Posts Tagged ‘questions’

Retroactive Hope

I  have been enjoying the television series Mad Men as of late. My boyfriend and I weren’t really into watching television, but we got hooked and plowed through all four seasons a few months ago. And now I’ve been re-watching it. It is a well-written series with meticulous attention to visual detail. The cast is talented, and the leading actor is painfully handsome. This makes watching the often idiotic characters doing repeatedly idiotic things bearable. 

Furthermore, it is a show about advertising executives at a company (Sterling Cooper) who make large sums of money. Their biggest client is a tobacco company called Lucky Strike. The main characters are rich because they help propagate an addictive, dangerous drug. In spite of all this, it is an engaging, well-made show with solid acting.

The ubiquitous nature of smoking in the show reflects the time the show takes place in: the 1960s. It is both amusing and tragic to see people constantly and compulsively lighting up: while they exercise, when they wake up in the middle of the night, or even while they are pregnant. The acceptability of smoking and drinking while pregnant is frightening.

We now know better and look back on that time as perhaps naive, ignorant, or simply too hooked to be willing to face the facts. But of course, it is easy for me to judge 50 years later.

I wonder how our predecessors will look back on this time in a few generations. What stupidities will they laugh at? What, if anything, will become unacceptable?

I can only hope that sugar is exposed for what it is. It would be great if people would look back and shake their heads in shame at the prevalence of high fructose corn syrup the way we shake our heads in shame at a smoking pregnant woman.

I hope lists like this are taught  in schools along side the dangers of smoking, hard drugs, and drinking. And that cutting dietary sugar becomes part of the standard treatment protocol for treating ADHD, Autism, GI dysfunction, diabetes, hormonal imbalances, hypertension, chronic fatigue, cancer, etc

Sigh, to dream.


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 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…

The New Pollution

One can follow the perfect diet and stick to an optimal supplementation protocol, but the truth is that we are inundated with environmental toxins every day. They can impede efforts to heal.  I have been aiming to reduce my exposure to some of these toxins:

1. Fluoride: Ever since one of my doctors told me it is a counterproductive carcinogen, I’ve been playing around with different fluoride-free toothpastes. Tom’s of Maine and Burt’s Bees have some decent toothpastes. I currently am using Jason’s toothpastes. In terms of sheer functionality, all of these do a good job of cleaning my teeth (and I have no cavities). I am, however, still in search of the right flavor. I’m a big cinnamon fan and not much of a mint person; Jason’s Cinnamon Mint flavor will have to do.

2. Chlorine: I just bought a shower filter, and I have been filtering my water twice (once with a PUR filter and once with a Brita filter).  Apparently chlorine is like an antibiotic: it kills the good bacteria in the gut. That’s just what I need. Apparently chlorine evaporates, however.

I was also reading in this book that chlorine and fluoride generate oxidized cholesterol/ oxysterols in the body. Oxysterols/oxidized cholesterol initiate plaque buildup in the arteries. Without oxidization, cholesterol is harmless to the arteries.

3. BPA: I just treated myself to a BPA-free water bottle from Camelbak. It’s a good size, pretty easy to clean, and has a permanent “straw” that doesn’t leak and keeps orally fixated people happily sipping.

This is just a beginning, however. I need to do  more research on decreasing the fluoride in the water I drink. My boyfriend suggested using a de-humidifier to provide drinking water: water from the air hasn’t been treated with chlorine or fluoride. But what other toxins might be present?

And most commercial water filters say that reduce the “taste and odor” of chlorine, but do they actually remove it?

If I had more money to spare, I’d invest in some stainless steel cookware and a glass tea kettle.

Can we trust anything in our daily surroundings anymore? When seemingly innocuous things like water and plastic can become destructive, it’s hard to resist paranoid cynicism.