Sneak Peak of my E-book Part 1

Good Day Folks!

With this post, I wanted to let everyone know that There will be a product in my store! The product is a 7-day startup guide.

In this guide, I take you through the first 7 days and I give you tips and tricks to help you turn this diet into a lifestyle. Later this week, I will be writing up a full post about it to let you know what you can purchase.

Today, however, I wanted to post part three of my three-part appendix on why we should avoid sugar.

Sugary Epidemic Batman!

Let’s start this section with another long quote from a journal article, but this time it is just from the abstract. I want to clarify why I oftentimes say diabesity instead of obesity and diabetes.

Here is the quote from the abstract:
The relationship between obesity and diabetes is of such interdependence that the term ‘diabesity’ has been coined. The passage from obesity to diabetes is made by a progressive defect in insulin secretion coupled with a progressive rise in insulin resistance. Both insulin resistance and defective insulin secretion appear very prematurely in obese patients, and both worsen similarly towards diabetes[9].

The main point I want to zero in on is the role of insulin in our current epidemic. Before I dive into the issue, I want to talk about the reason the rise in diabetes and obesity are truly an epidemic, I am not calling it that for effect, I am simply using the same verbiage that the medical journals, PhDs, Doctors and other influential people from this field are using. Speaking of Doctors, a paper by Robert Lustig called, “Sickeningly Sweet: Does Sugar Cause Type 2 Diabetes? Yes” gives us a good set of numbers to look at so we can get a thumbnail sketch of our current health breakdown. The paper starts off mentioning that, “type 2 diabetes mellitus is a hallmark disease, affects more than 25% of the adult population in the United States… while prediabetes is currently estimated to be present in up to 40% of adults[10].” That means in a group of 20 friends statistically speaking 5 would be a type 2 diabetic, and 8 others would be on the road to diabetes, That means only 7 out of every 20 people are actually healthy individuals.

So, should we assume that only our fat friends are obese and suffering from type 2 diabetes? Not quite, to add a further wrinkle, the article also states that, “People forget that 20% of morbidly obese individuals are metabolically healthy and have normal life spans, while up to 40% of normal-weight adults harbour metabolic perturbations similar to those that occur with obesity, including hypertension, dyslipidemia, nonalcoholic fatty liver disease and cardiovascular disease[10].” So your scale weight does not determine your risk for diabetes, then why did I send to much time talking about diabesity? This is because the common factor is, our bodies becoming desensitized to insulin; you can become insulin resistant no matter if you are obese or not, heck age isn’t even a factor anymore.

Dr. Lustig also mentions, “children as young as 1 through 10 years of age now manifest these same biochemical processes[10].” Let that sink in for a moment. Dr. Lustig said 1-year-old infants are developing type 2 diabetes. Keep in mind this is not type 1 (put simply type 1 is an autoimmune disease where your body does not/ cannot make insulin), but it is type 2. Again type 2 is caused by insulin resistance, meaning these babies are getting more sugar than their developing bodies can handle.

When I read that, I had to fight off a mixture of tears and anger, because my little guy in 9 months, how can a child that can barely walk be given of much insulin that they cannot regulate it. That makes no sense to me. Again this is where I refer back to the paper because Dr. Lustig also brings up similar question about the cause of insulin resistance, “So what is the cause, a cause that everyone is exposed to? And how is it that children experience this degree of metabolic dysfunction[10]?”

He then goes on to answer:
Most people consider sugar (i.e. fructose-containing compounds) to be just “empty” calories. Rather, the studies mentioned herein demonstrate that the fructose moiety of sugar is toxic in chronically high dosage unrelated to its calories and is a significant contributor to metabolic syndrome. Sugar recapitulates all the chronic detrimental effects on long-term health, as does alcohol. This is why our children now get the diseases related to alcohol (type 2 diabetes, nonalcoholic fatty liver disease) without consuming alcohol. Sugar meets all the public health criteria for regulation[10].

Said another way: Sugar is not empty calories, but they are toxic calories, along the same lines are alcohol, in terms, the need for regulation, and it is along the same lines as other controlled addictive substances.

Wow, this sweet section blew up… it was originally only going to be 1-2 typed pages. In the words of Tolkien, “the tale grew in the telling.” Also, I seem to have the gift of gab when I get excited about what I am writing about. Since I mentioned things I get excited about, it is finally time to talk all things grains! Well, see how long this tale grows. See you in the next section.

Resources (these are the resources for the three-part section instead of the one section I posted):

[1]: https://www.heb.com/product-detail/sun-maid-raisin-bread-cinnamon-swirl/2017755

[2]:http://www.sunmaid.com/products-details/raisin-bread-chocolate-covered-raisins-raisin-muffins-cookie-mix.html

[3]:https://www.fda.gov/Food/IngredientsPackagingLabeling/FoodAdditivesIngredients/ucm094211.htm

[4]: https://health.gov/dietaryguidelines/dga2010/dietaryguidelines2010.pdf

[5]: http://sugarscience.ucsf.edu/hidden-in-plain-sight/#.WmrPKjdG200

[6]: http://bjsm.bmj.com/content/early/2017/08/23/bjsports-2017-097971

[7]:https://www.smithsonianmag.com/smithsonian-institution/when-did-Americans-Lose-British-accents-ask-smithsonian-180955291/

[8]:https://www.researchgate.net/publication/233750937_Sack_and_sugar_and_the_aetiology_of_gout_in_England_between_1650_and_1900

[9]:https://www.ncbi.nlm.nih.gov/pubmed/16311223

[10]: http://www.canadianjournalofdiabetes.com/article/S1499-2671(15)30072-1/pdf

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