Artificial Sweeteners Are Not Healthy Or Natural
Originally published on February 28, 2023
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A study came out yesterday called “The artificial sweetener erythritol and cardiovascular event risk,” published in the Journal, Nature, February 27, 2023, showing a near 200% increased risk for heart attacks and stroke in people using erythritol sweeteners.
The near two-fold increase in Major Adverse Cardiac Events (M.A.C.E.), including death, compared the lowest 25% use to the highest 25%.
It is important to note that the 200% higher risk was compared using a lot vs. just some erythritol, but not comparing using some to using none.
We already know that using any artificial sweeteners increases MACE compared to non-users, summarized in a paper published in the British Medical Journal (BMJ) last year titled, “Artificial sweeteners and risk of cardiovascular diseases: results from the prospective NutriNet-Santé cohort.”
The irony is that many people use this artificially manufactured sweetener to avoid sugar and the associated diseases of diabetes and heart disease when a 200% increased risk, as shown above, puts the risk levels for MACE at par with diabetes and heart disease! Just now, without the sugar it replaced.
Let’s be honest. Most people selectively use this and other sweeteners for drinks, coffee, and some baking, but do not replace all sugar, thus maintaining diabetes and heart disease risk and adding the MACE risk.
So why is it so hard for people to give up sweets?
Because we are hardwired to love it!
Fructose from fruit is the sweetest substance we can find in nature and is 2.5 times sweeter than glucose.
Eating fructose numbs the hormonal receptors that cause us to feel satisfied from eating, so we don’t feel full from eating it, and it cranks up the hunger hormone to make us hungrier for more.
The result is the perfect hormonal equation for overeating.
But why would our body seem to set us up for dietary overeating like that?
In the development of our genetic evolution, fructose was only found during the late summer and for a very short period of time. When we found it, we ate it, loved it, and we ate all we could while we could.
But still, why?
Simply put, fructose is metabolized directly into fat, liver fat to be specific, and is not circulated to the rest of the body or used there.
Liver fat is stored for medium-term use. Glucose is stored in the liver and muscle as glycogen for short-term use, and body fat is held under the skin for long-term use.
Visceral fat is stored to get us ready for some sort of action. Bears do it for hibernation, birds for migration, fish for their dormant season, and so on.
Humans activate the addiction pathway when eating fructose and storing visceral/liver fat to get ready for the winter months of scarcity or fasting.
The problem is we don’t hibernate, migrate, have a dormant season, or fast, so the preparation gets us ready for action, and we do nothing.
The result is a year-round fed state preparing us for an action that never comes and leads us to fatty liver, insulin resistance, and eventually weight gain, addiction, and all chronic metabolic diseases.
The good news is that the medium-term fat that accumulates in the liver and viscera can be easily accessed and reduced very effectively through different types of intense exercise and rotational fasting models.
The bad news is that once we start that metabolic fat accumulation and stay in that chronic fed state for years or decades, it changes our physiology (DAMP = Damage-Associated Molecular Patterns) and causes damage (Advanced Pathological Insulin Resistance Spectrum).
The damage can be reversed, but losing weight or lowering cholesterol or blood sugar levels will not fix it. It takes a lot more work but still beats the alternative.
More on exactly how this is done and what you can do to stop this process or reverse it can be found on my page or in my group, “Insulin Friendly Fasting Secrets.”
If you are beyond the point of reading more and need to make a change now, contact me, and we can see what can be done today!
We can do better,