Thursday, April 29, 2010

Tender cuts of meat for the grill: Filet mignon and bison

Filet mignon is one of the tenderest cuts of beef. It is also one of my favorites. Filet mignon comes from the tenderloin area (see this picture), which is not a weight-bearing area and thus is very tender. The bison cuts I get here in South Texas are close in terms of tenderness, but not as tender, probably because they are from the round area.

One steak of either filet mignon or bison will yield about 100 g of cooked meat, with 30 g of protein and 10 g of fat. About half of that fat will be saturated and half monounsaturated (as in olive oil). It will provide you with plenty of vitamins (particular B vitamins) and minerals. Good amounts of selenium, phosphorus, zinc and potassium.

On the photo below (click on it to enlarge), the bison steak is at the top. The other pieces are all filet mignon cuts. They are all medium-cooked. I cooked two plates of these, for 6 people. All ate to satisfaction, with a side salad. The leftovers are delicious for breakfast in small amounts.

For the filet mignon, I think you really have to go to a specialty meats store (butcher) and make sure that they cut the smaller tail end of the tenderloin muscle. You will be paying a lot for it, so it makes sense to be choosy. Experience butchers will cut it right in front of you and won’t mind your choosiness.

Below is a simple recipe; simple like most of the recipes on this blog. I like my meals quick and delicious.

- Prepare some dry seasoning powder by mixing sea salt, garlic power, chili powder, and a small amount of cayenne pepper.
- Season the steaks at least 2 hours prior to placing them on the grill.
- Grill with the lid on, checking the meat every 10 minutes or so. (I use charcoal, one layer only to avoid burning the surface of the meat.) Turn it frequently, always putting the lid back on.
- If you like it rare, 20 minutes (or a bit less) may be enough.

These are as tender as any piece of beef can possibly get. No need for any tenderizer juices during seasoning. If you are doing both filet mignon and bison together, either eat only bison or bison first. Because once you taste the filet mignon, the bison cut may taste a bit hard!

For me the filet mignon is a 10-dollar per pound treat for special occasions. The price of the bison cut is about the same, at least here in Laredo, Texas, where I get it shipped from Dakota via my local supermarket. You can also get it online.

By the way, some folks like to say that bison is the “salmon of the prairie”. This is in reference to bison’s omega-3 content. Well, here is the polyunsaturated fatty acid composition of 100 g of bison steak: 29 mg of omega-3, and 197 mg of omega-6. For salmon it is 1424 mg of omega-3, and 113 mg of omega-6.

Salmon of the prairie or not, I love it!

Wednesday, April 21, 2010

Interesting links


2016 Virtual Paleo Summit presentation

Health Data Analysis with HCE

Managing Multiple Health Variables with HCE

Ned Kock interviewed on Episode 477 of The Livin’ La Vida Low-Carb Show with Jimmy Moore

Reality check

Many people fall prey to scams that are presented as valid alternative medicine options for diseases that are psychosomatic in nature. The sites below can be helpful in avoiding these scams.


Somatic symptom disorder

Various health sites

Below is a list of links to web sites that deal with health issues in general. These have been moved from the previous “favorite links” area to this post so that some space could be saved on the main page of the blog. Some of these sites are excellent sources of research-based and reliable information. Others are somewhat light in content, but still interesting.

Alan Aragon

Animal Pharm

Ancestralize Me!

Anthony Colpo

Arthur De Vany

At Darwin's Table

Athletics by Nature

Barefoot Ted's Adventures

Beef and Whiskey

Big Muscles Fast

Blaine's Low Carb Kitchen

Blood Sugar 101

Body by Science

Body Recomposition


Brad Pilon's Blog

Canibais e Reis

Cholesterol and Health

Colorado State University's Physiologic Effects of Insulin

Conditioning Research

Cooling Inflammation

Cut the Carb

David Mendosa

Diabetes Update

Diet Doctor

Discover Magazine Online

Dr. Bernstein's Diabetes Solution

Dr. Gabe Mirkin

Dr. Michael R. Eades

Dr. Nemechek's Integrative Medicine

Dr. Ron Rosedale

Entropy Production

Ernestine Shepherd

Evolution for Everyone

Evolutionary Psychiatry

Evolving Thoughts by John Wilkins

Exercise Prescription on the Net

Experiments in Lifestyle Design by Tim Ferriss

Fat Head

Fit 2 Fat 2 Fit

Free the Animal

Grassroots Health

Girl Gone Primal

Gnolls by J. Stanton

Health News Review

Healthcare Epistemocrat


Homo Consumericus

Hunt, Gather, Love

Hunter Gatherer


ItsTheWooo's The Scribble Pad

John Hawks Weblog

Julianne's Paleo & Zone Nutrition Blog

Lean Gains

Low-Carb for You

Lucas Tafur

Mark's Daily Apple

Matt Metzgar's Blog

Maxwell Murphy

Metabolism Society

Michael Barker's Type 2 Ketosis Prone Diabetes

Muscle and the City


My Carb Sane-Asylum

My Carb Sane Chronicles

Natural Messiah


Nigee's Diet & Nutrition Blog

Nourishing by Heart

Nutrition and Physical Regeneration

Nutrition, Health & Heart Disease

Omega-6 Fat News Commentary

Paleo Clinic

Paleo Diet

Paleo Hacks


Patrick Ward's Optimum Sports Performance

Pay Now Live Later

Philosophy of Weight Management

Prague Stepchild

Primal Montain

Primal Wisdom

Principle Into Practice

Protein Power


Rambling Outside the Box

Ramblings of a Carnivore

Raw Food SOS

Ray Peat

Robb Wolf

Ron Brown's The Myth of Loose Skin

Sandwalk by Laurence Moran

Scooby's Home Bodybuilding Workouts

Seth Roberts's Blog

Skyler Tanner

Sock Doc - Natural Injury Treatment & Prevention

Son of Grok

Spark of Reason

Stella Style

Survivorman - Discovery

That Paleo Guy

The Carnivore Health Weblog

The Daily Lipid

The Evolution & Medicine Review

The Heart Scan

The Healthy Skeptic

The Livin' La Vida Low-Carb Show

The Paleo Diet

The Paleo Diet Blog

The Weston A. Price Foundation

Theory to Practice

Vitamin D Council

Vitamin D Wiki


Whole Health Source

Wikipedia - Strength Training

Wildly Fluctuating

Zero Currency, Moneyless World - By Daniel Suelo

Zeroing in on Recovery

Zoe Harcombe

180 Degree Health

Tuesday, April 13, 2010

Long-term adherence to Dr. Kwaśniewski’s Optimal Diet: Healthy with high LDL cholesterol

This is a study (Grieb, P. et al., 2008; full reference at the end of this post) that I read a few years ago, right after it came out, and at the time I recall thinking about the apparent contradiction between the positive effects of the Optimal Diet and the very elevated LDL cholesterol levels among the participants. I say “contradiction” because of the established and misguided dogma among medical doctors, particularly general practitioners, that decreasing LDL cholesterol levels is the best strategy to avoid cardiovascular disease.

The Optimal Diet is one of the best examples of a healthy diet where LDL cholesterol levels are generally high, in fact much higher than most people are willing to accept as healthy today. (In this study, LDL cholesterol levels were calculated based on the Friedewald equation.)

It is not uncommon to see people concerned about their high LDL cholesterol levels after adopting a low carbohydrate diet. (A low carbohydrate diet is, generally speaking, a high fat diet.) This study shows that this is a rather common thing, and also that it is not something that those who experience it should be too concerned about. To be convinced of this, one can always do a VAP test (see this post for a link to a sample VAP test report) and check his or her LDL particle pattern.

The study presents the Optimal Diet as the Polish equivalent to the Atkins diet. It states that the Diet’s main characteristic is maintaining the proportion of proteins:fat:carbs. in the range of 1:2.5-3.5:0.5, with no restriction on the amount of food consumed. In fact, as you will see in this post, more than 70 percent of the calories consumed by the study participants came from fat.

Easily digestible carbohydrate-rich foods are not part of the Optimal Diet. More specifically, the following foods were listed as not being allowed in the Optimal Diet: sucrose, sweets, honey, jam, white rice, bread, starches in general, beans, potatoes (only in small amounts), and sweetened drinks. Also, the Optimal Diet is definitely a low carbohydrate diet, but not what is often referred to as a "very low carbohydrate diet". In this study, the typical carbohydrate intake per day was around 60 g.

Thirty-one healthy people participated in the study, 17 women and 14 men. The average age was 51.7 (standard deviation: 16.6). They had self-reportedly adhered to the Optimal Diet for at least 1 year prior to the study; the average period of adherence was 4.1 years (standard deviation: 1.9). So, the vast majority had been on the diet for more than 2.2 years, about half for 4.1 years or more, and about one-sixth for more than 6 years. (Check this post if you want to know how these figures can be calculated based on the average period of adherence and the standard deviation.)

The table below (click on it to enlarge) shows anthropometric and physiologic characteristics of the participants. Note that longer adherence to the Optimal Diet (right end of the table) was associated with lower systolic and diastolic blood pressure, as well as lower body mass index (BMI). (It was also associated with lower height and BMR, so I am guessing that more women tended to be long-term adherers than men.) Most of the participants had BMIs in the normal range, with only one in the obese category. That was a 43-year-old man who followed the diet for 1.5 years; he had a BMI of 34.1.

The macronutrient distribution of the Optimal Diet is shown on the table below (click on it to enlarge), as followed by the participants. As you can see, protein intake was not that high; about 53.9 g per day on average for men, a bit less for women. Note the percentage of calories from fat: more than 77 percent for men and 72 percent for women. Given the BMIs just discussed, one can safely say based on this that eating a lot of fat did not make the participants fat.

The table below (click on it to enlarge) has some interesting health markers. Note that free fatty acids (FFAs) were elevated. This is to be expected, as these folks were burning fat for energy most of the time, and not as much glucose. The FFAs are not really “free”, but bound to a protein called albumin, which is abundant in human blood. FFAs yield large quantities of adenosine triphosphate (ATP), the main energy “currency” used by the body.

These levels of FFAs are also usually associated with mild ketosis, where ketones are produced by the body and used for energy. Unlike albumin-bound FFAs, ketones are soluble in water, and thus circulate freely through the blood. The mild ketosis experienced by the participants was possibly to the point where ketones showed in the urine. The article mentions this, and provides a measure of beta-HB (beta-hydroxybutyrate, a ketone body), which is elevated as expected, but does not provide urine or other blood ketone measures (e.g., blood acetone levels). Also note the fairly healthy fasting glucose levels, slightly higher in men than in women, but fairly low overall. Fairly healthy insulin levels as well; at the high end of what Stephan at Whole Health Source would recommend, but still significantly lower than the average insulin level in the U.S. at the time of the article's publication.

Finally, the table below (click on it to enlarge) shows lipids and a few other measures. Total cholesterol was on average a bit more than 278 mg/dL. LDL cholesterol was a bit higher than 188 mg/dL on average; high enough to make most doctors cringe today. Based on the means and standard deviations provided, we can estimate that about 16 percent of the participants had LDL cholesterol levels higher than 228.1 mg/dL. About 2.5 percent of the participants had LDL cholesterol levels higher than 268 mg/dL. And this is all after adhering to the diet for a relatively long period of time; even higher LDL cholesterol levels might have occurred right after adoption.

Yet average HDL cholesterol was a very high and protective 71.6 mg/dL. This high HDL and the relatively low triglycerides suggest a large-buoyant non-atherogenic LDL particle pattern.

Average HOMA(IR), a measure of insulin resistance, was a low 1.35 mU/mmol; strongly indicating, together with the relatively low fasting glucose levels, that the participants were far from being pre-diabetic, let alone diabetic.

Diabetes is a strong risk factor for cardiovascular disease, and many other health complications; much more so than elevated LDL cholesterol.

The Optimal Diet does not seem to be a diet for bodybuilders, but I would say that, overall, Peter at Hyperlipid has chosen a diet that makes some sense.


Grieb, P. et al. (2008). Long-term consumption of a carbohydrate-restricted diet does not induce deleterious metabolic effects. Nutrition Research, 28(12), 825-833.

Sunday, April 11, 2010

The Friedewald and Iranian equations: Fasting triglycerides can seriously distort calculated LDL

This post has been revised and re-published. The original comments are preserved below. Typically this is done with posts that attract many visits at the time they are published, and whose topics become particularly relevant or need to be re-addressed at a later date.

Friday, April 9, 2010

The huge gap between glycemic loads of refined and unrefined carbohydrate-rich foods

I often refer to foods rich in refined carbohydrates in this blog as among the most disease-promoting agents of modern diets. Yet, when one looks at the glycemic indices of foods rich in refined and unrefined carbohydrates, they are not all that different.

The glycemic index of a carbohydrate-rich food reflects how quickly the food is digested and generate a blood glucose response. Technically, it is measured as the area under a two-hour blood glucose response curve following the consumption of a portion of the food with a fixed amount of carbohydrates.

A measure that reflects much better the underlying difference between foods rich in refined and unrefined carbohydrates is the glycemic load, which is the product of the glycemic index of a food by the carbohydrate content in a 100 g portion of the food.

The glycemic load is also the reason for one known fact among diabetics. If a diabetic person eats a very small amount of a high glycemic index food, he or she will have a relatively small increase in blood sugar. If that person consumes a large amount of the same food, the increase in blood sugar will be dramatic.

The table below (click on it to enlarge) shows the remarkable differences between the glycemic loads of foods rich in refined and unrefined carbohydrates. It was taken from an article co-authored by Loren Cordain, Michael R. Eades, and Mary D. Eades (full reference at the end of this post).

At the time of this post’s writing, the article from which the table above was taken had a solid number of citations to it; a total of 74 citations on Google Scholar’s database. It is an excellent article, which I highly recommend reading in full (the link to the online full text is at the end of this post).

What is the reason for the differences in glycemic loads?

The answer is that foods rich in unrefined carbohydrates, even those with a high glycemic index (such as potatoes), are also packed with a number of other things – e.g., micronutrients, fiber, water, and even some protein. An Irish (white) potato is 75 percent water. By comparison, cereal, without milk added, is about 1 percent water. You have to add a lot of whole milk to it to make it a bit healthier. And even unsweetened whole milk is about 5 percent sugar.

There was nothing even remotely similar to modern foods rich in refined carbohydrates in the diet of our Paleolithic ancestors. In fact, the types of food rich in refined carbohydrates shown on the table above are very recent, typically dating back to less than a hundred years ago. That is, they are so recent that it is unlikely that any of us have genetic adaptations to those types of food.

Once one’s glucose metabolism is seriously impaired, which seems to be associated with consumption over many years of refined carbohydrates and sugars (as well as some genetic predisposition, which may have evolved among some of our ancestors), then even the foods with high glycemic index and low glycemic load (e.g., potato) will lead to highly elevated glucose levels if eaten in more than very small amounts.

Insulin resistant individuals should avoid even foods with high glycemic index and low glycemic load, as well as any food that significantly increases their blood glucose levels after a meal, because highly elevated glucose levels are toxic to various tissues in the body. The longer those highly elevated serum glucose levels are maintained, the more damage is done; e.g., 2 hours as opposed to 30 minutes at 180 mg/dl. One reason why they are toxic is because they lead to high levels of protein glycation; this is a process whereby sugar binds to protein and “warps” it, impairing its functions.

Generally speaking, the more glycation is going on in our body, the more accelerated is the aging process.


Loren Cordain, Michael R. Eades, Mary D. Eades (2003). Hyperinsulinemic diseases of civilization: More than just Syndrome X. Comparative Biochemistry and Physiology: Part A, 136, 95–112.

Tuesday, April 6, 2010

Low fasting triglycerides: A marker for large-buoyant LDL particles

Small-dense LDL particles are particles that are significantly smaller than the gaps in the endothelium. The endothelium is a thin layer of cells that line the interior of arteries. Those gaps are about 25-26 nanometers (nm) in diameter. Small-dense LDL particles can contribute a lot more to the formation of atheromas (atherosclerotic plaques) in predisposed individuals than large-buoyant LDL particles.

Note that typically LDL particles are about 23-25 nm in diameter in most people, and yet not everybody develops atheromas. It is illogical to believe that evolution made LDL particles within those ranges of size to harm us, given the size of the gaps in the endothelium, unless you believe in something like this joke theory. There are underlying factors that make individuals much more prone to the development of atheromas than others.

One of those factors is chronic inflammation, which is caused by: chronic stress, excessive exercise (aerobic or anaerobic), and a diet rich in refined carbohydrates (e.g., white bread, pasta) and refined sugars (e.g., high fructose corn syrup, table sugar).

Can a standard lipid profile report tell me anything about my LDL particle pattern?

Yes, check you fasting triglycerides. If they are below 70 mg/dL, it is very likely that you have a predominance of large-buoyant LDL particles in your blood. That is, your LDL particle pattern is most likely Pattern A (see figure below, from:, the least atherogenic of the patterns identified by a Vertical Auto Profile (VAP) test. This test is more sophisticated than a standard lipid profile test, where the LDL cholesterol is typically calculated. For a discussion of a sample VAP test report, see this post.

So, you can get a rough idea about your LDL pattern type only by checking your fasting triglyceride levels on a standard lipid profile test report, if you cannot or do not want to have a VAP test done. The higher your fasting triglyceride levels are, above 70, the more likely it is that your LDL particle pattern is Pattern B, which is the most potentially atherogenic pattern.

Large-buoyant LDL particles often lead to high measured LDL cholesterol levels. This situation is analogous to that of water-filled balloons. If you have 10 balloons, each holding 0.5 L of water, then your total water amount is 5 L. If the same balloons are filled with 1 L of water each, then your total water amount is 10 L. That is, even though the number of LDL particles (analogous to the number of balloons) may be the same as that of a person with low LDL cholesterol, large-buoyant LDL particles have more cholesterol (water content in each balloon) in them, and lead to higher measured LDL cholesterol (total amount of water in the balloons) levels.

This leads to the counterintuitive situation where your LDL cholesterol levels go up, and your risk of developing cardiovascular disease actually goes down.

Also worth keeping in mind is that fasting triglyceride levels are strongly and negatively correlated with HDL cholesterol levels. The higher your fasting triglyceride levels are, usually the lower are your HDL cholesterol levels. The latter are also provided in standard lipid profile reports.

How do you decrease your fasting triglycerides?

A good way to start is to do some of the things that increase your HDL cholesterol.


Elliott, W.H., & Elliott, D.C. (2009). Biochemistry and molecular biology. 4th Edition. New York: NY: Oxford University Press.

Lemanski, P.E. (2004). Beyond routine cholesterol testing: The role of LDL particle size assessment. CDPHP Medical Messenger, May 2004.

Sunday, April 4, 2010

Genetic clustering of metabolic disorders: Meet your relatives

As noted in this post, it is possible for a food-related trait to evolve to fixation in an entire population in as little as 396 years; not the millions of years that some believe are necessary for mutations to spread.

Moreover, evolution through fixation can occur in the absence of any selective pressure. That is, traits that are neutral with respect to fitness may evolve by chance, particularly in small populations. (A group of 100 individuals who made it to the Americas after a long and grueling trek would fit the bill.) This rather counterintuitive phenomenon is known as genetic drift (Hartl & Clark, 2007; Maynard Smith, 1998).

Fast evolution of traits certainly applies to polygenic traits, such as traits associated with nutrient metabolism. Polygenic traits are traits that are influenced by multiple genes, with those genes acting together to influence the expression of the trait.

Moreover, a mutation in one single pleiotropic gene (a gene that influences various traits) can lead to dramatic changes in interconnected phenotypic traits. This includes traits associated with complex processes involving multiple body tissues, such as glucose and fat metabolism.

Some disagree, arguing that complex traits need much longer to evolve. I wish I could be convinced of that; it would make our understanding of health issues and related predictions a lot easier. For example, we could zero in on Homo erectus as our target for an ideal Paleolithic diet.

Unfortunately, when you look around, you see people with food allergies, metabolic disorders, and other food- and lifestyle-related complications; and those problems cluster among people who seem to share recent common ancestors. Interestingly, in many cases those people do not look alike, in spite of sharing common ancestors.

For example, here in South Texas, it is clear that people from Amerindian ancestry (like me, although mine is from South America) are a lot more predisposed to diabetes than others. There are exceptions, of course; we are talking about probabilities here. Especially common here in South Texas are people with South and Central American Indian ancestry; less common but also represented are descendants of North American Indian tribes such as the Kickapoos.

Very recent food inventions, such as refined carbohydrates, refined sugars, omega-6-rich vegetable oils, and hydrogenated fats are too new to have influenced the genetic makeup of anybody living today. So, chances are, they are bad for the vast majority of us. Sure, a small percentage of the population may not develop any hint of diseases of civilization after consuming them for years, but chances are they are not going to be as healthy as they could be.

Other not so recent food inventions, such as olive oil, certain types of bread, certain types of dairy etc. may be better, in terms of overall health effects, for some people than for others. In fact, they may be particularly health-promoting for certain groups of individuals. The reason may be found in inherited metabolic traits. Learning about your ancestors could be helpful in this respect. The problem is that many people's ancestry is quite mixed; again, I give myself as an example - South American Indian, German, Italian, Portuguese ... and who knows what else.

Another, easier and perhaps more effective, way to figure out what particular foods, and in what quantities, may be healthy for you is to keep in touch with close and distant biological relatives; e.g., grandparents, parents, siblings, cousins (family gathering photo below from: It is likely that you share genes with them. If several of them developed a particular disease, and they consumed a lot of a certain type of food prior to that, then maybe that food should not be part of your diet.

This may also help you avoid making serious mistakes regarding health issues by acting too fast in response to laboratory test results. Relatives may share some quirky metabolic responses, which could be indicative of a disease at first glance and actually have no negative long term effects, and perhaps some positive ones.

For example, let us assume that a person, let us call her Mary, is in her early 50s and has been consuming a diet rich in refined carbohydrates and sugars for her entire life. Her fasting blood glucose looks pretty good at around 82 mg/dL.

Mary then adopts a diet that includes only vegetables and animal fat and protein. This new diet induces mild ketosis. She then notices that her fasting blood sugar is now 113 mg/dL, much higher than the previous 82 mg/dL. Mary’s doctor tells her that she may be pre-diabetic.

Mary knows that the change in diet was associated with the increase in fasting blood sugar, and reverts back to her diet rich in refined carbohydrates and sugars. Her fasting blood sugar goes down to 82 mg/dL, and she is happy. Her doctor congratulates her. However, she becomes obese and develops the metabolic syndrome in her late 50s, and several related diseases soon after.

Let us now look at a different scenario. After getting the 113 mg/dL fasting blood sugar reading on a mildly ketogenic diet, Mary talks to as many of her living relatives as she can. She asks many questions and finds out that a few of them were big meat and veggie eaters and had the same metabolic response. They are in their 60s and 70s and have no hint of diabetes. In fact, they are relatively lean and fairly healthy. She then sticks to her diet of only vegetables and animal fat and protein for life, and never develops the metabolic syndrome.

This fictitious case is based on the idea that low carbohydrate diets that induce mild ketosis may also induce physiological (not pathological) insulin resistance, leading to a version of the much talked about dawn phenomenon. This phenomenon, in this context, seems to be related to our good friend, but much maligned, palmitic acid. Several bloggers discussed it in excellent posts. Peter at Hyperlipid blogged about it here and here; Stephan at Whole Health Source blogged about it here.

Now, going back to keeping in touch with close and distant relatives. It is important to check your relatives’ lifestyle patterns as well, because diet is not everything, even though it is a major contributor to health outcomes. By lifestyle patterns I mean things like level and type of physical activity, sunlight exposure (which strongly influences vitamin D levels), and frequency and quality of social interactions (which reduce stress).

Regarding social interactions, it is worth noting that humans are highly social beings, and social isolation is almost universally detrimental to both mental and physical health.


Hartl, D.L., & Clark, A.G. (2007). Principles of population genetics. Sunderland, MA: Sinauer Associates.

Maynard Smith, J. (1998). Evolutionary genetics. New York, NY: Oxford University Press.

Thursday, April 1, 2010

Body mass index and cancer deaths in various US states

Ancel Keys is often heavily criticized for allegedly originating the fat phobia that we see today in the US and other countries, perhaps with good reason. But he has also made many important contributions to the health sciences.

One of them was the index known as body mass index (BMI), calculated based on a person's weight and height. Unlike other measures, such as body fat percentage and body fat mass, BMI is very easy to calculate; divide your weight (kg) by your height (m) squared.

BMI is strongly correlated with body fat percentage, and body fat mass. Very muscular people are exceptions; they may have a high BMI and yet reduced body fat.

Excessive body fat mass leads to chronic inflammation, due in part to elevated circulating levels of pro-inflammatory hormones such as tumor necrosis factor-alpha (cute name eh?).

Chronic inflammation, in turn, leads to increased incidence of cancer.

Thus it should be no surprise that having a BMI above 30 (obesity level) is strongly correlated with cancer death rates; see graph below (click on it to enlarge), from: Florida, 2009 (full reference at the end of this post).

The correlation for the graph above is a high 0.702, calculated as the square-root of the R-squared value shown at the bottom-right. The R-squared is the percentage of explained variance for cancer deaths, meaning that nearly 50 percent of the cancer deaths are "explained", or caused, by the BMI percentages.

One more reason to bring body fat down to healthy levels.

How do you do that? A good way to start is to replace refined carbohydrates and sugars with natural sources of protein and fat in your diet; eggs included, no need to worry about dietary cholesterol.


Florida, R. (2009). The geography of obesity. Creative Class, Nov. 25.