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Type-2 Diabetes, genes and gene expression

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Two recent news articles announced discovery of 13 gene variants that make us susceptible to developing type-2 diabetes later in life. The point of this article is that you don't have to be a victim of genetic variants; you may be more susceptible to some disease of aging, but you don't have to accept it as your fate. The variants discussed are called Single Nucleotide Pair variants or SNPs.  SNPs are the simplest variation that a gene can have; only one letter in the code is changed in a place that changes the molecule produced from the gene. It is like the word "confiscate" being changed to the word "codfilcate". That letter sequence change has two SNPs in the code changed, but each involves only a single letter change, as opposed to 2 or more adjacent letters changed.

In these studies, thirteen new SNPs have been found in genes relating to glucose metabolism, blood sugar levels, insulin levels and insulin resistance. If you have one or more of these variants, they may make you more susceptible to developing the problems associated with metabolic syndrome and type-2 diabetes, but they don't necessarily insure that you will. There are choices that minimize the probability, and these choices involve what you eat, when you eat and whether you move your body enough to keep your metabolic hardware working properly. The health science industry is hoping to benefit much with this genetic information - primarily by making drugs that will treat the symptoms of this now epidemic "disease",  which will allow us to continue eating the wrong foods and watching TV, while buying drugs-for-life to abate the symptoms.

 

The real cause of this epidemic is how we eat, and how we move our muscles, which strongly affects our gene expression. Our eating and exercise patterns dramatically control which of our genes are turned on and which are turned off, and are far more important than this catalog of SNPs in determining our health and fitness as we age. This is critical to understand. The most profound of recent science relates to just how dominant the influence of food and exercise is on gene expression and health or the lack thereof. If you eat primarily sugar-laden foods with altered fats or proteins, you turn on the genes required for building large fat stores and ramping up inflammation; genes that slow your metabolism, slow down thyroid and adrenal gland function, inflame your arteries, destroy your joints and shrink your brain.

The primary health-killing food culprits are:

  • Refined and hydrogenated fats and oils in place of natural oils as found in seeds, nuts, fruits (such as olive and avocado) and grains.
  • Manufactured food products that are loaded with sugar and high fructose corn syrup, altered oils, "flavorings", MSG, chemical preservatives, and have natural vitamins, oils and minerals removed and replaced by synthetic pseudo-nutrients.
  • The rampant use of soft drinks, diet or sugar-filled, instead of real water for liquid intake.
  • Grain-finished meats and farmed fish with much lower levels of omega-3 fats than they would have if naturally feeding on their wild diet.
  • Eating belly-stretching amounts of food at mealtime - every excess above needed calories promotes the expression of genes required to store calories as fat and leads to reduced ability to burn fat for energy.

When we eat also had a powerful influence on gene expression. The primary impacts of eating too frequently are elevated baseline insulin level and interruption of leptin signaling. This is a recent discovery, and not well understood. We can control our appetite by snacking between meals, so that we don't feel compelled to gorge at meal time. The popular wisdom is that eating healthy (real) foods like nuts or fruit or vegetables (not potato chips and other junk) suppresses binging and overeating patterns. Most people who use this strategy do lose significant weight and girth, and keep it off for years. What is less understood is that this pattern leads to persistently elevated leptin and insulin in the blood, and eventually drives your metabolism toward metabolic syndrome anyway. This author is a classic example: low body fat for decades, controlled by consistent exercise and eating small, frequent meals, but eventually acquiring all the symptoms of metabolic syndrome, including high fasting blood sugar, sky high cholesterol and triglycerides and the need for a quad bypass operation in 2001 at the age of 61.

The not-so-obvious reasons for this are rigorously developed and explained in Byron Richards' book Mastering Leptin, the 3rd edition of which was published in 2009. If you really want to understand leptin, insulin, the obesity epidemic and why we get fatter as we age, this is a great book to read carefully. His solution is very simple, and it has worked very well for this writer:

  • Eat 3 reasonably sized meals per day; never eat to fullness
  • Eat nothing and drink only water between meals, allowing 5-6 hours for insulin to return to baseline and the liver to supply blood sugar made from stored fats
  • Make Breakfast a meal with significant protein intake
  • Eat nothing after dinner or before bedtime - this is the critical time for the liver to perform its detox functions and to convert stored fat to energy for repair and restoration overnight
  • Reduce carbohydrate intake, get most carbs from fibrous vegetables, not starchy sources like grains and potatoes

When you put these strategies into action, energy levels rise, appetite slackens, the brain works better and the desire for excess carbohydrates goes away. For the vast majority of people, the obesity epidemic is a matter of food choices, meal size and spacing, and lack of regular physical movement. Carrying excess body fat is for most people a fast track to rapid aging and degenerative disease. Don't wait for the medical industry to come up with another drug to fix it - we already have the tools to eliminate the problem.



By Frank Wilhelmi BSE, ME
All rights reserved. Any reproducing of this article must have the author name and all the links intact.

Author: BSE, ME

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