We know that an accumulation of fat on the interior of artery walls–known as plaque–causes artheriosclerosis and contributes to heart disease. What a recent study has shown is that low-density lipoprotein (LDL, the “bad” cholesterol) plays a role in the signaling pathways of certain proteins by affecting how they relate to other proteins.
Dishevelled and Frizzled
Certain proteins in the body (Wnt) are the traffic cops between cells; they orchestrate and influence how cells interact and develop. A particular protein, called Dishevelled, can be found at the branch point of these cell interactions. Cholesterol activates a chemical called beta-catenin that is responsible for embryonic development and adult cell stabilization. Stimulation of this chemical affects Dishevelled and how it acts with other proteins.
The activated protein is transformed into Frizzled, which then enriches the cholesterol and other LDL-related proteins. This chemical transaction then, in turn, affects the signaling pathway from whence it came.
Because high levels of LDL cholesterol–without the balancing of high-density lipoprotein (HDL, the “good” cholesterol)–affect how cells interact and distracts them from normal communication, abnormal cells can develop. Cancer.
This discovery not only indicts LDL in its part in the development of cancer but it isolates the specific reason why: by virtue of its effect on the cellular communication system. The lead researcher from the University of Illinois summarizes:
“We know that things like high-fat diets, which boost cholesterol levels, have been linked to an elevated incidence of cancer. Our research provides a mechanism for how cholesterol promotes pathways that lead to cancer…Our research points to a new regulatory role for cholesterol, and also presents an exciting new therapeutic target for suppressing canonical [involving beta-catenin] Wnt signalling to treat or prevent cancer.”
The hope is that, by narrowing the specific protein responsible for this chain of events, a drug can be developed that will disrupt the binding of LDL to Dishevelled, preventing abnormal cell growth.
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Better yet, if we reduce the amount of LDL in the body and achieve a balance between LDL and HDL, we can prevent the attachment of cholesterol to the protein on a cellular level to begin with.
Cholesterol isn’t the bad guy, per se–we need this substance in our bodies to protect nerve fibers and allow the conduction of electricity. It is also necessary for the production of certain hormones, like cortisol, estrogen, and testosterone. By making a few changes, we can rebalance cholesterol levels, painlessly and pharmaceutical-free.
If you are overweight or concerned about your cholesterol level, ask your healthcare provider to test for it. You’ll then have a starting point, a benchmark by which to rate any changes you make.
- Stop or drastically reduce eating processed foods and trans fat. Today. These are artificial and the body doesn’t metabolize them properly. The additives and fat hang around in the body and stick to artery walls.
- Increase intake of coconut oil and fiber from whole grains (like quinoa) and vegetables. Eat more fish that is rich in omega-3 fatty acids. Use olive, coconut, or sesame oils in cooking rather than vegetable and seed oils like corn, soy, and canola. These latter fats are heavily processed and have virtually no nutritional value.
- By all means, exercise more. However you like. Exercise raises heart rate, promotes blood oxygenation (cancer doesn’t like oxygen) and circulation, and makes every cell in your body work better. You’ll sleep better, feel better, and look better.
- Cut out refined and added sugars. It is excess glucose that causes high cholesterol and weight gain, not fat.
High LDL isn’t a death sentence, it’s a red flag. Pay attention and adjust and you’ll have plenty more laps left to go before the checkered flag.