with meat and fat lowers long-term blood sugar, lowers insulin levels, and improves markers of glucose metabolism and diabetes.

 

The following facts are also true:

1.       Diabetes rates are increasing more rapidly than CRC rates

2.       Diabetes rates are increasing in children and young adults³⁶

 

I’m sure its entirely obvious where I’m going with this by now, but I’ll share an image from last year’s post on red meat and diabetes to drive home the point:

 

 

Red meat doesn’t cause diabetes and in fact can be instrumental in reversing it. In reality, this discussion on CRC is basically just “red meat doesn’t cause diabetes” with extra steps. Red meat consumption has never been legitimately linked to the development of CRC - A minority percentage of epidemiolocal papers suggest a weak link between the two only by utilizing survey data that fails to fully account for meaningful confounding factors.

On the contrary, insulin levels are directly, strongly, and significantly linked to the development of CRC. As reflected by ever-increasing rates of diabetes and ever-earlier onset of the disease, population levels of blood sugar and insulin continue to increase. If one begins with the (scientifically-valid) premise that impaired glucose metabolism, elevated insulin, and other diabetic complications are directly influential in the onset of CRC, it is effectively inescapable that the increasing rates of diabetes (and young adult diabetes) must portend an increase in young adult CRC as well.

To the degree than any dietary factor is influencing the increase in CRC incidence and mortality, it is these – excess consumption of sugar and processed carbohydrate, chronically elevated blood sugar, and long-term elevated insulin are directly involved in the development of CRC. Red meat, for decades now lumped with smoking, drinking, sugar, and a sedentary lifestyle as the vices of chronic disease, is occasionally caught in the crossfire of weak epidemiological science.

News articles and “expert” advice will likely continue to focus on the minor, weak, indirect link and urge you to prudently fight CRC by eliminating meat despite the lack of evidence to support this position. I’ll do the opposite – if you want to reduce your risk of colorectal cancer, focus on the direct link more than an order of magnitude stronger. Reduce your insulin levels by reducing or eliminating sugar, grains, and other processed carbohydrates, and make a real, meaningful difference in your risk of developing cancer, diabetes, and a host of other chronic diseases. Don’t blame the meat.

1.               Colon cancer is killing more younger men and women than ever, new report finds. NBC News. Published January 17, 2024. Accessed January 18, 2024. https://www.nbcnews.com/health/health-news/colon-cancer-deaths-younger-men-women-report-rcna134084

2.               Siegel RL, Giaquinto AN, Jemal A. Cancer statistics, 2024. CA: A Cancer Journal for Clinicians. n/a(n/a). doi:10.3322/caac.21820

3.               Colorectal Cancer Prevention | How to Prevent Colorectal Cancer. Accessed January 18, 2024. https://www.cancer.org/cancer/types/colon-rectal-cancer/causes-risks-prevention/prevention.html

4.               What Can I Do to Reduce My Risk of Colorectal Cancer? | CDC. Published February 23, 2023. Accessed January 18, 2024. https://www.cdc.gov/cancer/colorectal/basic_info/prevention.htm

5.               How to prevent colorectal cancer. Harvard Health. Published February 1, 2014. Accessed January 18, 2024. https://www.health.harvard.edu/cancer/how-to-prevent-colorectal-cancer

6.               Bouvard V, Loomis D, Guyton KZ, et al. Carcinogenicity of consumption of red and processed meat. The Lancet Oncology. 2015;16(16):1599-1600. doi:10.1016/S1470-2045(15)00444-1

7.               Norat T, Bingham S, Ferrari P, et al. Meat, Fish, and Colorectal Cancer Risk: The European Prospective Investigation into Cancer and Nutrition. JNCI: Journal of the National Cancer Institute. 2005;97(12):906-916. doi:10.1093/jnci/dji164

8.               Larsson SC, Rafter J, Holmberg L, Bergkvist L, Wolk A. Red meat consumption and risk of cancers of the proximal colon, distal colon and rectum: The Swedish Mammography Cohort. International Journal of Cancer. 2005;113(5):829-834. doi:10.1002/ijc.20658

9.               Huang J, Liao LM, Weinstein SJ, Sinha R, Graubard BI, Albanes D. Association Between Plant and Animal Protein Intake and Overall and Cause-Specific Mortality. JAMA Internal Medicine. 2020;180(9):1173-1184. doi:10.1001/jamainternmed.2020.2790

10.             Sinha R, Cross AJ, Graubard BI, Leitzmann MF, Schatzkin A. Meat intake and mortality: a prospective study of over half a million people. Arch Intern Med. 2009;169(6):562-571. doi:10.1001/archinternmed.2009.6

11.             Cohen_cornellgrad_0058F_10285.pdf. Accessed June 25, 2023. https://ecommons.cornell.edu/bitstream/handle/1813/51613/Cohen_cornellgrad_0058F_10285.pdf?sequence=1#page=111

12.             Orlich MJ, Singh PN, Sabaté J, et al. Vegetarian dietary patterns and the risk of colorectal cancers. JAMA Intern Med. 2015;175(5):767-776. doi:10.1001/jamainternmed.2015.59

13.             Ma J, Giovannucci E, Pollak M, et al. A Prospective Study of Plasma C-Peptide and Colorectal Cancer Risk in Men. JNCI Journal of the National Cancer Institute. 2004;96(7):546-553. doi:10.1093/jnci/djh082

14.             Kaaks R, Toniolo P, Akhmedkhanov A, et al. Serum C-peptide, insulin-like growth factor (IGF)-I, IGF-binding proteins, and colorectal cancer risk in women. J Natl Cancer Inst. 2000;92(19):1592-1600. doi:10.1093/jnci/92.19.1592

15.             Tsujimoto T, Kajio H, Sugiyama T. Association between hyperinsulinemia and increased risk of cancer death in nonobese and obese people: A population-based observational study. International Journal of Cancer. 2017;141(1):102-111. doi:10.1002/ijc.30729

16.             Fung TT, Hu FB, Schulze M, et al. A dietary pattern that is associated with C-peptide and risk of colorectal cancer in women. Cancer Causes Control. 2012;23(6):959-965. doi:10.1007/s10552-012-9969-y

17.             Chen L, Li L, Wang Y, et al. Circulating C-peptide level is a predictive factor for colorectal neoplasia: evidence from the meta-analysis of prospective studies. Cancer Causes Control. 2013;24(10):1837-1847. doi:10.1007/s10552-013-0261-6

18.             Xu J, Ye Y, Wu H, et al. Association between markers of glucose metabolism and risk of colorectal cancer. BMJ Open. 2016;6(6):e011430. doi:10.1136/bmjopen-2016-011430

19.             Tsai CJ, Giovannucci EL. Hyperinsulinemia, Insulin Resistance, Vitamin D, and Colorectal Cancer Among Whites and African Americans. Dig Dis Sci. 2012;57(10):2497-2503. doi:10.1007/s10620-012-2198-0

20.             Jenab M, Riboli E, Cleveland RJ, et al. Serum C-peptide, IGFBP-1 and IGFBP-2 and risk of colon and rectal cancers in the European Prospective Investigation into Cancer and Nutrition. International Journal of Cancer. 2007;121(2):368-376. doi:10.1002/ijc.22697

21.             Wei EK, Ma J, Pollak MN, et al. A prospective study of C-peptide, insulin-like growth factor-I, insulin-like growth factor binding protein-1, and the risk of colorectal cancer in women. Cancer Epidemiol Biomarkers Prev. 2005;14(4):850-855. doi:10.1158/1055-9965.EPI-04-0661

22.             Djiogue S, Nwabo Kamdje AH, Vecchio L, et al. Insulin resistance and cancer: the role of insulin and IGFs. Endocr Relat Cancer. 2013;20(1):R1-R17. doi:10.1530/ERC-12-0324

23.             Leroith D, Scheinman EJ, Bitton-Worms K. The Role of Insulin and Insulin-like Growth Factors in the Increased Risk of Cancer in Diabetes. Rambam Maimonides Med J. 2011;2(2):e0043. doi:10.5041/RMMJ.10043

24.             Yoon YS, Keum N, Zhang X, Cho E, Giovannucci EL. Hyperinsulinemia, insulin resistance and colorectal adenomas: A meta-analysis. Metabolism. 2015;64(10):1324-1333. doi:10.1016/j.metabol.2015.06.013

25.             McKenzie AL, Hallberg SJ, Creighton BC, et al. A Novel Intervention Including Individualized Nutritional Recommendations Reduces Hemoglobin A1c Level, Medication Use, and Weight in Type 2 Diabetes. JMIR Diabetes. 2017;2(1):e6981. doi:10.2196/diabetes.6981

26.             Westman EC, Yancy WS, Olsen MK, Dudley T, Guyton JR. Effect of a low-carbohydrate, ketogenic diet program compared to a low-fat diet on fasting lipoprotein subclasses. International Journal of Cardiology. 2006;110(2):212-216. doi:10.1016/j.ijcard.2005.08.034

27.             Yancy WS, Olsen MK, Guyton JR, Bakst RP, Westman EC. A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia. Ann Intern Med. 2004;140(10):769-777. doi:10.7326/0003-4819-140-10-200405180-00006

28.             Garg A, Grundy SM, Unger RH. Comparison of Effects of High and Low Carbohydrate Diets on Plasma Lipoproteins and Insulin Sensitivity in Patients With Mild NIDDM. Diabetes. 1992;41(10):1278-1285. doi:10.2337/diab.41.10.1278

29.             Gower BA, Chandler-Laney PC, Ovalle F, et al. Favourable metabolic effects of a eucaloric lower-carbohydrate diet in women with PCOS. Clinical Endocrinology. 2013;79(4):550-557. doi:10.1111/cen.12175

30.             Yuan X, Wang J, Yang S, et al. Effect of the ketogenic diet on glycemic control, insulin resistance, and lipid metabolism in patients with T2DM: a systematic review and meta-analysis. Nutr Diabetes. 2020;10(1):1-8. doi:10.1038/s41387-020-00142-z

31.             Gu Y, Yu H, Li Y, et al. Beneficial Effects of an 8-Week, Very Low Carbohydrate Diet Intervention on Obese Subjects. Evidence-Based Complementary and Alternative Medicine. 2013;2013:e760804. doi:10.1155/2013/760804

32.             Meng Y, Bai H, Wang S, Li Z, Wang Q, Chen L. Efficacy of low carbohydrate diet for type 2 diabetes mellitus management: A systematic review and meta-analysis of randomized controlled trials. Diabetes Research and Clinical Practice. 2017;131:124-131. doi:10.1016/j.diabres.2017.07.006

33.             Huntriss R, Campbell M, Bedwell C. The interpretation and effect of a low-carbohydrate diet in the management of type 2 diabetes: a systematic review and meta-analysis of randomised controlled trials. Eur J Clin Nutr. 2018;72(3):311-325. doi:10.1038/s41430-017-0019-4

34.             Nielsen JV, Joensson EA. Low-carbohydrate diet in type 2 diabetes: stable improvement of bodyweight and glycemic control during 44 months follow-up. Nutrition & Metabolism. 2008;5(1):14. doi:10.1186/1743-7075-5-14

35.             Unwin DJ, Tobin SD, Murray SW, Delon C, Brady AJ. Substantial and Sustained Improvements in Blood Pressure, Weight and Lipid Profiles from a Carbohydrate Restricted Diet: An Observational Study of Insulin Resistant Patients in Primary Care. International Journal of Environmental Research and Public Health. 2019;16(15):2680. doi:10.3390/ijerph16152680

36.             CDC. By the Numbers: Diabetes in America. Centers for Disease Control and Prevention. Published October 25, 2022. Accessed January 20, 2024. https://www.cdc.gov/diabetes/health-equity/diabetes-by-the-numbers.html

The Study That MIGHT Change Lipidology

Last weekend, UCLA cardiologist Dr. Matthew Budoff presented preliminary baseline data at the World Congress on Insulin Resistance, Diabetes, and Cardiovascular Disease that could theoretically, potentially, eventually, help turn the fields of lipidology and cardiology on their heads. 

The first of its kind prospective (ie. forward-looking) study directly assesses arterial plaque and calcification in a population of individuals with extremely high LDL-C resulting from a very low carbohydrate diet (Why this happens HERE). This population, while not entirely uncommon, is largely unstudied and may offer a number of clues to the true nature of lipid behavior and cardiovascular disease. 

Why is this? Because these individuals have very, very high LDL-C - an average of 272 mg/dl. Remember, conventional medical guidance considers an LDL-C above 100 mg/dl to be "high" while average is something around 120 mg/dl. 272 mg/dl is way past the 99th percentile and is more than 40% higher than the American Heart Association's threshold for automatic, no-questions-asked high-intensity statin therapy. Factor in the subject's average age of 56 years and they should, in theory, seem like a no-brainer for lipid-lowering therapy. 

These people should be at extreme risk for cardiovascular disease, should they not? Well, yes...if the traditional paradigm is correct. But the lipid-heart hypothesis is not nearly the settled science the AHA, pharmaceutical companies, and the medical establishment would have you believe. Instead, there are I believe two principle theories by which atherosclerotic cardiovascular disease may develop: 

•  Theory 1 is that LDL-C and LDL particles themselves are the direct, primary, and uniquely necessary elements of atherosclerotic disease. Elevated levels of LDL particles and LDL-C increase your risk for such disease by increasing the chance that, over time, more and more of these particles will become trapped in the wall of the blood vessel and ultimately lead to the development of plaque, arterial occlusion, etc. This is the common theory advanced by the medical industry. 

• Theory 2 is that LDL particles damaged as a result of oxidative stress or hyperglycemia are the target of immune cells whose function is to trap the damaged particles for recycling and removal. When poor metabolic efficiency, hyperglycemia, and increased oxidative stress lead to an excessive number of damaged LDL particles, this process occurs at a greatly increased rate. The development of plaque, arterial occlusion, etc. is fundamentally an inability of the body to remove and recycle these damaged particles as quickly as they accumulate. I've written many thousands of words about why I favor this theory. 

Now the subjects in this study are excellent candidates to test these theories because they not only have very high LDL-C, but also good metabolic health (HDL = 90, Triglycerides = 64, BP = 117/76, A1C = 5.4%). This means the key sentence in Theory 2 ("poor metabolic efficiency, hyperglycemia, and increased oxidative stress...") is of limited relevance and allows a unique opportunity to compare the two theories. If Theory 1 is correct, these individuals should rapidly develop cardiovascular disease. If Theory 2 is correct, they should not.

So far we only have preliminary, baseline date, which you can watch be presented HERE, but which I'll summarize briefly:

CAC and plaque scores for low-carb and control groups

• The researchers assessed two direct measures of atherosclerotic disease - coronary artery calcification and a "total plaque score" (calculated via CT angiography). These were measured in both the low-carbohydrate group and a control group matched for age, metabolic health, etc. The only major difference between the two groups was LDL-C, which was more than twice as high in the low-carb group. 

• The researchers will assess both of these metrics again in another year to assess any disease progression in each group

• The majority of subjects in each group had coronary artery calcification scores (CACs) of 0, indicating no calcification (CACs of significantly at-risk individuals commonly range from 100-400 or higher).

• Total Plaque Score is calculated from 0 to 45 (0-3 at each of 15 different potential plaque sites). In the low-carb group, the median subject had a TPS of 0 with an interquartile range (the middle 50%) of 0-2. No subject had a TPS greater than 12. The control group had a median TPS of 1 with an interquartile range of 0-4. The difference between the two groups was not statistically significant. 

• There was no difference in CAC or TPS between the low-carb, high LDL-C group and the control group.

• There was no relationship in either group between LDL-C levels and measured plaque.

Now, it should be noted that CACs and TPSs of 0 are not particularly remarkable. In fact a little more than half of 56 year olds have a CAC of 0 (you can play around on this NLHBI site if you'd like to see). Its normal and healthy to be free of coronary calcification. But what makes this study so potentially fascinating is that these subjects aren't considered "healthy" in a traditional sense. Years of extremely high LDL-C should predict the impending doom of atherosclerosis, but so far at least this group shows little and often no disease progression whatsoever. In fact, their cardiovascular disease state is indistinguishable from matched subjects with good metabolic health and no elevated LDL-C. 

We'll have to wait until 2024 for follow-up results, in which actual plaque progression in each group will be compared. But if two groups with similar metabolic health yet vastly different LDL-C levels continue to demonstrate identical disease states (or the lack thereof), it would lend significant credence to the notion that metabolic health and other associated factors, rather than LDL Cholesterol, drive chronic cardiovascular disease. Ideally, this would help launch a number of other studies to further challenge common assumptions and explore underappreciated aspects of lipidology and cardiovascular disease. Will that be the case? TBD...

Fuck Around and Find Out....

 ....That Your Underlying Health Is Still in the Trash

This is probably going to get long, and I’m kind of a broken record at this point. This will be the third post this year in which I detail the ways in which I’ve been unable to move fully past my autoimmune condition, or made a mistake, or failed to be as absolutely diligent as is necessary to keep my neurological symptoms at bay. I’ve messed up, again, and the ramifications of doing so have me deeply contemplative. So I’m gonna monologue for a bit.

I won a race a couple months ago. It was amazing, truly one of the greatest days of my life. I overcame so much to get to that point. I wrote about it here – About keeping neurological complications at arm’s length and about the unusual ways in which my body failed to respond like I’m accustomed to when racing.

When things are bad, as they’ve been lately, my fine motor control and muscle function are noticeably impaired to a degree of, I dunno….lets say 30 percent. I twitch and shake, I bump into things, I drop things, I struggle sometimes with balance. I had none of those problems during the race. But it was still there, just a little…tiny…bit. Lets call it 2 or 3 percent now instead. My legs wouldn’t respond quite the right way when running hard. They cramped and seized early in the race and I had to fight my body the last 45 minutes of the race. I won in large part, I think, not by outright running faster but by taking risks on the technical sections and being willing to go all the way over the edge to win a small local race.

I had been eating a lot of dried mango in the week leading into the race. It was a food I had been eating a bit with some regularity in small amounts, but only now was consuming the way I had been consuming blueberries and bananas. And for whatever reason, it doesn’t work for me. It induces neurological symptoms, to at least some degree. It became apparent as I experimented the week after the race that the symptoms I described before my first race – “intermittent headaches, cervical numbness, peripheral fatigue and tingling” – came and went in concert with appreciable mango consumption.

Ok, so we found another food I probably shouldn’t be eating. Easy enough – In fact I raced again the following week to better physical results. This race was hillier and longer, a 25k trail race (or 26.5k, but who’s counting?) in what they call “Mountain Maryland.” I lost – my 23^rd (!!!) career runner-up finish – but raced sooooo much better than I had the week prior. The two of us ran together for 20k before I totally exploded hiking up a ~30% climb with about 4 miles to go. While the week prior my body rebelled in the early miles, this time I had no such problems. I raced normally, and it was great. At this point, in early November, I felt so, so good about things.

A couple days later I got a flu shot. This was the third time since the onset of my autoimmune condition that I’d done so. The first two were basically fine – bad side effects, but difficult to assess any transient effect on my neurological symptoms as they were far more present generally one and two years ago. I had a day of obnoxious side effects again, and took it easy the day after. On day 2, I ran twice just like I had planned. Problem was I shook and trembled the entire way. I felt completely detached from my legs, which simply didn’t move the way I wanted them to. It’s so weird to describe – its like the dial-up internet of motor function, like I can think about moving my leg and then sit and wait for it to finally happen. It’s a very shaky and unstable feeling.

Anyway, I ran twice. Had to stop a bunch to rest. Finally shuffled my way though an awkward 15 miles. And you know what? I did it again the next day. I felt worse and worse as the run progressed, but I got it done. And again the day after that, but this time 22 miles of suck. My resting heart rate was super elevated, I was having hot flashes, my limbs went numb whenever I sat down, my neck and head hurt like hell. But I shuffled through 22 miles anyway. Because I was too stubborn not to. And then I finally snapped a little bit. Those three days had been my worst in months. I was only weeks removed from feeling 100% normal and had 2 more races scheduled in the next few weeks. I was, to put it mildly, frustrated. And I gave into those emotions – I pigged out on cheese, salami, Naked fruit smoothies, plantain chips. Nothing acutely terrible, but several things at once that would all negatively impact my health and symptoms.

The next week, on Thanksgiving, still not feeling quite normal, I trudged through a few miles with my wife before completely giving up mid-run. Things just weren’t right and I had had enough. I told her I was done, I went home and, this time, I gave in completely. It was Thanksgiving after all, family was in town, and I hadn’t been quite right in a couple weeks or more. So what fucking difference would it make if I just let go and acted like a normal person? I drank hard cider, ate mashed potatoes and gravy, ate ice cream…I did Thanksgiving. And I cooked a good turkey, dammit.

And I felt it. I forced my way through the next day with ibuprofen and coffee (itself a major trigger of symptoms that I’ve avoided for some time), but spent the next couple days, including my 33^rd birthday, largely in bed. For months I had planned to run 33 miles on my birthday. Its something I had done a couple times when younger and wanted to do again, in part as an exclamation point on my triumph over my autoimmune condition. Instead I spent the day as I described above - I twitched and shook, I bumped into things, I dropped things, I struggled sometimes with balance. I laid on the couch and all my limbs went numb. I had a really bad day.

It was, frankly, really depressing. And this is part of where I get particularly contemplative – for two and a half years I’ve felt like I’m not allowed be upset, or to feel disheartened or frustrated when things are bad. Honestly I feel I’ve been, at least in part, conditioned to feel that way. I’ve been dismissed so frequently that every time I allow myself to experience any human emotion, I feel like I’m providing ammunition to all the doctors who look at half a dozen adverse autoimmune markers and still think this is all in my head.

Last year I had a doctor accuse of me of not actually wanting to be healthy. I tried to explain how massive a difference diet made – a year later literally a difference between winning races and spending all day stuck in bed, numb and twitchy. My approach was not only working, it was and is validated by dozens of studies and academic papers, and a functional understanding of evolutionary biology. But I couldn’t explain why I was approaching things the way I was, because she was raising her voice and cutting me off. She was accusing me of leaning into it, of choosing this, and enjoying this in some perverse way. She was accusing me, if I declined to take an antidepressant for my dizziness, numbness, migraines, impaired motor control, and stabbing neck, face, and cerebral pain, of choosing this for myself and refusing to actually solve the problem. This doctor was not alone in her assumptions.

I was positive for literally every marker of neuropsychiatric lupus. Symptoms of that condition include acute confusional state, anxiety disorder, cognitive dysfunction, mood disorder, and psychosis. I suffered (and when things are bad, still sometimes suffer) from every one of those symptoms. Suffering from mental, neurological, or cognitive symptoms does not mean I’m making this shit up. I’m not faking anything because I like the attention, and I do not want to be sick. It is, contrary to the opinion of seemingly every doctor and every fucking wannabe medical expert, possible for the nervous system to be subject to actual physical damage. Or to be the focus of a persistent autoimmune condition. It does not have to be a goddamn serotonin problem. It does not have to be a mental health problem. It can be a real, legitimate, physical disease.

But its been suggested, over and over, by doctors and “experts” and even normal people in my life that its all in my head. And I think I fight that specifically as hard as I can, for as long as I can. It frankly fucking sucks to be so diligent about everything you do, all day every day. It sucks to not be able to eat “normal” food without going numb and tripping up the stairs.  I should never have done what I did. I should never have eaten those things. I shouldn’t have given in and invited a greater relapse of neurological problems.

But I did. I gave in. Twice in less than two weeks I failed to be optimistic, and tough, and strong. I’ve so relentlessly pursued a return to health and fitness. I’ve run and lived and existed through so much pain and discomfort and impaired function and every so often I’ve failed to keep my head screwed on straight. And it makes me fail like a failure. Like I’ve compromised myself as a person, and proved right all the doctors and people who think I’m making this up, or who think I’m some kind of vaccine conspiracy theorist, or have completely refused to honestly engage with me for whatever other reason.

So where am I now? I’m trying to let go of all that and move on. I don’t really expect anyone wants to read all this but being open about my experiences helps me do those things. I’m trying to forgot about the doctors who have dismissed my condition or tried to simply diagnose me with depression, and accept that every so often I’m going to feel unhappy and frustrated with where my health is at, and that’s fine. I’m trying to accept it as part of the process, rather than view it as weakness or failure. More immediately, I’m about to start my third week- (or so) long fast. I actually feel pretty decent now and am exercising a bit, but given that my underlying health hasn’t progressed as far as I’d been assuming a month or two ago, I think it prudent to fast for a while and see if I can’t take another significant step forward.

Within two weeks, I’m going to feel “perfect” and be running every day. I’ll get back to it, training every day and eating the few things that don’t trigger any symptoms (no mango!) with no real plans to expand my diet any time soon. I don’t think there will be any racing until maybe April or so, but I’m planning on being in much better shape than I was this fall. I don’t have any specific goals in mind right now, but I do think my best races are still in front of me. I am persistently optimistic that this will be the case. And I’m hoping to get there, and be fully healthy, some time in the next calendar year. I guess we'll see...

Thanks for reading. All the best

So... I Won a Race

What: Lake Fairfax 10 Mile

When: October 29, 2023

Where: Reston, Va

Stats: Trail Race, ~10 miles, ~1000ft ascent

Result: 1st Overall, 1:13:09 (Results, Strava)

I won a race!

It wasn’t a big race. But it was, without question, the biggest race of my life.

Because it was a day I used to legitimately believe would never come. I didn’t run for over a year and a half, and frankly spent most of that time far more concerned with ever again living a fully functional life - With making it out the other side, with moving and sleeping and thinking like a normal healthy person. When I couldn’t stand up out of bed or walk in straight line, racing was often the furthest thing from my mind. And even if I made it back to some kind of normalcy, for some two years I never really believed I’d seriously compete at the front of another race.

But…. here we are. More than four full years after crossing the finish at Kona I finally, finally, finally found myself back on a start line. A much smaller, more low-key start line – a local race with about a hundred people. But a perfect first race back, and one I’d been counting the days to for quite some time.

Chamonix

How’d I get here, from a summer update that was still less than optimal?

Things have honestly gone extremely well lately. I’ve been delicate and disciplined and careful with every aspect of my health. For a good eight weeks anyway I’d been training daily with virtually no neurological symptoms at all. That even included a trip to Europe (running and hiking in Chamonix, France, it turns out, is basically unbeatable) during which I managed to avoid dietary or lifestyle “mistakes” of any kind. Without a doubt, this was the best stretch so far.

The week of the race wasn’t exactly perfect, however, and I wasn’t even fully certain I’d race on Sunday if things didn’t come around a bit. Nothing was terribly bad by any stretch, but I felt limited/impaired enough (by intermittent headaches, cervical numbness, peripheral fatigue and tingling) after work on Thursday and Friday that the race was in at least some degree of doubt. But, Sunday came as the neurological symptoms went, and before I knew it I was racing again.

 I don’t really know what to write about the actual race. It was a cool little event! A 10(ish?) mile trail race put on by a fantastic local race company. Mostly single track through the woods, but not particularly technical or hilly as far as single track through the woods goes. There was like 1000m of easy grass and dirt before the trail part, and a friendly guy named Scott pulled me out way too fast for my current fitness. I finally let him go and assumed he was gone for good, but I kept catching glimpses of him through the trees and finally pulled all the way back almost eight miles in.  

My legs had been rebelling since the early miles, in a crampy/seizey kind of way. Found this very frustrating, since I had run the first half of the course at roughly race effort the week before with no such problems. The nerve pain/tingling from the previous days was gone but it felt like I was having a lot of trouble producing the force I wanted (it doesn’t help at all that I’ve barely run hard in years). This actually felt more pronounced on the super smooth, runnable sections where Scott kept putting additional meters into me.

Catching up on the more twisty/technical section seemed like the only chance to press an advantage - Hammered it down a tight, somewhat rocky downhill to open a gap and just tried to hold on the rest of the way. Kept the legs in one piece the last ten minutes and ended up about 30 seconds clear by the end after what turned into about as painful a last mile or two as I remember. A relative lack of race fitness, a total lack of any hard training, and some minor lingering neuro problems combined to create a frankly strange end of race experience, where I felt my body fighting to keep everything together rather than being strictly limited by flat-out aerobic output. 

Finishing didn’t feel like I expected it to. When I had played it through in my mind over and over in the weeks leading in to the race, I imagined I’d be highly emotional at the finish. The thought of winning a race three weeks out had been making me emotional, after all. But in the moment, it was basically the opposite - It was probably the least emotionally present I’d ever been winning a race. Part of it was everything I just wrote about not being in great shape to race – trying to pull it all back together laying in the finishing chute leaves little room for emotion. Part of it was that the gravity of the moment just wasn’t hitting me like I thought it might.

 

I was incredibly excited to be sure– basically bubbling over really. But in that sense it was just like any other race, any other good result. I just felt so much joy and relief to finally be home. Not until my wife finished a bit later did I feel any of the “emotional” bits I expected. And not until I started writing this has it really sunk in that I’m really racing again, and doing it without any apparent consequence to my health.

But I am racing again! And for a second time in short order. I’m writing this the Thursday after Lake Fairfax, with plans for race number two already this Sunday, a fairly low-key 25k trail race in western Maryland. It took a day or so longer to feel recovered than it might have a few years ago, but the legs are ready to go and I feel better from a basic health perspective than I did a week ago. Let’s see if we can make it two in a row! Onward and upward!

Chamonix Ibex