Archive for the ‘info’ Category

“I am Jill’s Liver.”

Some months back, I was lucky enough to have seen the Bodies Exhibition.  The cross-sectioned bodies give you an up close, three-dimensional, and most importantly, real view of the human body.

It was eye-opening. One of the most notable things to me was how big the liver was in comparison to the stomach, heart, or brain. It helped me to realize how amazing the liver is.  Most know how obviously vital the brain and heart are. The liver, however, doesn’t seem to get the attention it deserves. At three pounds,  it’s the largest glandular organ in the body. This might be fitting because the liver has a lengthy to-do list:

  • Filtering blood from the digestive tract before sending it to the rest of the body.
  • Detoxifying chemicals and metabolizes drugs.
  • Producing 80% of the body’s cholesterol needs. The liver adjusts its production according one’s diet: the more cholesterol one consumes, the less cholesterol it makes and vice versa.
  • Processing fructose.
  • Converting thyroid hormone from T4 (inactive form) to T3 (active form).
  • Using its significant storage capacity to house glycogen and  Vitamins A, D, K, and B12.
  • Secreting bile which aids in fat digestion.
  • Making proteins essential for blood clotting.

The liver is clearly a hard worker. It does its best to clean up the toxins we ingest and/or are exposed to. I was tempted to write the post in the first person as a homage to this scene in Fight Club, but I decided it might get ridiculous rather quickly. But honestly, it’s important to love your liver. The consequences of mistreating it are far-reaching:

Hepatitis: There are several types, but they are different forms of inflammation in the liver.

Non-Alcoholic Fatty Liver Disease (NAFLD): This is when excessive fat stores in the liver. This can lead to hepatitis and cirrhosis. The symptoms can include chronic fatigue, jaundice, upper abdominal discomfort, and edema.

Cirrhosis: This occurs when fibrous tissue builds up in the liver from replacing dead liver cells. Symptoms often don’t appear until the liver gradually shows signs of not being able to carry out its duties.  When they do show up, someone with cirrhosis might experience fatigue, nausea, loss of appetite and libido, sensitivity to medications (since the liver processes them), easy bruising/bleeding, etc.

Liver Cancer: The most common type of liver cancer is Hepatocellular carcinoma, and it is most commonly caused by Cirrhosis. Those with Hepatitis B or C are more likely to develop this form of liver cancer. Liver cancer shares many of the symptoms listed above. It can also cause gastrointestinal bleeding and liver failure. Liver cancer is mostly fatal: it can kill a patient within a year.

Like the liver, researchers are noting that the number of liver disease-related deaths has been underestimated. If viral hepatitis, liver cancer and obesity-related fatty liver diseases are included, then deaths from liver disease bump from the 12th leading cause of death to the 8th. And liver disease is the fourth leading cause of death for those between 45 and 64.

Furthermore, the liver plays a key role in the development of insulin resistance. Researchers have found that the liver makes and secretes a hormone  that causes insulin resistance: they found higher levels of selenoprotein P (SeP) in diabetic people in comparison with nondiabetic people. Furthermore, when researchers gave healthy mice SeP, they became insulin resistant, and their blood sugar increased. When they were given treatment to block SeP, their insulin resistance and blood sugar decreased.

This begs the question, “What do I have to do to keep my liver healthy?” The first place to start is to keep the major liver offenders in check: alcohol, cigarettes, trans fats, and sugar. Since the dangers of alcohol, cigarettes, and trans fats are more well-known, I will focus on fructose.

More and more studies are linking high levels of fructose consumption with fatty liver disease. Glucose is a sugar that is processed by every cell in the body; fructose, however, can only be processed by the liver. So eating lots of fructose makes the liver work harder. And, as the list at the beginning of this post illustrates, the liver is a 3 pound beast with more important things to do.

Interestingly, there is evidence that obesity and insulin resistance are greater risk factors for developing fatty liver than moderate alcohol consumption.

Fatty liver is an insidious disease. People with fatty liver are five times more likely to develop type 2 diabetes than those without fatty liver. Fatty liver is also correlated to insulin resistance and elevated serum lipids. And if fatty liver goes on untreated, it can lead to cirrhosis which can lead to cancer. Fatty liver develops earlier on the timeline of liver disease progression. Fortunately, there is plenty one can do to maintain liver health before it is too late:

  • Eat medium chained triglycerides like coconut oil, ghee, and MCT oil. These fats do not require bile, so they do not tax the liver.
  • Keep alcohol consumption slow and moderate. If this is difficult, seek professional help.

The Hormone That Cried Wolf

Gary Taubes wrote an interesting article in the New York Times. He outlines the studies indicating that excess sugar consumption  leads to fatty liver, insulin resistance,  obesity, diabetes, heart disease, and some cancers. He queries his way through the evidence to try to answer the question, “Is sugar toxic?”

First of all, let’s start out with some facts:

1. Taubes establishes that refined sugar (sucrose) is a 50-50 mixture of fructose and glucose. Fructose is what makes sugar sweet, which might partly explain the popularity of high fructose corn syrup, which is 55% fructose and 45% glucose. So  the maligned high fructose corn syrup is only 5% higher in fructose content than regular refined sugar.

2. It’s important to know that the body metabolizes fructose and glucose differently: the liver processes fructose, and every cell in the body processes glucose.  Complex carbs (rice, bread) are broken down into glucose.  The more fructose one consumes, and the smaller amount of time one consumes it in (say if it’s in a drink), then the harder the liver has to work.

3. The pancreas secretes insulin to respond to foods that raise our blood sugar, namely carbohydrates and sugars. The insulin scoops the excess sugar from our bloodstream and stores it in the liver and muscles in the form of glycogen. But if the reserves are full or too much sugar was consumed, the cells begin to ignore insulin.  The exhausted pancreas needs to pump out more insulin to get the same effect, and and the sugar is eventually stored in fat cells.

4. The process described above is called insulin resistance. To restate, this is when the pancreas cannot secrete enough insulin to manage rising blood sugar levels because the cells become resistant to insulin. Consequently,  the excess sugar and insulin remain in the blood stream for longer.  Chronic insulin resistance is also known as metabolic syndrome.

5. More and more evidence is linking sugar consumption with insulin resistance.

6. Insulin resistance and chronically elevated insulin levels are accepted as a significant risk factor (if not a precursor) to diabetes, obesity,  high blood pressure, low HDL cholesterol levels (the “good cholesterol”), and high triglycerides.

7. The World Health Organization’s International Agency for Research on Cancer studied large populations in 2004. Their findings state one is more likely to get cancer if they are insulin resistant, obese, and/or diabetic. Other researchers are finding this as well.

8. Furthermore, cancer researchers are finding that excess insulin (a symptom of insulin resistance) promotes tumor growth, and the cells of several human cancers need insulin for fuel/blood sugar. Insulin resistance seems to be at the center of several cumulative diseases.

9. Researchers currently studying insulin resistance assert that the accumulation of fat in the liver (fatty liver disease) is the likely cause of insulin resistance. Accumulation of fat  in the liver. According to the second point listed above, the liver processes fructose. So what causes fat to accumulate in the liver? Is it sugar, fructose consumption in particular? Yes, yes it is.

And if one were to look at the facts from a bird’s eye view, this would appear to be the case. For example, in the 1980’s, each American was consuming an average of 75 pounds of sugar per year (according to the USDA). One in seven were obese and 6 million were diabetic. Sugar consumption per person increased to 90 pounds a year in the early 2000’s. By then, one in every three were diabetic, and 14 million were diabetic.

The Centers for Disease Control and Prevention now estimate that 75 million Americans have metabolic syndrome. The information below is from the Centers for Disease Control and Prevention:

Unfortunately, while there is plenty of similar “circumstantial evidence” correlating sugar consumption to obesity and diabetes. The National Institutes of Health aren’t funding many viable studies that produce conclusive results. Taubes points out the flaws in several of the studies relating sugar consumption to insulin resistance:

  • There are studies that link consuming beverages sweetened with fructose to insulin resistance; however, refined sugar is half fructose and half glucose.
  •  The dosages used are perhaps too high (8-10 cans of Coke a day).
  • Insulin resistance, heart disease, and diabetes require several months to several years to develop. One meal or a few weeks’ worth of meal studies aren’t enough to establish whether or not  it is a culprit.

One reason why there has been so little attention given to sugar’s effects is because the people asserting that sugar is toxic are also advocating that saturated fat is harmless. In the 1970’s scientist John Yudkin did just this, and his work was not taken seriously because of the increasing prevalence of anti-fat biases. Dr. Atkins faced similar criticisms. Yet the fact remains that,trans fats aside, fat intake does not result in insulin resistance.

America has been quite busy with demonizing fat that it seems to have not noticed the elephant in the room: sugar. Sadly, as a result, we have little conclusive, time-tested evidence to portray sugar accurately to the general public. Thus the cycle continues: people continue to see fat as the bad guy while downing the insulin-producing sugars.

 However, Tabues is not asserting that just because many scientists have failed to exercise objectivity means we should passively wait around for them to do their jobs:

If sugar just makes us fatter, that’s one thing. We start gaining weight, we eat less of it. But we are also talking about things we can’t see–fatty liver, insulin resistance, and all that follows. Officially, I’m not supposed to worry because the evidence isn’t conclusive, but I do.

Keeping sugar intake to a minimum, watching how you feel, and keeping track of your stats (weight, blood pressure, cholesterol, triglycerides, thyroid function) is the most important research you can do.

Furthermore, plain old common sense helps. Insulin is at the center of it all. Sugar and carbohydrate consumption triggers insulin secretion; fat consumption does not. Chronically elevated insulin leads to diabetes, weight gain, high blood pressure, lower HDL cholesterol, metabolic syndrome, and even cancer. These are facts, and you can act accordingly.

Shifting Standards

Let food be your medicine and medicine be your food.-Hippocrates

Food most certainly has the power to be medicine. It also has the power to be disease-causing (which, in my book, makes it not food). I have been interested in nutrition and healthy eating for about 10 years now. And during these years, my definition of what is healthy has clearly changed.

I remember during my vegan days I used to be very anti-cheese because of its fat and dairy content. It was a topic my college roommate and I could not discuss without getting into an intense disagreement (along with abortion).Now, I learn that aged cheese is low in lactose and doesn’t spike one’s blood sugar. And I cannot deny its deliciousness. I won’t be eating cheese anytime soon, but in my dietary evaluation schema, cheese has been upgraded from “bad” to “okay.”

Another thing I have noticed that people often say foods are healthy, and then they support this statement by saying something like, “It’s has no cholesterol or trans fat.” The absence of a [so-called] negative ingredient is not enough to characterize a food as healthy.

Here are some ideas for criteria measuring how healthy of a food is:

1. Nutrient Density: Nutrients provide our bodies with what they need to function. Essential nutrients like vitamins A, D, B12, glutamine, protein, calcium, etc cannot be produced by our bodies, so they must be derived from food. If a food only provides one or two nutrients, then it’s not really nutrient dense. The more nutrients per serving, the more nutrient dense a food is.

2. Blood Sugar Impact: Low sugar and low carb is usually the best choice. Why? Because insulin resistance plays a central role in weight gain, prediabetes, diabetes, heart disease, etc.  When you ingest sugar, blood sugar rises, and the pancreas releases the amount of insulin needed to take the excess glucose and store it in the liver and muscles as glycogen.

But if your glycogen reserves are already filled up (depending your activeness and the amount of sugar you ate), then there is no room for that excess glucose in the liver or muscles. This begins the process of insulin resistance: the pancreas needs to pump out more insulin to get the same effect, the excess glucose and insulin remain in the blood stream for longer, and the sugar is eventually stored in fat cells. Furthermore, high blood sugar levels are inflammatory (which relates to the 4th point listed below).

Simply put, eating less sugar creates less of a need for insulin. Not all sugars affects our blood sugar levels the same, however. Each food’s blood sugar impact has been quantified by the glycemic index.  Foods with a lower GI rating are less likely to quickly assault blood glucose levels; this staves off accumulating insulin resistance, weight gain, inflammation, and ultimately diabetes and heart disease.

3. Authenticity: Did the food grow out of the earth, or was it processed and put in a box? Was it grown with pesticides, or was it grown organic? Were the animals treated and fed well (grass-fed), or were they oppressed and pumped with hormones? Are there ingredients you struggle to pronounce, or do you know what’s in it?

4. Immune-friendly: Do the foods contain any ingredients that trigger allergic responses? Do they create oxidative stress or contain lectins and consequently require an immune response? Allergens such as gluten, lactose, peanuts, soy, etc. can be quite problematic. And polyunsaturated fats are prone to oxidation.

5. Bioavailability: How fresh is the food? How far did it travel to get to your plate? What kind of preparation and/or  heat heat does it require to maximize one’s benefit? How easily can the body assimilate the nutrients in the food? Are there anti-nutrients?

For example, most grains, legumes, nuts, and seeds contain varying amounts of anti-nutrients known as phytic acid. They are anti-nutrients because they bind to minerals and take them out of the body with them. In other words, they prevent our bodies from getting the chance to gain benefit from minerals. Soaking, sprouting, and cooking these foods can reduce this.

I almost miss the simple days of simply counting calories, carbs, fats, proteins, etc. But I’m happy knowing that I’m getting closer and closer to a more accurate, holistic paradigm of what it means to eat in a way that keeps the doctor away.

Speaking of advertising…

I think I should just let these speak for themselves:

And now for some rebuttal:


Gotta spread the word about this toxin. Because it may be an obvious evil to people in the nutrition nerd community. But it is sadly quite ubiquitous. And eliminating it is only the tip of to toxic iceberg.

The Heart of the Matter (Part III)

The purpose of this post is to explain the process of atherosclerosis formation, or how plaque accumulates and hardens in the arteries resulting in terrible yet preventable things like high blood pressure, heart attacks, and strokes.

The traditional paradigm states that dietary saturated fat and cholesterol build up in the arteries over time to form arterial plaque. More recent research shows something different: arterial plaque is the result of arterial damage, inflammation, and oxidation.

It is important to know that the conventional view of cholesterol is negligent and oversimplified: they label HDL as the good cholesterol and LDL as the bad cholesterol. But there is more to the story: HDL stands for high density lipoprotein, and LDL stands for low density lipoprotein.  HDL and LDL are the proteins that carry cholesterol throughout the blood. We measure cholesterol by the amounts of these lipoproteins.

The key fact is that the smaller the lipoprotein, the more dangerous they are; smaller lipoproteins are significantly more likely to damage arterial walls than bigger lipoproteins.  More importantly, not all LDL poses a risk: it is the small, dense form of LDL cholesterol  that is most likely to injure the the arteries. An analogy from this post effectively gets the point across:

Think of it this way. Small, dense LDL are like BBs. Large, buoyant LDL are like beach balls. If you throw a beach ball at a window, nothing happens. But if you shoot that window with a BB gun, it breaks.

Knowing this, we can go through the basics of how atherosclerosis forms: 

1. The artery is injured.

2.  White blood cells (also called Leukocytes) rush to the scene and enter the arterial wall.

3.  They consume the offending LDL.

4. Depending on how much there is for the white blood cells to deal with, they become overtaxed with LDL cholesterol and become foam cells.

5. As these foam cells accumulate over time, they form fatty streaks.

6. In attempt to heal, smooth muscle cells cover the plaque resulting in a fibrous cap that is what clogs up the artery.

7. If the inflammation continues, the build-up progresses, and the fibrous caps become increasingly susceptible rupturing which in turn leads to blood clots or heart attacks.

To summarize, atherosclerosis begins when the artery is injured, and if the same factors that caused the initial injury persist, then the resulting, long-term inflammatory response to the injury causes a build-up of arterial plaque. Plaque cannot form unless there is a lesion/damaged spot. The American Heart Association, the government, reputable doctors, and skeptics alike are studying and documenting this.

Then what are these factors that cause the initial arterial injury? And what other factors increase the risk of  a continued inflammatory response?

Oxidation: One way to explain oxidation by starting out with its antithesis: antioxidants. Antioxidants are somewhat of a buzz word; we know they are good for preventing cancer. This is because they inhibit oxidation, a chemical reaction that can produce free radicals. Free radicals damage cells because they are missing electrons and try to take back electrons by attacking cells; antioxidants counteract this process. In short, oxidation causes cellular damage. And when the immune system senses damage, it produces an inflammatory response.

Cholesterol has been labeled as one of the main culprits in causing heart disease; however, cholesterol enables several essential functions that would require an entire other blog post to cover. It is true that there are dangerous forms of cholesterol:  as previously stated, the smaller and more dense the lipoprotein, the more likely it is to hurt the artery. Furthermore, the smaller the LDL, the more likely it is become oxidized. Oxidized LDL poses a significant threat to arterial walls.

So if you have high levels of small, dense, oxidized LDL looking for other cells to bully and steal electrons from, then you are in trouble, because that can cause an arterial injury.

So then what changes will decrease the your levels of small, dense, oxidized LDL?

  • Reduce your polyunsaturated fat (PUFA) intake. Unsaturated fat has a positive connotation in our culture (just like how cholesterol has a negative connotation). However not all unsaturated fats are the same: PUFAS are very prone to oxidation and consequently producing free radicals; monounsaturated fats are more stable. Unfortunately, PUFAs are ubiquitous and misconstrued as “heart healthy.” Avoid consuming processed foods, too many nuts, and soybean, canola, and corn oil.
  • Manage your blood glucose with a low-sugar diet. As I previously explained, high blood glucose levels and growing insulin resistance keep glucose in the bloodstream for longer. This increases the chances of glycation and Advanced Glycation End-products (AGEs): this is when a sugar molecule binds to a protein or fat molecule without an enzyme to digest that sugar. The result is an AGE which wreaks havoc by damaging cells and requiring the immune system to create an inflammatory response (which sounds an awful lot like oxidation and free radicals).
  • Eat healthy fats like butter, olive oil, and coconut oil. Gasp! Did I just say butter? But butter is a saturated fat. Yes, yes it is. And saturated fat rarely oxidizes. Furthermore, compared to grains, healthy fats are a superior source of energy because they do not elevate blood sugar levels or trigger an insulin response thus decreasing the risk of glycation and AGEs.
  • Don’t smoke, be completely sedentary, or eat trans fats and HFCS. These points are obvious and consequently do not merit elaboration.

There is plenty of evidence to support the connection between blood sugar, glycation, oxidation, and developing heart disease:

  • Oxidation and inflammation are observed as key players in arterial plaque accumulation.

In conclusion, heart disease is not as simple as this:

It is more accurately represented by this:

For more information, I recommend the following:

The Heart of the Matter (Part II)

The purpose of this post is to explain in relatively simple terms how excessive carbohydrate consumption increases triglyceride (fat) and blood pressure levels (aka the risk factors for developing heart disease). I will preface this by making clear that this is a complex process that I will not pretend to understand in its entirety; however, there are some basic concepts behind the process of arterial plaque formation that I’m aiming to outline.

For the sake of clarity, I will start off with an obvious but crucial fact: all carbohydrates we consume (e.g. candy, white flour, whole wheat bread, oatmeal, pasta, legumes, high sugar fruits, agave nectar, evaporated cane juice, quinoa, etc)  are broken down into sugar, or glucose.

Complex carbohydrates take longer to break down, so they cause a more gradual (and consequently less damaging) spike in our blood sugar; unfortunately, in the end, they all become blood sugar which triggers the need for insulin, a hormone secreted by the pancreas that manages our blood sugar levels. This leads into a discussion of the variables in developing heart disease: 

1. Insulin Resistance:  When you ingest sugar, blood sugar rises, and the pancreas releases the amount of insulin needed to take the excess glucose and store it in the liver and muscles as glycogen. This is certainly useful for having energy reserves stored for later if need be.

But if your  glycogen reserves are already filled up (depending your activeness and the amount of sugar you ate), then there is no room for that excess glucose in the liver or muscles. This begins the process of insulin resistance: the pancreas needs to pump out more insulin to get the same effect, the excess glucose and insulin remain in the blood stream for longer, and and the sugar is eventually stored in fat cells.

2. Glycation: Glucose should not be present in the bloodstream for longer than necessary; the longer it floats in the bloodstream, the higher the risk of glycation. Glycation occurs when a sugar molecule like glucose or fructose  binds to a protein  or fat molecule without the protective help of an enzyme. Without an enzyme to moderate the reaction that protein or fat molecule gets damaged.

More importantly, this reaction leads to advanced glycated end-products (AGEs). AGEs can degrade any cell in the body, and the accumulation of their destruction signals an inflammatory response.

3.Inflammation: Generally speaking, inflammation is defined as the immune system’s response to damaged cells, foreign invaders, toxins, etc. If you hurt your leg, it might swell and bruise. While it hurts, this is the immune system initiating the healing process. This is an example of a straightforward case of acute inflammation.

Chronic, low-level inflammation, on the other hand, keeps your body in a state of alarm: the immune system is waging a constant battle that is neither significantly traumatic nor ignorable. This battle often requires the expenditure of cytokines and various types of  infection-fighting white blood cells like monocytes and macrophages. The longer the inflammation goes on, the higher the risk of tissue damage.  In short, regular, excessive carb/sugar consumption leads to chronic AGEs which lead to chronic inflammation.

Below is an image of a glucose molecule binding to a protein molecule to produce an AGE that triggers an immune response from a macrophage:

Luckily, there are ways to quantify inflammation and blood glucose levels. Inflammation is often measured via a white blood cell count (WBC) and C-Reactive Protein (CRP) level. A 1-h plasma glucose test measures short-term (one hour to be exact) blood sugar levels, and Hemoglobin A1c (HbA1c) measures long-term blood glucose levels. Knowing this, let’s tie the evidence together:

  • There is a link between inflammation and insulin resistance: this study establishes a connection between insulin resistance and inflammation, again, in nondiabetic people. Inflammatory markers like CRP and white blood cell counters were associated with insulin resistance, and CRP levels were positively correlated to weight.
  • High blood sugar levels have been studied as a risk factor for heart disease. Another study also finds a connection between HbA1c levels (long-term blood glucose) and heart disease.
  • AGEs are correlated to to inflammation and atherosclerosis in diabetics.
  • Chronic inflammation is also strongly correlated to heart disease. One study observed a higher incidence of aortic inflammation with people who have inflammatory rheumatic disease than those with no inflammatory diseases.

So if atherosclerosis isn’t the mere accumulation of dietary fat and cholesterol, then how does it form?

To be continued….

The Heart of the Matter (Part I)

Learning about my own symptoms, blood test result history, and state of health has helped me to learn about the variables that contribute to being healthy. They aren’t always what they seem to be.

I want to expound on the fact that my triglycerides ( the amount of fat in my blood) have decreased over the past six years in spite of all of the butter, coconut oil, olive oil, and  mac nut oil  I’ve been eating almost daily for about a year now.  Triglycerides are the best predictor of nascent heart disease:  higher triglyceride levels increase chances of that excess fat hardening in and clogging up your arteries.

So I’ve been eating more fat, and less fat is showing up in my blood.  Why would that be? Let’s take some general “before” and “after” pictures of my diet and lifestyle:

  • When I was 21, I ate Larabars, Stonyfield farm yogurt, Natural Ovens bagels, dark chocolate, peanut butter, walnuts,  tofu, fake soy meat,  fruit, wheat pasta, POM juice, broccoli, and carrots. My triglycerides were 65 mg/dL.
  • When I was 25, I started to decrease my sugar intake when I figured out I had Candida. I didn’t give up sugar or grains entirely (I still ate oatmeal, apples, cheerios, dark chocolate, etc) but I definitely started to transition into a low carb and high fat diet. My triglycerides were 54 mg/dL.
  • I am 26, and I eat  3-5 daily servings of vegetables along with 2-4 eggs, nuts, and the fats mentioned above. I will have the occasional starchy acorn squash or sweet potato about twice a month. My triglycerides are 45 mg/dL.
  • It should also be noted that when I was 21 I did more exercise than I do now. (And, to add to the irony further, my current weight is 10 pounds less than my weight then).

So then what’s the difference? I have switched from grain-based carbs to vegetable-based carbs, removed the sugar, and replaced carbs/sugar with fat for my energy source.

My experience is not an isolated incident. There are several other studies manipulating the same variables that yield similar results:

  • In a low carb/high-fat vs. low fat/high carb study, the low carb/high fat group had a significant reduction in triglycerides, blood pressure, and VLDL (the worst of the bad cholesterol) after six months.
  • This study links carbohydrate restriction with reduced body weight, LDL cholesterol, and triglyceride levels.
  • A meta-study recently published in the American Journal of Clinical Nutrition summarized data from 21 cardiovascular disease studies entailing 350,000 people over a span of 14 years and the results are in: saturated fat does not cause heart disease.
  • Given all the mainstream emphasis on low-fat diets, I was surprised to read that even the American Heart Association says that a diet composed of 60% or more of carbohydrates is at a higher risk of developing unhealthy triglyceride levels.

Wow. My understanding of excessive sugar consumption is expanding: it isn’t just about managing a predominately female issue like Candida (although men can are not exempt); it’s about preventing cumulative and fatal illnesses like heart disease.

The key question is why does excessive carbohydrate consumption increase triglyceride and blood pressure levels? And why doesn’t saturated fat consumption increase triglyceride levels?

It certainly makes sense to think that eating foods with saturated fat and cholesterol would contribute to heart disease: the plaque that hardens in the arteries is composed of fat and cholesterol.

However, the development of heart disease is a consequence of interdependent factors: chronically increased insulin levels feed into inflammatory and oxidation responses which create a breeding ground for raised triglycerides, blood pressure, weight, etc.

To be continued…