Updated: May 6, 2019
We have always heard that being overweight is unhealthy. To be sure, science has never identified a level of fat that is a risk, per se. However, recently studies have attempted to tell us that there is actually a paradox that exists whereby being overweight may help protect some patients with an increasingly long list of medical problems, including pneumonia, burns, stroke, cancer, hypertension, and heart disease from premature death.
But that’s not the whole story, it never is. The paradox is flawed for a myriad of reasons including the fact that overweight people suffer more disease than healthy ones, and they live shorter lives overall. To be clear, scientists do not yet agree on what the paradox means for health, and more concerning, many are beginning to accept the evidence behind it.
That’s actually quite scary.
The paradox is this: fat people have a better chance of survival from disease than thin ones. The premise is not entirely inaccurate, but its not because the person was fat. It’s more likely that life threatening diseases, such as cancer, cause the patient to lose a lot of weight, and that weight loss places the patient at risk of death. It stands to reason that the more you can lose, the better your chance of survival.
But let’s look at this scientifically (and logically too). First off let’s look at a study by the NHS (British National Health). This study was not a small study. This study involved 3.5 million people of which 766,900 (21.9%) were considered obese with other risk factors and 518,000 (14.9%) were obese with no risk factors other than being overweight.
The researchers found that the obese participants had a 50% greater likelihood of heart disease, 7% more likely to suffer stroke and twice as likely to suffer heart failure.
For those who were obese but had no additional risk factors, they were 2.6 times more likely to get a heart attack, 58% more likely to suffer from a stroke, 3.8 times more likely to get heart failure and 2.2 times more likely to suffer from peripheral vascular disease.
So, the problem with this new line of thinking, that fatter is better, is fundamentally flawed. For those with disease a little extra padding might help them survive the ordeal of treatment. However, the very reason they may have needed treatment in the first place was due to the extra padding! Not only a paradox, but an ironic one at that.
Perhaps the issue is the way we think about fat. It is very dangerous to assume that the fat cell is simply a reservoir for the storage of fat and nothing else. This cannot be further from the truth.
Let’s first look at disease. Anytime someone presents with any form of disease, including chronic illness, the underlying factor is uncontrolled cellular inflammation. This cellular inflammation is a factor in cardiovascular disease, diabetes, cancer, arthritis and most all auto-immune complaints and just about any disease.
While we used to think that being obese was a symptom; an inconvenient risk factor, today it is actually considered a disease. Why you ask would it be? The answer is simple. It is now known that obesity always presents with low grade, chronic inflammation which, if left unchecked, is a gateway to the development of metabolic and cardiovascular disease. In short, obesity is a precursor to disease because it causes chronic inflammation, which leads to disease. Obesity is now akin to high cholesterol and high blood pressure as a predictor of what’s to come.
Before we get into this, yes, it is true that inflammation is a protective reaction of the human body to irritation, which leads to healing. But acute irritation, such as from tendonitis is considered short term (we call it acute) while chronic inflammation (long term) is, well, chronic.
To explain this concept, but still keep things simple, let me explain a little about the inflammation cycle. At the point of injury, the body responds by several protective mechanisms that usually include both muscle spasm and muscle inactivation. This is followed by the production of fluid around the area (swelling) to further protect that area.
The next step is generated by the nervous system. It involves the release of chemicals which enhance pain. Again, this is protective. It stops you from ignoring movements that might cause more damage.
Around and between all your cells is a fluid filled space called the extracellular space. The fluid in that space is called Interstitial Fluid. This fluid is a vital part of your circulatory and cell-nutrition system. Not only do you have fluid pumping through your arteries, and returning to your heart from your veins, but you also have a lymphatic system that drains old cells, bacteria, immune system cells etc. from your body and eventually out.
Your veins return about 20% of this fluid pumped from your heart back to your heart.
The other 80% is Interstitial Fluid in your extracellular space, and that is returned by the lymphatic system and eventually eliminated from your body.
So, when fluid gets trapped in the area, it means that the extracellular space gets filled up with more and more fluid. Which we now call edema.
Nutrition now has a harder time getting to its target cells because the extra fluid in the area reduces cellular absorption. Thus, you can essentially starve cells when you have inflammation going on, which reduces the health of that cell.
So, short term this is not a huge issue. Acute irritation from an injury is a protective response and allows for tissue recovery. But, when the inflammation gets chronic, as in the case of obesity, the chemical messengers, derived from different cellular activities begin to cause a decline in that cells activity and the swelling reduces its ability to receive proper nutrition. The long-term effects lead to a weaker cell. See the difference?
Now, the fat cell (which is not a simple holding reservoir) is now considered part of your immune system whereby it is able to contribute to the health (and decline) of your body in many ways. Visceral fat, which is the deep fat around your organs (considered belly fat), is associated with chronic low-grade inflammation. Visceral fat is also considered the single most problematic contributor to metabolic disease through insulin resistance and the promotion of atherosclerotic plaque accumulate in the blood vessels.
The second most problematic contributor is inactivity. However, when you combine visceral fat accumulate with inactivity, poor nutrition and advancement in age, the effects of inflammation become more pronounced.
It turns out that visceral fat is highly metabolic and causes an increase in cytokine activity. Cytokines are a class of protein that is involved with pain and inflammation. In visceral fat, they are called adipokines, meaning they are secreted by the fat cell. But that’s not the end of the story. This constant low-grade inflammation also forces changes in leptin, resistin and adiponectin.
Adiponectin is considered an antiatherogenic agent. That means it helps prevent the development of atherosclerotic plaque and also slows the progression of plaque accumulate in the arteries, specifically the heart vessels. It’s mechanism of doing this is to inhibit adhesive molecules (such as sclerotic-LDL) from contributing to the formation of a blockage. In the liver and skeletal muscle, it serves to promote insulin sensitivity and lower triglycerides. However, visceral fat lowers the concentration levels of adinonectin, which in turn leads to a higher accumulation of plaque and lower sensitivity to insulin (that means belly fat increases the risk of blocked arteries, heart attacks and strokes and type II diabetes).
Leptin is "the hormone of energy expenditure". It is a hormone which is produced by adipose cells. Leptin helps regulate the metabolism and also inhibits ghrelin, the hunger hormone. It acts in conjunction with the hypothalamus.
In obesity, the over accumulation of fat cells leads to a decreased sensitivity to leptin. This results in an inability to detect satiety despite high energy stores and high levels of leptin. In other words, your body cannot detect when it is full, leading to overeating.
This change in leptin due to visceral fat has been recognized to contribute to insulin resistance and, since it increases fat accumulation by blocking satiety, it contributes to low-grade inflammation and cardiovascular risk factors.
Finally, with increases in visceral fat we find an increase in resistin. Resistin is also known as adipose tissue-specific secretory factor or C/EBP. It too increases in concentration with obesity, contributes to inflammation and may be associated with the progression of arteriosclerotic plaque formation. It also promotes insulin resistance. It’s a big word with a bad affect.
The resistance to insulin is a mechanism whereby the cells do not respond to normal levels of insulin anymore. The cells now require more than is produced and so the cell fails to absorb blood sugar and thus leads to diabetes. Insulin resistance as it’s called, is also influenced by free fatty acids (free floating fats that have not been stored in the fat cell yet or attached themselves to a glycerol molecule to become triglycerides).
These fatty acids are liberated from the visceral fat and absorbed by the liver. Visceral fat release certain chemicals and fatty acids into the portal system (that which supplies the liver) where it influences the liver and spleen. But less understood is the fact that the portal system is specialized whereby it also connects the organs and the liver. Any excess fat in the portal system is also shared by the other organs, all of which act negatively with the effects of insulin resistance. The more the accumulate of fat, the worse the effects. This has an effect on the sympathetic system where by there is a heightened activity of the breakdown of fat into fatty acids, creating more fatty acids (fat) in the blood, producing more beta cell activity, reduced insulin clearance and eventually high insulin in the blood. In other words, diabetes.
Two of the markers medical science uses to measure inflammation is interleukin-6 (IL-6) and C-reactive protein. IL-6 levels are typically found as high as 50% greater in the portal system of obese patients. Since IL-6 correlate well with C-reactive protein levels, you can quickly see how detrimental visceral fat can be to your health. C-reactive protein is well associated with cardiovascular and peripheral vascular disease.
Based on the research, it is evident that low-grade inflammation is a leading cause of atherosclerosis, diabetes, cancer and coronary heart disease and premature death and visceral fat is central to that inflammation. So being overweight is nowhere near being healthy.
The question is how do we get rid if visceral fat?
There are three things that you need to focus on to change your visceral fat content. First, and perhaps most important, is to cut back on sugars and starches (processed carbs). This will begin to switch your body into taking fat as a fuel rather than burn the readily assessible sugars from carbs and sugary foods.
Another benefit of cutting carbs is that it lowers insulin levels, and insulin sensitivity, something that leads to diabetes and coincidentally less fat burning.